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Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease

3rd Edition

Developed by the Council on Renal Nutrition of the National Kidney Foundation

Editor: Linda McCann, RD, CSR, LD


Satellite Healthcare
Redwood City, CA
Primary Reviewers: Alice Chan, RD, CSR, LD Houston, Texas
Lori Lambert, MS, RD, CDE Boston, MA
Secondary Reviewers: Susan Reams, RD, CSR, LD Des Moines, IA
Nancy Spinozzi, RD (Peds) Boston, MA

FORWARD

This revision of the Pocket Guide was undertaken to update trends in clinical practice and to incorporate the recommendations of
the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (K/DOQI). Every effort was made to obtain and
provide the most up to date information. Where information differs from previous versions or references, the most recent was used.
As is common with such a resource, and in view of the rapidly developing K/DOQI guidelines, it is difficult to find a point at which
publication moves forward rather than wait for new guidelines and initiatives. Thus, the revision and review process has been lengthy,
affecting the publication of this edition of the pocket guide.
For those who are new to this resource, the primary goal has been to compile nutrition assessment information in a concise and
abbreviated format so that it could truly be a “pocket guide.” In the interest of keeping it concise each piece of information is
evaluated for inclusion with that primary goal in mind. The balance between too much and too little information is difficult to achieve
because of the wide variation of practice within the target audience. For experienced clinicians, the book may provide a concentrated
source of information they know and use on a regular basis. For the less experienced clinician, it may provide a base on which to
build clinical expertise. My hope is that the Pocket Guide will provide tools that enhance the commitment to consistent, high quality
nutrition care for all chronic kidney disease (CKD) patients.

Where appropriate and available, references are cited for further exploration of a particular topic. The book is not all inclusive. In
some cases the information is a compilation from many sources and input from experienced renal dietitians. On almost every topic
there will be varied opinions. The information herein is not meant to dictate clinical practice, but to provide practical resources. It is
the responsibility of individual clinicians to keep their knowledge base current and to interpret and modify their resources to reflect the
policies, procedures, and philosophies of the specific practice setting.
-Linda McCann, RD, CSR, LD

This book was published with an educational


grant to the NKF-Council on Renal Nutrition from

Redwood City, CA
www.satellitehealth.com
Net Nutrition A-Z

The K/DOQI seal


ensures accurate
interpretation of the
K/DOQI clinical
30 East 33rd Street practice guidelines.
The symbol has been
New York, NY 10016 added to the pages that
(800) 889-2210 were reviewed and
approved by K/DOQI.
www.kidney.org

© 2005 National Kidney Foundation, Inc. All Rights Reserved


Pocket Guide to Nutrition Assessment of the Patient with Chronic Kidney Disease

Acronyms and Abbreviations


AA/aa - Amino acids
ABW – Adjusted body weight
AIDS- Acquired immune deficiency syndrome
ARF - Acute renal failure
APD - Automated Peritoneal Dialysis( )TjETEMC /P </MCID 8.10.00is
Pocket Guide to Nutrition Assessment
of the Patient with Chronic Kidney Disease
TABLE OF CONTENTS

Introduction

Chapter 1: Nutrition Assessment Charts, Tables, and Formulas


Practical Steps to Nutrition Assessment - Adult Patients 1-2
K/DOQI Assessment and Monitoring Recommendations 1-3
Tips for Effective Assessment, Interviewing, and Teaching 1-4
Height Estimation From Knee Height 1-5
Height Estimation From Arm Span 1-6
Determination of Frame Size by Elbow Breadth 1-7
Determination of Frame Size by Wrist Circumference 1-8
Patient Determined Frame Size 1-9
Methods to Determine Body Weights for Nutrient Calculations 1-10
Standard Body Weight 1-11
Metropolitan Life Height and Weight Tables for Adults-Male 1-12
Metropolitan Life Height and Weight Tables for Adults-Female 1-13
Weight for Height Tables for Filipinos 1-14
Desirable Body Weight Based on BMI 1-15
Estimating Dry Weight 1-16
Clinical Signs of Fluid Status In Dialysis Patients 1-17
Usual Fluid Intake and Output in Adults Without Kidney Disease 1-17
Weight Comparison Formulas 1-18
Adjusted Body Weight for the Obese or Underweight Patient 1-19
Weight Estimation in Amputees 1-20
Body Mass Index 1-21
Body Mass Index Classifications 1-22
Creatinine Index (For estimating Edema-free Lean Body Mass) 1-23
Sample Calculation of Edema-free Lean Body Mass 1-24
Body Surface Area Nomogram 1-25
Body Surface Area Formulas 1-26
Arm Anthropometrics 1-27
Reference Values for the Triceps Skinfold Thickness – Male 1-28
Reference Values for the Triceps Skinfold Thickness – Female 1-29
Reference Values for Mid-arm Muscle Circumference - Male/Female 1-30
Reference Values for Mid-upper Arm Muscle Area – Male 1-31
Reference Values for Mid-upper Arm Muscle Area – Female 1-32
Other Measures of Body Composition 1-33
Subjective Global Assessment 1-34 to 1-41
Criteria For Estimation of Performance or Functional Status 1-42
Dietetic-Specific Nutritional Diagnostic Codes (D-S NDCs) 1-43 to 1-47
Medical Nutrition Therapy (MNT) 1-48
Common Physical Signs of Malnutrition 1-49 to 1-50

© 2005 National Kidney Foundation, Inc. All Rights Reserved 1


Pocket Guide to Nutrition Assessment
of the Patient with Chronic Kidney Disease
Chapter 2: Laboratory Values/Drug Nutrient Interactions
General Information 2-2
Conversion Formulas 2-3
Laboratory Tests 2-4 to 2-18
Possible Non-Dietary Causes of Hyperkalemia in Kidney Disease 2-19
Signs and Symptoms of Abnormal Serum Potassium 2-20
Acidosis/Acidemia 2-21
Acidosis/Alkalosis 2-22
Na+/K+ Content of Salt and Salt Substitutes 2-23
Drugs That May Impair Absorption or Utilization of Nutrients 2-24
Drug Nutrient Interactions 2-25
Potential Nutrition Effects of Common Immunosuppressive Drugs 2-26
Herbal Supplements 2-27 to 2-28

Chapter 3: Nutrient Calculations


General Information 3-2
Daily Nutrient Recommendations for Kidney Disease 3-3 to 3-4
Nutrition Recommendations for CKD Patients Not on Dialysis 3-5
L-Carnitine Supplementation in MD Patients 3-6
Nutrient Recommendations for the Pregnant Dialysis Patient 3-7
Nutrient Recommendations for AIDS 3-8
Harris Benedict Formula for Determining Basal Energy Expenditure 3-9
Suggested Adjustment Factors for Energy Needs During Acute Illness 3-9
Estimated Body Weight and Energy Needs in Para- and Quadriplegia 3-10
Estimates of Calories Absorbed From Peritoneal Dialysate 3-11 to 3-12
National Renal Diet Food Choice Lists (Nutrient Averages) 3-13 to 3-14
Vitamins Formulated for CKD Patients 3-15
Considerations for a Kosher Diet 3-16
Available Fiber, Potassium, and Phosphorus in Common High Fiber Cereals 3-17
Composition of Milk and Milk Substitutes 3-18

Chapter 4: Special Considerations for the Diabetic Patient


Common Symptoms, Treatments, and Definitions of Diabetes 4-2
Stages of Diabetic Nephropathy 4-3
Recommended Dietary Modification in Diabetic Nephropathy 4-4
Types and Actions of Insulin 4-5
Oral Hypoglycemic Agents 4-6
Glycated Hemoglobin 4-7
Hypoglycemia 4-8
Modifications for Acute Illness in Insulin Dependent DM 4-9
Food Glucose Equivalents to 15 gm Carbohydrate 4-10
Diabetic Gastroparesis 4-11
Other Nutrition Issues for Diabetics 4-12

© 2005 National Kidney Foundation, Inc. All Rights Reserved 2


Pocket Guide to Nutrition Assessment
of the Patient with Chronic Kidney Disease

Chapter 5: Special Considerations for the Elderly Patient


Education Considerations for the Elderly 5-2
DETERMINE: A Nutrition Checklist for the Elderly 5-3
Potential Influences on Nutrition Status in the Elderly 5-4
Physiological Changes in the Elderly 5-5
Body Composition Changes in the Elderly 5-6
Decrease in Physiological Function at 80 Years of Age 5-6
Incidence of Malnutrition in the Elderly 5-7
Subjective Global Assessment 5-8

Chapter 6: Hyperlipidemia in CKD


General Patterns of Hyperlipidemia in CKD 6-2
Patients At Risk for Developing Cardiovascular Complications 6-3
National Cholesterol Education Program (HCEP) 6-4
Target Lipid Levels/Therapeutic Lifestyle Changes 6-5
Antihyperlipidemic Drugs 6-6 to 6-7
Approximate Cholesterol Content of Common Foods 6-8

Chapter 7: Anemia in CKD


Anemia 7-2
Terminology Used to Describe Cell Alterations in Anemia 7-2
Types and Characteristics of Anemia 7-3
Laboratory Values Used to Diagnose Anemia 7-4
Interpretation of Iron Status Parameters 7-5
Iron Balance in CKD Patients 7-6
Laboratory Values Used to Diagnose Iron Deficiency in CKD 7-7
Estimation of Iron Needs: Recommendations for Repletion 7-8
Iron Supplements 7-9
Reasons for Inadequate Response to Epogen therapy 7-10

Chapter 8: Bone Metabolism and Disease in CKD/Urolithiasis


Management of Osteodystrophy in CKD 8-2
Osteodystrophy of CKD: Types and Characteristics 8-3
Negative Effects of Hyperphosphatemia 8-4
Hyperphosphatemia Due to Release of Phosphorus From Bone 8-4
Phosphorus Density of Common Foods 8-5
Phosphate Binding and Calcium Supplementation 8-6
Calcium Compounds 8-7
Potential Side Effects of Calcium-Based Binders 8-7
Common Name Brands of Calcium-Based Binders/Supplements 8-8
Combination Binders with Calcium 8-8
Other Phosphate Binders 8-9
Available Vitamin D and Vitamin D Analogs-Oral and IV 8-10
Use of Active Vitamin D or Vitamin D Analogs 8-11
Protocols for the Administration of Vitamin D and Vitamin D Analogs 8-12

© 2005 National Kidney Foundation, Inc. All Rights Reserved 3


Pocket Guide to Nutrition Assessment
of the Patient with Chronic Kidney Disease

Chapter 8: Bone Metabolism and Disease in CKD/Urolithiasis (cont)


Manufacturers’ Suggested Dosing Guidelines for Vitamin D or Analogs 8-13
Factors Affecting Therapeutic Response to Vitamin D/analogs in 8-14
Hyperparathyroidism
Management of Adynamic (Low Turnover) Bone Disease 8-15
Formulas for Adjusted Calcium/Ionized Calcium Calculation 8-16
Symptoms of Hyper- and Hypocalcemia 8-17
Etiology of Hypercalcemia 8-17
Potential Indications for Parathyroidectomy 8-18
Common Clinical Course After Parathyroidectomy 8-19
Urolithiasis (Nephrolithiasis/Kidney Stones) 8-20
Treatment of Calcium Stones 8-21
Hyperoxaluria 8-22
Oxalate Content of Common Foods 8-23
Soft Tissue Calcification and Calcific Uremic Arteriopathy (Calciphylaxis) 8-24

Chapter 9: Malnutrition in CKD


Adult Malnutrition 9-2
Factors that Can Cause or Exacerbate Malnutrition in CKD 9-3
Evaluation of Weight Loss Over Time 9-4
Critical Proteins for Assessing Malnutrition 9-5
Guidelines for Enteral Feeding 9-6
Enteral Nutrition Supplements 9-7
Specialty Nutrition Bars/Cookies/Puddings 9-8
Modular Products 9-9
Oral Amino Acids 9-10
Tube Feedings-Special Considerations for CKD 9-11
Common Tube Feeding Sites 9-12
Tube Feeding Formulas 9-13
Common Tube Feeding Products 9-14
Intradialytic Parenteral Nutrition (IDPN) 9-15
Gastrointestinal Motility Studies 9-16
IDPN Solutions 9-17
Recommended TPN Solution for Acute or CKD 9-18
Nutrient Calculations for Parenteral Nutrition 9-19
Nutrition Support Monitoring Guidelines in the Stable Dialysis Patient 9-20
Intraperitoneal Amino Acids as Nutrition Support in PD 9-21
Clinical Associations with Negative Nitrogen Balance/Estimation of Nitrogen 9-22
Balance

© 2005 National Kidney Foundation, Inc. All Rights Reserved 4


Pocket Guide to Nutrition Assessment
of the Patient with Chronic Kidney Disease

Chapter 10: Adequacy of Dialysis and Urea Kinetic Modeling


General Information 10-2
K/DOQI Suggested Adequacy Targets, 2001 10-2
Kinetic Modeling Glossary 10-3 to 10-5
Methods of Measuring Hemodialysis Adequacy 10-6
Parameters That Affect Adequacy 10-7
Formal Urea Kinetic Modeling (Kt/V) Components 10-7
Body Water Volume 10-8
Volume From Surface Area (VSA) Calculation Formulas 10-9
Differences Between Single Pool and Double Pool Kinetics 10-10
Hemodialysis Formulas for Urea Kinetic Modeling (UKM) 10-11
Summary of K/DOQI Hemodialysis Adequacy Recommendations 10-12
Common Causes of Delivered Kt/V Unequal to Prescribed 10-13
Steps to Error Analysis of Formal HD UKM 10-14
Helpful Information for Analysis of UKM Results 10-15
Error Analysis for Formal UKM 10-16 to 10-18
Dialyzer Characteristics 10-19
Formulas to Estimate Equilibrated Kt/V 10-20
Formulas for Other Measures of Adequacy 10-21
Daily Hemodialysis 10-22
Peritoneal Dialysis Adequacy Formulas 10-23 to 10-24
Summary of K/DOQI PD Adequacy Guidelines 10-25
Kinetic Modeling Formulas for CKD Not on Dialysis 10-26
Nutrition Intervention Based on nPNA 10-27
Glomerular Filtration Rate Calculations 10-28

Chapter 11: Special Considerations for the Pediatric Patient with CKD
Note Page 11-2
Nutrition Assessment of the Pediatric Patient 11-3
Practical Steps to Nutrition Assessment of Pediatric Patients 11-4
Assessment of Protein/Energy Status in Pediatric Patients 11-5
Mid-Arm Circumference (MAC) Reference Values 11-6
Triceps Skinfold Thickness 11-7
Estimated Mid-Arm Muscle Circumference 11-8
Formula for Mid-Arm Muscle Circumference and Area 11-9
Formulas for Calculating Standard Deviation Scores 11-9
50th Percentile for Height in Boys/Standard Deviation Values for Height in Boys 11-10 to 11-11
50th Percentile for Height in Girls/Standard Deviation Values for Height in Girls 11-12 to 11-13
50th Percentile for Weight in Boys/Standard Deviation Values for Weight in Boys 11-14 to 11-15
50th Percentile for Weight in Girls/Standard Deviation Values for Weight in Girls 11-16 to 11-17
Pediatric Laboratory Values That Are Different From Adult Values 11-18
Estimating Calorie and Fluid Needs of Pediatric CKD Patients 11-19
Guidelines for Choosing an Infant Formula 11-20
Pediatric Formulas Used in CKD 11-21

© 2005 National Kidney Foundation, Inc. All Rights Reserved 5


Pocket Guide to Nutrition Assessment
of the Patient with Chronic Kidney Disease

Chapter 11: Special Considerations for the Pediatric Patient with CKD (cont.)
Average Number and Volume of Feedings for an Infant Without CKD 11-21
Nutrient Recommendations for Pediatric Patients (ARF, CKD, HD, PD, Transplant) 11-22-11-26
Bone Abnormalities in Pediatric Patients with CKD 11-27
Malnutrition in Pediatric Patients with CKD 11-28
Guidelines for Enteral Feedings in Pediatric Patients with CKD 11-29
Guidelines for Tube Feedings in Pediatric Patients with CKD 11-30
Guidelines for Parenteral Nutrition in Pediatric Patients with CKD 11-31
Guidelines for Urea Kinetic Modeling in Pediatric HD Patients 11-32
Guidelines for Adequacy Testing in Pediatric PD Patients 11-33
Calcium Urolithiasis/Hyperoxaluria 11-34
Pediatric References 11-34

© 2005 National Kidney Foundation, Inc. All Rights Reserved 6


Chapter 1:
NUTRITION ASSESSMENT
CHARTS, TABLES, AND
FORMULAS

PRACTICAL STEPS TO NUTRITION ASSESSMENT-ADULT PATIENTS

1. Review the medical history (concurrent diseases, drug/nutrient interactions, hospitalizations, weight changes,
comparison of current weight to usual and standard, conditions that interfere with
ingestion/absorption/mastication/elimination).
2. Diet history including “normal” for the patient and changes in appetite or intake, food intolerances, pica behavior,
religious diet restrictions, past diet modifications and instruction, patient’s understanding of diet and disease,
educational level, patient’s perspective of weight changes, food preferences, use of salt and sugar, food allergies,
typical meal pattern/food frequency record, use of supplements, urine output, physical/economic/psychological
problems, family/other support, activity level, and sleep patterns.
3. Anthropometric measurements/physical examination: measured height, frame size, weight, subjective global
assessment, arm anthropometrics (triceps skinfold, mid-arm muscle circumference Page 1-27 to 1-32), and general
appearance. (Subjective Global Assessment: Page 1-34 to 1-41).
4. Review of chemistries look for values that identify areas of concern (nutrition/immune status, state of uremia,
bone status, electrolyte status, iron status, vitamin/mineral status, hydration status, glycemic control).
5. Assess current intake Kcal, carbohydrate, protein, fat, Na+, K+, Ca++, P, fluid, vitamins, minerals.
6. Assess/develop nutrition problem list with prioritized interventions.
7. Develop individualized diet prescription/meal pattern with appropriate diet modifications for nutrition
problems and individual preferences. Be as liberal as possible to promote adequate intake and good nutrition
status.
8. Instruct patient/other; provide written materials at predetermined level of education/understanding.
9. Follow-up within one to three months to assess appropriateness of diet modification as well as patient
satisfaction and understanding. Modify plan as appropriate.
10. Reevaluate on a regular basis whenever the patient has a change in status such as significant weight change,
extended hospitalization, or acute illness.

1-2
K/DOQI ASSESSMENT AND MONITORING RECOMMENDATIONS:

Parameter Frequency
Serum albumin Monthly
nPNA At least: monthly-HD; every 4 months-PD
% Usual dry weight (post dialysis or post-drain) Monthly
% Standard body weight Every 4 months
Subjective Global Assessment Biannually
Diet interview/diary Biannually
Anthropometrics, DEXA, Prealbumin, Creatinine As needed
Index, Creatinine, Urea Nitrogen, Cholesterol

Adapted from: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

TIPS FOR EFFECTIVE ASSESSMENT, INTERVIEWING, AND TEACHING

• Introduce yourself.
• Make eye contact and use a receptive posture.
• Explain what you will be doing.
• Assess prior learning.
• Gear information to the individual’s knowledge and education.
• Ask open-ended questions without leading responses.
• Utilize food models or other references to enhance accuracy of patient responses.
• Acknowledge patient responses.
• Limit the time spent and the volume of information given at each session.
• Give written material to reinforce verbal instructions.
• Identify and use patient-specific motivational factors.
• Encourage the patient to participate in his or her own nutritional care and to ask questions.
HEIGHT ESTIMATION FROM KNEE HEIGHT

Knee height is highly correlated with stature and may be used


to estimate height in persons who are unable to stand.

Use a knee height caliper with the knee bent at a 90-degree


angle while the patient is in a supine position. Measure the
distance from the heel to the top of the knee on the outside
of the left leg (or the nonaccess leg).

Take two successive measurements. They should agree within 5 mm.

Male height (cm) = (2.02 x knee height cm) - (0.04 x age) + 64.19

Female height (cm) = (1.83 x knee height cm ) - (0.24 x age) + 84.88

Reference: Chumlea WC, Roche AF: Nutritional Assessment of the Elderly through Anthropometry,
Ross Laboratories, Columbus, Ohio, 1987

1-5

HEIGHT ESTIMATION FROM ARM SPAN

Arm span is approximately equal to height (within 10% error) in both men and women, although it usually slightly
overestimates height.

With the arms fully extended and parallel to the ground, measure the distance from the tip of the middle finger on one
hand to the tip of the middle finger on the other hand. It may be easiest to measure across the patient’s back.

References: Clinical Geriatrics, Lippincot Co. Philadelphia, PA, 1979


Simko M, et al: Nutrition Assessment - A Comprehensive Guide for Planning Intervention,
ASPEN Publications, 1995

1-6
DETERMINATION OF FRAME SIZE BY ELBOW BREADTH (K/DOQI)

1. Have the patient stand, facing you with feet together. Ask him or her to extend the right arm in front of the body
with the forearm at a 90-degree angle, the inside of arm facing the body, and the fingers pointing up.

2. Place the thumb and index finger (or calipers with blades up) against the two prominent bones on either side of the
elbow, exert firm pressure to minimize influence of soft tissue, measure the distance between your thumb and
index finger or the caliper blades. Take the reading while the arm is still bent and in the caliper and measure to the
nearest 0.1 cm. Measure twice and use the average of the two measurements.

3. Determine the frame size using the patient’s height and elbow breadth on the chart below. Use frame size to
determine standard or ideal body weight.

Male Female
Age Small Medium Large Small Medium Large
18 - 24 ≤6.6 >6.6 and <7.7 ≥7.7 ≤5.6 >5.6 and <6.5 ≥6.5
25 - 34 ≤6.7 >6.7 and <7.9 ≥7.9 ≤5.7 >5.7 and <6.8 ≥6.8
35 - 44 ≤6.7 >6.7 and <8.0 ≥8.0 ≤5.7 >5.7 and <7.1 ≥7.1
45 - 54 ≤6.7 >6.7 and <8.1 ≥8.1 ≤5.7 >5.7 and <7.2 ≥7.2
55 - 64 ≤6.7 >6.7 and <8.1 ≥8.1 ≤5.8 >5.8 and <7.2 ≥7.2
65 - 74 ≤6.7 >6.7 and <8.1 ≥8.1 ≤5.8 >5.8 and <7.2 ≥7.2
Adapted from: Frisancho AR: New standards of weight and body composition by frame size and height for assessment of nutritional status
of adults and the elderly. Am J Clin Nutr 40: 808-819, 1984

1-7

DETERMINATION OF FRAME SIZE BY WRIST CIRCUMFERENCE

Use a fiberglass tape to measure the circumference of the right (or nonaccess) wrist just beyond the wrist bone toward
the hand. If the right wrist is swollen or enlarged for any reason, use the left wrist. Note which wrist is measured (for
subsequent measurements) and record the measurement in cm.

Frame Size = __Height (cm)___


Wrist circumference (cm)

CONVERSION TABLE

Males Frame Size Females


>10.5 Small >11.0
9.6 - 10.5 Medium 10.1 - 11.0
<9.6 Large <10.1
Reference: Gant JP: Handbook of Parenteral Nutrition, W.B. Saunders, Philadelphia, 1980

1-8
PATIENT-DETERMINED FRAME SIZE
For a patient-determined frame size, have the patient encircle the non-dominant wrist with the thumb and index finger
of the dominant hand at the level of the radius and ulnar styloid process. Note whether the thumb and index finger
overlap, meet, or do not meet. This method is not precise.

Frame Size Indicator


Small Thumb and index finger overlap
Medium Thumb and index finger meet or touch
Thumb and index finger do not meet or
Large
touch
Reference: Page CP, et al: Nutritional Assessment and Support - A Primer
2nd Edition, Williams & Wilkins, Baltimore, 1994

METHODS TO DETERMINE BODY WEIGHTS FOR NUTRIENT CALCULATIONS

1.* Standard Body Weight: Median body weight of normal Americans of the same height, gender, skeletal frame
size, and age range from the NHANES II data. (K/DOQI) (Page 1-11)
2.* Adjusted Body Weight: Use for obese or lean patients who are <95% or 115% standard body weight. (K/DOQI)
(Page 1-19 for formula).
3. Desirable Body Weight - Metropolitan Life Insurance Height and Weight Tables for Adults, 1983
(Pages 1-12 to 1-13)
4. Hamwi method - Not recommended; based on older NHANES data.

*K/DOQI Clinical Practice Guidelines for Nutrition in CRF recommend that standard and adjusted body weights,
#1 and # 2 above, be used to calculate nutrient levels. Some of the categories within the NHANES standard body
weight table were determined with small numbers of patients or linear regression and may be inappropriate for an
individual patient. Clinical judgment and longitudinal assessment of body weight should be utilized with other nutrition
measures to assess response to nutrition therapy and to make adjustments. Adoption of a consistent method of
determining body weight will simplify comparison of data and research within the renal community.

References: Simko M, et al: Nutrition Assessment: A Comprehensive Guide for Planning Interventions ASPEN, 1995
Alpers D, Stenson W, Bier D: Manual of Nutritional Therapeutics, Lippincott, Williams & Wilkins, 2002
Kopple JD, et al: Proposed Glossary for Dialysis Kinetics. Am J Kidney Dis 26(6):963-981, 1995
NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl
2, June, 2000
STANDARD BODY WEIGHT (K/DOQI)
NHANES II – Average 50th percentile weights for men and women by age, height, and frame size in the US.
Note: Some categories are based on a small sample of patients or estimated with linear regression and may not be appropriate for
an individual patient. Use clinical judgment in applying these standard body weights.

Male/age 25 - 54 years 55 - 74 years Female/age 25 - 54 years 55 - 74 years


Frame (Htcm) S M L S M L Frame (Htcm) S M L S M L

157 64 68 82 61 68 77* 147 52 63 86 54 57 92

160 61 71 83 62 70 80 150 53 66 78 55 62 78

163 66 71 84 63 71 77 152 53 60 87 54 65 78

165 66 74 79 70 72 79 155 54 61 81 56 64 79

168 67 75 84 68 74 80 157 55 61 81 58 64 82

170 71 77 84 69 78 85 160 55 62 83 58 65 80

173 71 78 86 70 78 83 163 57 62 79 60 66 77

175 74 78 89 75 77 84 165 60 63 81 60 67 80

178 75 81 87 76 80 87 168 58 63 75 68 66 82

180 76 81 91 69 84 84 170 59 65 80 61* 72 80

183 74 84 91 76* 81 90 173 62 67 76 61* 70 79

185 79* 85 93 78* 88 88 175 63* 68 79 62* 72* 85*

188 80* 88 92 77* 95 89 178 64* 70 76 63* 73* 85*

*Estimated with linear regression formula


Reference: Frisancho AR: New Standards of weight and body composition by frame size and height for assessment of nutritional status of adults
and the elderly. Am J Clin Nutr 40:808-819, 1984
1-11

METROPOLITAN LIFE HEIGHT AND WEIGHT TABLES FOR ADULTS, 1983 MALES,
Ages 25-59

Height Small Frame Medium Frame Large Frame


feet cm lbs kg lbs kg lbs kg
5' 1" 154.9 128-134 58.2-60.9 131-141 59.5-64.1 138-150 62.7-68.2
5' 2” 157.5 130-136 59.1-61.8 133-143 60.4-65.0 140-153 63.6-69.5
5' 3" 160.0 132-138 60.0-62.7 135-145 61.4-65.9 142-156 64.5-70.9
5' 4" 162.6 134-140 60.9-63.6 137-148 62.3-67.2 144-160 65.5-72.7
5' 5" 165.1 136-142 61.8-64.5 139-151 63.2-68.6 146-164 66.4-74.5
5' 6" 167.6 138-145 62.7-65.9 142-154 64.5-70.0 149-168 67.7-76.4
5' 7" 170.2 140-148 63.6-67.2 145-157 65.9-71.4 152-172 69.1-78.2
5' 8" 172.7 142-151 64.5-68.6 148-160 67.2-72.7 155-176 70.5-80.0
5' 9" 175.3 144-154 65.5-70.0 151-163 68.6-74.1 158-180 71.8-81.8
5' 10" 177.8 146-157 66.4-71.4 154-166 70.0-75.5 161-184 73.2-83.6
5' 11" 180.3 149-160 67.7-72.7 157-170 71.4-77.3 164-188 74.5-85.5
6' 0 182.9 152-164 69.1-74.5 160-174 72.7-79.1 168-192 76.4-87.3
6' 1" 185.4 155-168 70.5-76.4 164-178 74.5-80.9 172-197 78.2-89.5
6' 2" 188.0 158-172 71.8-78.2 167-182 75.9-82.7 176-202 80.0-91.8
6' 3" 190.5 162-176 73.6-80.0 171-187 77.7-85.0 181-207 82.3-94.1

Reprinted with permission. Height is without shoes. Weight includes indoor clothing-5lbs. (Light- weight pants/
T-shirt = 2 lbs, Sweatshirt/Jeans = 3.5 lbs, Sweatsuit/T-Shirt = 3 lbs.)

1-12
METROPOLITAN LIFE HEIGHT AND WEIGHT TABLES FOR ADULTS, 1983
FEMALES, Ages 25-59

Height Small Frame Medium Frame Large Frame


feet cm lbs kg lbs kg lbs kg
4' 9” 144.8 102-111 46.4-50.0 109-121 49.5-55.0 118-131 53.6-59.5
4'10" 147.3 103-113 46.8-51.4 111-123 50.0-55.9 120-134 54.5-60.9
4'11" 149.9 104-115 47.3-52.3 113-126 51.4-57.2 122-137 55.5-62.3
5' 0 152.4 106-118 48.2-53.6 115-129 52.3-58.6 125-140 56.8-63.6
5' 1" 154.9 108-121 49.1-55.0 118-132 53.5-60.0 128-143 58.2-65.0
5' 2" 157.5 111-124 50.5-56.4 121-135 55.0-61.4 131-147 59.5-66.8
5' 3" 160.0 114-127 51.8-57.7 124-138 56.4-62.7 134-151 60.9-68.6
5' 4" 162.6 117-130 53.2-59.0 127-141 57.7-64.1 137-155 62.3-70.5
5' 5" 165.1 120-133 54.5-60.5 130-144 59.0-65.5 140-159 63.6-72.3
5' 6" 167.6 123-136 55.9-61.8 133-147 60.5-66.8 143-163 65.0-74.1
5' 7" 170.2 126-139 57.3-63.2 136-150 61.8-68.2 146-167 66.4-75.9
5' 8" 172.7 129-142 58.6-64.5 139-153 63.2-69.5 149-170 67.7-77.3
5' 9" 175.3 132-145 60.0-65.9 142-156 64.6-70.9 152-173 69.1-78.6
5' 10" 177.8 135-148 61.4-67.3 145-159 65.9-72.3 155-176 70.5-80.0
5' 11" 180.3 138-151 62.7-73.6 148-162 67.3-73.6 158-179 71.8-81.4

Reprinted with permission. Height is without shoes. Weight includes indoor clothing 2-5 lbs. (Light-weight
pants/T-shirt = 2 lbs, Sweatshirt/Jeans = 3.5 lbs, Sweatsuit/T-Shirt = 3 lbs.)

1-13

WEIGHT FOR HEIGHT TABLES FOR FILIPINOS (Ages 25-65)

Male Female
Htcm Wtkg Htcm Wtkg Htcm Wtkg Htcm Wtkg
140 34.4-42.0 161 49.1-60.1 129 29.5-36.0 150 41.9-51.3
141 35.1-42.8 162 49.9-60.9 130 30.1-36.3 151 42.6-52.0
142 35.8-43.7 163 50.6-61.8 131 30.7-37.5 152 43.1-52.7
143 36.5-44.6 164 51.3-62.7 132 31.3-38.2 153 43.7-53.4
144 37.2-45.4 165 52.0-63.5 133 31.9-38.9 154 44.3-54.1
145 37.9-46.3 166 52.7-64.4 134 32.5-39.7 155 44.9-54.9
146 38.6-46.2 167 53.4-65.2 135 33.1-40.4 156 45.5-55.6
147 39.3-48.0 168 54.1-66.1 136 33.6-41.4 157 46.1-56.4
148 40.0-48.9 169 54.8-67.0 137 34.2-41.8 158 46.7-57.1
149 40.7-49.7 170 55.5-67.8 138 34.8-42.6 159 47.3-57.8
150 41.4-50.6 171 56.2-68.7 139 35.4-43.3 160 47.9-58.5
151 42.1-51.5 172 56.9-69.6 140 36.0-44.0 161 48.5-59.3
152 42.8-52.3 173 57.6-70.4 141 36.6-44.8 162 49.1-60.0
153 43.5-53.2 174 58.3-71.3 142 37.2-45.5 163 49.7-60.7
154 44.2-54.0 175 59.0-72.1 143 37.8-46.2 164 50.3-61.4
155 44.9-54.9 176 59.7-73.0 144 38.4-47.3 165 50.8-62.2
156 45.6-55.8 177 60.4-73.9 145 39.0-47.6 166 51.4-62.9
157 46.3-56.3 178 61.1-74.7 146 39.6-48.4 167 52.0-63.6
158 47.0-57.5 179 61.8-75.6 147 40.2-49.1 168 52.6-64.3
159 47.8-58.4 180 62.6-76.4 148 40.8-49.8 169 53.2-65.0
160 48.4-59.2 181 63.2-77.3 149 41.4-50.5 170 53.8-65.8
Reference: (Adapted) Nutritionist-Dietitian’s Association of the Philippines, Diet Manual, 4th Ed. 1994
1-14
DESIRABLE BODY WEIGHT BASED ON BMI
Weight tables are not readily available for all cultures or nationalities. In addition, the standard weight tables for the U.S. population often seem
inappropriate for those from other countries or cultures. Since BMI is used in many countries to assess “desired” weight, the table below provides
weights for BMI from 20-25 and for BMI from 23.6-24 (suggested as the best range for survival in HD patients).1 The clinician should compare
these ranges to the “normal” adult weight as a way of determining a “desired” weight that is reasonable for the individual patient.

Height Wt Range kg Wt Range kg Height Wt Range kg Wt Range kg


in/cm BMI 20-25 BMI 23-24 in/cm BMI 20-25 BMI 23-24
53/134.6 36.2-45.3 41.7-43.5 66/167.6 56.2-70.3 64.6-67.3
54/137.2 37.6-47.0 43.3-45.2 67/170.2 57.9-72.4 66.6-69.5
55/139.7 39.0-48.8 44.9-46.8 68/172.7 59.7-74.6 68.6-71.6
56/142.2 40.5-50.6 46.5-48.6 69/175.3 61.4-76.8 70.6-73.7
57/144.8 41.9-52.4 48.2-50.3 70/177.8 63.2-79.0 72.7-75.9
58/147.3 43.4-54.3 49.9-52.1 71/180.3 65.0-81.3 74.8-78.1
59/149.9 44.9-56.1 51.7-53.9 72/182.9 66.9-83.6 76.9-80.3
60/152.4 46.5-58.1 53.4-55.7 73/185.4 68.8-86.0 79.1-82.5
61/154.9 48.0-60.0 55.2-57.6 74/188.0 70.7-88.3 81.3-84.8
62/157.5 49.6-62.0 57.0-59.5 75/190.5 72.6-90.7 83.5-87.1
63/160.0 51.2-64.0 58.9-61.5 76/193.0 74.5-93.2 85.7-89.4
64/162.6 52.9-66.1 60.8-63.4 77/195.6 76.5-95.6 88.0-91.8
65/165.1 54.5-68.1 62.7-65.4 78/198.1 78.5-98.1 90.3-94.2
1
References: Kopple JD, Zhu X, Lew NL, Lowrie EG: Body weight for height relationships predict mortality in maintenance hemodialysis
patients. KI 56:1136-1148, 1999
Alpers D, Stenson W, Bier D: Manual of Nutritional Therapeutics, Lippincott, Williams, Wilkins, 2002
1-15

ESTIMATING DRY WEIGHT


142 mEq/L X Liters of NTBW = Liters of actual
Pre-dialysis serum sodium (mEq/L) body water

142 mEq/L = normal state of hydration

NTBW = Normal Total Body Water is calculated by multiplying the patient’s pre-dialysis weight by the average
percentage of body water for males (60%) and females (50%). A lower value (males - 57% and females -
47%) should be used in muscle wasted or overweight dialysis patients.

Example: Male, pre-dialysis weight of 63 kg, serum sodium of 131 mEq/L, and low muscle stores.

63 x 0.57 = 35.91

142 mEq/L x 35.91 = 5099.22 = 38.9 (Actual TBW)


131 mEq/L 131

38.9-35.9 = 3 kg excess body fluid

63 kg - 3.0 kg = 60.0 kg Estimated Dry Weight

(This formula does not consider fluid in tissues, so can only be used as one aspect of assessing dry weight).

Reference: Smith, et al. Formulation of Dry Weight Calculation. Contemp Dial & Nephr, May, 1990

1-16
CLINICAL SIGNS OF FLUID STATUS IN DIALYSIS PATIENTS
Fluid Overload Dehydration
Gain >4% body weight between Minimal weight gain/weight loss between treatments
treatments
Hypertension (onset or increase in BP) Hypotension/orthostatic fall in blood pressure

Peripheral edema, ascites, pleural Collapsing veins/difficult venipuncture


effusion Cool extremities
Left ventricular failure with rales in Decreased skin turgor
lungs, labored breathing while supine,
third heart sound
Dilution of the serum can cause some Concentration of the serum can cause some laboratory values to
laboratory values to be falsely low be falsely high

USUAL FLUID INTAKE AND OUTPUT IN ADULTS WITHOUT KIDNEY DISEASE

Intake Output
Fluid ingestion: about 1000 to 2000 cc/day Urine: normal 1000-2000 cc/day; varies to maintain
(Influenced by salt intake/eating patterns) fluid balance; decreases to negligible in CKD
Fluid from solid foods: 800-1000 cc/day Perspiration: minimal except in hot climate
Evaporation: 450 cc/day each from skin/respiration
Oxidative metabolism: 200 to 300 cc/day Stool: approximately 100 cc/day

Reference: Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins,
1997
1-17

WEIGHT COMPARISON FORMULAS

Percent Standard Body Weight Actual Body Weight x 100


(% SBW) Standard Body Weight
(K/DOQI) (See page 1-11)
Percent Desirable Body Weight Actual Body Weight x 100
(% DBW) Desirable Body Weight
(See pages 1-12 and 1-13)
Percent Usual Body Weight Actual Body Weight x 100
(% UBW) Usual Weight
Percent Weight Change (Previous Weight - Actual Weight) x 100
(% Wt Change) Previous Weight

Standard body weight may also be called “Relative” body weight


1
Reference: Kopple JD, et al: A proposed glossary for dialysis kinetics. Am J Kidney Dis 26(6):963-981, 1995

1-18
Adjusted body weight for the obese or Underweight Patient* (K/DOQI) 1

Adjusted body weight (BW)= edema-free BW + [(standard BW - edema-free BW) x 0.25]


*Adjust when patient’s weight is < 95% or >115% of standard body weight (page 1-11).

Examples of K/DOQI adjustment:


Underweight patient: Actual BW 60, Standard BW 80 so Adjusted BW = 60 + [(80 - 60) x 0.25]
Adjusted BW = 60 + [20 x 0.25]
Adjusted BW = 60 + 5 or 65 (Traditional adjustment = not applied to underweight patients)
Overweight patient: Actual BW 80, Standard BW 60 so Adjusted BW = 80 + [(60-80) x 0.25]
Adjusted BW = 80 + [-20 x 0.25]
Adjusted BW = 80 - 5 or 75 (Traditional adjustment = 65)

The K/DOQI adjustment is less extreme than the traditional adjustment with the rationale that patient compliance might be enhanced
with more modest step-wise alterations in nutrient intake. Thus, the K/DOQI adjusted weight is used to calculate a starting point for
nutrient levels, but requires periodic reassessment of weight and recalculation of needs as the patient’s status changes. As part of the
recommended research in the nutrition guidelines, renal clinicians are asked to utilize and test the K/DOQI formulas to validate their
accuracy and usefulness.
Traditional Adjustment2: Adjusted BW = IBW + [(Actual BW - Ideal BW x 0.25)]
The originally published adjustment formula as was developed for obese individuals (>125% of ideal BW) with the understanding
that fatty tissue is less metabolically active than lean tissue and requires different nutrient levels for maintenance. Thus, nutrient
recommendations based on actual BW were likely to overestimate needs and those based on ideal BW might underestimate the
needs of an obese individual. There was no application of the traditional formula to underweight patients since the research focussed
on obese patients. In the past, renal clinicians have recommended nutrient levels based on ideal weight for underweight patients.
Regardless of the formula employed, clinicians must consider the appropriateness of the adjustment for an individual patient.
1
Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, Am J Kidney Dis 35 (6) Suppl 2, June, 2000
2
Karkeck J. Adjustment for Obesity. ADA Renal Practice Group Newsletter, Winter, 3(1):6,1984
1-19

WEIGHT ESTIMATION IN AMPUTEES


To estimate the weight of persons with amputations for comparison to SBW (Page 1-11): To estimate the pre-
amputation BW, increase the post amputation BW by the percentage listed for the amputated appendage(s).

Example: Post-amputation BW is 62.2 kg with one below the knee (BK) amputation.
62.2 kg x 6.5% = 4.0 kg
4.0 kg to 62.2 = 66.2 (Underestimation due to use of post-amputation BW to calculate % lost)

To estimate the post-amputation BW, reduce pre-amputation BW by the % listed for the amputated appendage(s).

Example: Pre-amputation weight is 67 with one BK amputation.


67 kg x 6.5% = 4.4 kg
67 kg - 4.4 kg = 62.6 kg

To estimate volume (V) change after amputation: Post-amputation BW X pre-amputation V/pre-amputation BW

Example: Post-amputation BW = 62.2, pre-amputation V = 56, pre-amputation BW = 67


56/67 kg = 0.84
62.2 kg x 0.84 = 52.2 L (Assumes body water content does not change with amputation).

Upper Body % BW % BSA Lower Body % BW % BSA


Head, neck, trunk 49.7 C Foot 1.8 3.5
Hand 0.8 2.5 Lower leg, below knee 6.5 10
Forearm + hand 3.1 6 Leg, above knee 8.0 12.5
Entire arm 6.6 10 Entire leg 18.5 18
1-20
BODY MASS INDEX (BMI) (K/DOQI)
1. Standard Formula BMI = Weight (kg) 2. Simplified BMI = Weight (lbs) x 705
Height (m2) Height (in2)

Conversion to M2 Conversion to Inches2


Height M2 Height M 2
Height In2 Height In2
Feet /cm Feet /cm Inches/Feet Inches/Feet
4’9" / 144.8 cm 2.10 5’7" / 170.2 cm 2.90 57" / 4’9" 3249 67" / 5’7" 4489
4’10" / 147.3 cm 2.17 5’8" / 172.7 cm 2.98 58" / 4’10" 3364 68" / 5’8" 4624
4’11" / 149.9 cm 2.25 5’9" / 175.3 cm 3.07 59" / 4’11" 3481 69" / 5’9" 4761
5' / 152.4 cm 2.32 5’10" / 177.8 cm 3.16 60" / 5’0" 3600 70" / 5’10" 4900
5’1" / 154.9 cm 2.40 5’11" / 180.3 cm 3.25 61" / 5’1" 3721 71" / 5’11" 5041
5’2" / 157.5 cm 2.48 6' / 182.9 cm 3.35 62" / 5’2" 3844 72" / 6’0" 5184
5’3" / 160.0 cm 2.56 6’1" / 185.4 cm 3.44 63" / 5’3" 3969 73" / 6’1" 5329
5’4" / 162.6 cm 2.64 6’2" / 188.0 cm 3.53 64" / 5’4" 4096 74" / 6’2" 5476
5’5" / 165.1 cm 2.73 6’3" / 190.5 cm 3.63 65" / / 5’5" 4225 75" / 6’3" 5625
5’6" / 167.6 cm 2.81 6’4" / 193.0 cm 3.73 66" 5’6" 4356 76" / 6’4" 5776
Reference: Stensland SH, et al: Simplifying the calculation of body mass index for quick reference.
J of Am Dietetic Assoc. 90 (6):856, 1990

1-21

BODY MASS INDEX CLASSIFICATIONS


BMI Evaluation
Under 20 May be associated with health problems and malnutrition.
20 - 25 “Ideal” index range associated with the lowest risk of illness in people without kidney
disease.
25 - 27 May be associated with health problems related to overweight in some persons.
Over 27 Associated with increased risk of health problems related to obesity such as heart disease,
high blood pressure, and diabetes.
K/DOQI 23.6 for women and 24.0 for men
Note: Upper 50th percentile BMI may be best for survival in maintenance dialysis (MD)
patients. MD patients who are over 120% SBW or BMI >30 may benefit from weight
reduction, but the safety and efficacy of nutrient modification for weight loss needs to be
studied.
References: Classifications of Body Mass Index by Health and Welfare. Canada, 1988
NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, Am J Kidney Dis 35(6) Suppl 2, June, 2000

1-22
CREATININE INDEX (For estimating edema-free lean body mass):
The creatinine (Cr) index is defined as the creatinine synthesis or production rate and is used to assess skeletal muscle
mass. It is determined by the size of the skeletal muscle mass and the intake of creatine and creatinine. Creatinine
production is approximately proportional to skeletal muscle mass in metabolically stable adults who have consistent
protein intake. In MD patients creatinine is synthesized and serum levels rise at a rate that is approximately
proportional to somatic protein mass and dietary protein intake. The creatinine index is measured as the sum of
creatinine removed from the body (urine, dialysate, ultrafiltrate), any increase in the body creatinine pool, and the
creatinine degradation rate.

*Creatinine Index mg/24 hr = dialysate (ultrafiltrate) Cr mg/24 hr + urine Cr mg/24 hr + change in Cr body pool
mg/24 hr + Cr degradation mg/24 hr

Change in body creatinine pool mg/24 hr = (Final serum Cr mg/L - initial serum Cr) x (24 hour/time interval between
creatinine measurements) x (BW kg x 0.5 L/kg)

If body weight is variable:


Change in body creatinine pool mg/24 hr = [final serum Cr mg/L x (final BW kg x 0.5 L/kg)] - [initial serum Cr
mg/L x (initial BW kg x 0.5 L/kg)] x (24 hr/time interval between creatinine measurements)

Creatinine Degradation (gut) mg/24 hr = 0.038 dL/kg/24 hr x serum Cr mg/dL x BW kg


Edema-free lean body mass kg = 0.029 kg/mg/24 hr x Cr index mg/24 hr + 7.38 kg

*(Creatinine Index or Total creatinine production = creatinine excretion + creatinine degradation - See next page)

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, Am J Kidney Dis 35(6) Suppl 2, June, 2000

1-23

SAMPLE CALCULATION OF EDEMA-FREE LEAN BODY MASS

PD Patient:
Urine Volume = 475 Urine Creatinine mg/mL = 136
Effluent Volume = 12485 Effluent Creatinine mg/mL = 4.5
Serum Cr = 6.91
BW = 70.6

Cr degradation (gut) = 0.038 x (Scr x Wtkg)

= 0.038 x 6.91 x 70.6


= 18.6 mg/d

Cr production = Dcr x (Dv/100) + Ucr x (Uv/100)/1000


= 4.5 x (12485/100) + 136 x (475/100)
= 562 + 646
= 1208 mg/d

Creatinine Index (Total creatinine production) = 1208 + 18.6 or 1226.6 mg/d

Edema Free LBM = 0.029 x 1226.6 + 7.38 or 42.95 kg


Edema Free LBM = 61% of total weight is LBM

1-24
BODY SURFACE AREA NOMOGRAM

Wt Kg/Lbs Ht 58” 60” 62” 64” 66” 68” 70” 72” 74” 76”
38.6 85 1.27 1.30 1.33 1.36 1.39 1.42 1.45 1.48 1.51 1.54
40.9 90 1.30 1.33 1.36 1.39 1.43 1.46 1.49 1.52 1.55 1.58
43.2 95 1.33 1.36 1.39 1.43 1.46 1.49 1.52 1.55 1.58 1.62
45.5 100 1.36 1.39 1.42 1.46 1.49 1.52 1.56 1.59 1.62 1.65
47.7 105 1.39 1.42 1.45 1.49 1.52 1.55 1.59 1.62 1.65 1.69
50.0 110 1.41 1.45 1.48 1.52 1.55 1.59 1.62 1.65 1.69 1.72
52.3 115 1.44 1.48 1.51 1.55 1.58 1.62 1.65 1.68 1.72 1.75
54.6 120 1.47 1.50 1.54 1.57 1.61 1.65 1.68 1.72 1.75 1.78
56.8 125 1.49 1.53 1.57 1.60 1.64 1.67 1.71 1.75 1.78 1.82
59.1 130 1.52 1.55 1.59 1.63 1.67 1.70 1.74 1.77 1.81 1.85
61.4 135 1.54 1.58 1.62 1.66 1.69 1.73 1.77 1.80 1.84 1.88
63.6 140 1.57 1.60 1.64 1.68 1.72 1.76 1.79 1.83 1.87 1.90
65.9 145 1.59 1.63 1.67 1.71 1.75 1.78 1.82 1.86 1.90 1.93
68.2 150 1.61 1.65 1.69 1.73 1.77 1.81 1.85 1.89 1.92 1.96
70.5 155 1.63 1.68 1.72 1.76 1.80 1.83 1.87 1.91 1.95 1.99
72.7 160 1.66 1.70 1.74 1.78 1.82 1.86 1.90 1.94 1.98 2.02
75.0 165 1.68 1.72 1.76 1.80 1.84 1.88 1.92 1.96 2.00 2.04
77.3 170 1.70 1.74 1.78 1.83 1.87 1.91 1.95 1.99 2.03 2.07
79.6 175 1.72 1.76 1.81 1.85 1.89 1.93 1.97 2.01 2.05 2.09
81.8 180 1.74 1.79 1.83 1.87 1.91 1.96 2.00 2.04 2.08 2.12
86.4 190 1.78 1.83 1.87 1.91 1.96 2.00 2.04 2.09 2.13 2.17
90.9 200 1.82 1.87 1.91 1.96 2.00 2.04 2.09 2.13 2.17 2.22
Reference: Baxter Healthcare Training Seminar, Chicago, 1991

1-25

BODY SURFACE AREA (BSA) FORMULAS


1
Dubois and Dubois : BSA Adjustment for Amputation
BSA (m2) = 0.007184 X BW (kg)0.425 X Height (cm)0.725 Part of Body % Wt Loss %
BSA4
Gehan and George2:
Arm at shoulder 6.6 10.0
BSA (m2) = 0.0235 X Weight (kg)0.51456 X Height (cm)0.42246 Arm at elbow 3.1 6.0
Haycock3: (Pediatrics) Hand alone 0.8 2.5
Leg at hip 18.5 18.0
BSA (m2) = 0.024265 X Height (cm)0.3964 X Weight (kg)0.5378
Leg above knee 8.0 12.5
Mosteller5: Leg below knee 6.5 10.0
BSA (m2) = ([Ht(cm) X Wt(kg)]/3600)1/2 Foot alone 1.8 3.5
References: 1. Dubois D, Dubois AEF: A formula to estimate the approximate surface area if height and weight be known. Nutrition 5:303-311,
1989
2. Gehan E, George SL: Estimation of human body surface area from height and weight. Cancer Chemother Rep Part I 54:225-
235, 1970
3. Haycock GB, Chir B, Schwartz, et al: Geometric method of for measuring body surface area: A height-weight formula validated
in infants, children, and adults. J Pediatr 93:62-66, 1978
4. Tzamaloukas AH, Malhotra D: CrCl in amputees on CPD. Perit Dial Int 16:426, 1996
5. Mosteller RD: Simplified Calculation of BSA. N Eng J Med, 22;317(17):1098, 1987

1-26
ARM ANTHROPOMETRICS

Step I Mid-arm circumference (MAC)


1. With the patient standing (if possible) and at dry weight, measure the circumference of the patient’s right or nonaccess arm
using a fiberglass tape.
2. For the maximum accuracy, place the patient’s forearm across the stomach, measure and mark the midpoint between the
acromial and olecranon processes.
3. Have the patient relax the arm at his or her side and measure the arm circumference at the mark without compressing the
soft tissue. Record to the nearest 0.1 cm.

Step II Triceps skinfold (TSF)


1. With the patient’s arm relaxed at his or her side, pick up or lightly pinch a lengthwise double fold of skin with a thumb
and forefinger just above the marked midpoint. Have the patient open and close the fist to ensure that none of the
muscle is included in the pinch.
Note: It may be easiest to start the pinch below the midpoint and work the fingers up to the mark.
2. Hold the calipers parallel to the floor, place them over the fat fold at the mark, to a depth approximately equal to the
width of the fat fold. Release calipers while holding the pinch, and take the reading within 3 seconds. Repeat three (3)
times and record the average.

Step III Mid-arm muscle circumference (MAMC)


Calculate as follows: MAMC = MAC - (TSF X 0.314)

Step IV Mid-upper arm muscle area (MAMA)


2
Calculate as follows: MAMA = (MAMC) /12.56

Step V Evaluation
1. Compare values to reference standards and record the percent of standard. (Pages 1-28 to 1-32)
2. Use the patient as his or her own standard in subsequent measurements.

Note: Measurements on a significant MD population showed few differences from the HANES II norms.
Reference: Nelson E: Anthropometry in the Nutritional Assessment of Adults with ESRD. J Ren Nutr 1:162-172, 1991
1-27

REFERENCE VALUES FOR THE TRICEPS SKINFOLD THICKNESS (mm) – Male

Age Group Percentile


Years 5 10 15 25 50 75 85 90 95
15-15.9 5.0 5.0 5.0 6.0 7.5 11.0 15.0 18.0 23.5
16-16.9 4.0 4.0 5.1 6.0 8.0 12.0 14.0 17.0 23.0
17-17.9 4.0 4.0 5.0 6.0 7.0 11.0 13.5 16.0 19.5
18-24.9 4.0 4.0 5.5 6.5 10.0 14.5 17.5 20.0 23.5
25-29.9 4.0 4.0 6.0 7.0 11.0 15.5 19.0 21.5 25.0
30-34.9 4.5 4.5 6.5 8.0 12.0 16.5 20.0 22.0 25.0
35-39.9 4.5 4.5 7.0 8.5 12.0 16.0 18.5 20.5 24.5
40-44.9 5.0 5.0 6.9 8.0 12.0 16.0 19.0 21.5 26.0
45-49.9 5.0 5.0 7.0 8.0 12.0 16.0 19.0 21.0 25.0
50-54.9 5.0 5.0 7.0 8.0 11.5 15.0 18.5 20.8 25.0
55-59.9 5.0 5.0 6.5 8.0 11.5 15.0 18.0 20.5 25.0
60-64.9 5.0 5.0 7.0 8.0 11.5 15.5 18.5 20.5 24.0
65-69.9 4.5 4.5 6.5 8.0 11.0 15.0 18.0 20.0 23.5
70 -70.9 4.5 4.5 6.5 8.0 11.0 15.0 17.0 19.0 23.0
Adapted: Frisancho AR: Anthropometric Standards for the Assessment of Growth and Nutritional Status. The University of Michigan Press, 1993

1-28
REFERENCE VALUES FOR THE TRICEPS SKINFOLD THICKNESS (mm) – Female

Age Group Percentile


Years 5 10 15 25 50 75 85 90 95
15.0-15.9 8.0 9.5 10.5 12.0 16.5 20.5 23.0 26.0 32.5
16.0-16.9 10.5 11.5 12.0 14.0 18.0 23.0 26.0 29.0 32.5
17.0-17.9 9.0 10.0 12.0 13.0 18.0 24.0 26.5 29.0 34.5
18.0-24.9 9.0 11.0 12.0 14.0 18.5 24.5 28.5 31.0 36.0
25.0-29.9 10.0 12.0 13.0 15.0 20.0 26.5 31.0 34.0 38.0
30.0-34.9 10.5 13.0 15.0 17.0 22.5 29.5 33.0 35.5 41.5
35.0-39.9 11.0 13.0 15.5 18.0 23.5 30.0 35.0 37.0 41.0
40.0-44.9 12.0 14.0 16.0 19.0 24.5 30.5 35.0 37.0 41.0
45.0-49.9 12.0 14.5 16.5 19.5 25.5 32.0 35.5 38.0 42.5
50.0-54.9 12.0 15.0 17.5 20.5 25.5 32.0 36.0 38.5 42.0
55.0-59.9 12.0 15.0 17.0 20.5 26.0 32.0 36.0 39.0 42.5
60.0-64.9 12.5 16.0 17.5 20.5 26.0 32.0 35.5 38.0 42.5
65.0-69.9 12.0 14.5 16.0 19.0 25.0 30.0 33.5 36.0 40.0
70.0-74.9 11.0 13.5 15.5 18.0 24.0 29.5 32.0 35.0 38.5

Adapted: Frisancho AR: Anthropometric Standards for the Assessment of Growth and Nutritional Status. The University of Michigan Press, 1993

1-29

REFERENCE VALUES FOR MID-ARM MUSCLE CIRCUMFERENCE (cm)

Age Group Percentile


Years 5 10 25 50 75 90 95
18-24 23.5 24.4 25.8 27.2 28.9 30.8 32.3
M 25-34 24.2 25.3 26.5 28.0 30.0 31.7 32.9
A 35-44 25 25.6 27.1 28.7 30.3 32.1 33.0
L 45-54 24.0 24.9 26.5 28.1 29.8 31.5 32.6
E 55-64 22.8 24.4 26.2 27.9 29.6 31.0 31.8
65-74 22.5 23.7 25.3 26.9 28.5 29.9 30.7
F 18-24 17.7 18.5 19.4 20.6 22.1 23.6 24.9
E 25-34 18.3 18.9 20.0 21.4 22.9 24.9 26.6
M 35-44 18.3 19.2 20.6 22.0 24.0 26.1 27.4
A 45-54 18.8 19.5 20.7 22.2 24.3 26.6 27.8
L 55-64 18.6 19.5 20.8 22.6 24.4 26.3 28.1
E 65-74 18.6 19.5 20.8 22.5 24.4 26.5 28.1
Reference: Bishop CW, et al: Norms for Nutritional Assessment of American Adults by Upper Arm Anthropometry.
Am J of Clin Nutr 34:347, 1982

1-30
REFERENCE VALUES FOR MID-UPPER ARM MUSCLE AREA (cm) – Male

Age Group Percentile


Years 5 10 15 25 50 75 85 90 95
15.0-15.9 31.9 34.9 36.9 40.3 46.3 53.1 56.3 65.7 63.0
16.0-16.9 37.0 40.9 42.4 45.9 51.9 57.8 63.6 66.2 70.5
17.0-179 39.6 42.6 44.8 48.0 53.4 60.4 64.3 67.9 73.1
18.0-24.9 34.2 37.3 39.6 42.7 49.4 57.1 61.8 65.0 72.0
25.0-29.9 36.6 39.9 42.4 46.0 53.0 61.4 66.1 68.9 74.5
30.0-34.9 37.9 40.9 43.4 47.3 54.4 63.2 67.6 70.8 76.1
35.0-39.9 38.5 42.6 44.6 47.9 55.3 64.0 69.1 72.7 77.6
40.0-44.9 38.4 42.1 45.1 48.7 56.0 64.0 68.5 71.6 77.0
45.0-49.9 37.7 41.3 43.7 47.9 55.2 63.3 68.4 72.2 76.2
50.0-54.9 36.0 40.0 42.7 46.6 54.0 62.7 67.0 70.4 77.4
55.0-59.9 36.5 40.8 42.7 46.7 54.3 61.9 66.4 69.6 75.1
60.0-64.9 34.5 38.7 41.2 44.9 52.1 60.0 64.8 67.5 71.6
65.0-69.9 31.4 35.8 38.4 42.3 49.1 57.3 61.2 64.3 69.4
70.0-74.9 29.7 33.8 36.1 40.2 47.0 54.6 59.1 62.1 67.3
Adapted: Frisancho AR: Anthropometric Standards for the Assessment of Growth and Nutritional Status. The University of Michigan Press, 1993

1-31

REFERENCE VALUES FOR MID-UPPER ARM MUSCLE AREA (cm) – Female


Age Group Percentile
Years 5 10 15 25 50 75 85 90 95
15.0-15.9 24.4 25.8 27.5 29.2 33.0 37.3 40.2 41.7 45.9
16.0-16.9 25.2 26.8 28.2 30.0 33.6 38.0 40.2 43.7 48.2
17.0-17.9 25.9 27.5 28.9 30.7 34.3 39.6 43.4 46.2 50.8
18.0-24.9 19.5 21.5 22.8 24.5 28.3 33.1 36.4 39.0 44.2
25.0-29.9 20.5 21.9 23.1 25.2 29.4 34.9 38.5 41.9 47.8
30.0-34.9 21.1 23.0 24.2 26.3 30.9 36.8 41.2 44.7 51.3
35.0-39.9 21.1 23.4 24.7 27.3 31.8 38.7 43.1 46.1 54.2
40.0-44.9 21.3 23.4 25.5 27.5 32.3 39.8 45.8 49.5 55.8
45.0-49.9 21.6 23.1 24.8 27.4 32.5 39.5 44.7 48.4 56.1
50.0-54.9 22.2 24.6 25.7 28.3 33.4 40.4 46.1 49.6 55.6
55.0-59.9 22.8 24.8 26.5 28.7 34.7 42.3 47.3 52.1 58.8
60.0-64.9 22.4 24.5 26.3 29.2 34.5 41.1 45.6 49.1 55.1
65.0-69.9 21.9 24.5 26.2 28.9 36.6 41.6 46.3 49.6 56.5
70.0-74.9 22.2 24.4 26.0 28.8 34.3 41.8 46.4 49.2 54.6
Adapted: Frisancho AR: Anthropometric Standards for the Assessment of Growth and Nutritional Status. The University of Michigan Press, 1993

1-32
OTHER MEASURES OF BODY COMPOSITION

Methods Assessment of: Advantages Limitations


Dual Energy X-Ray Bone/bone mineral content, Validated high precision/pt Affected by hydration,
Absorptiometry fat mass, & lean body mass acceptance, low radiation, tissue density, assumption
(DEXA) can provide localized body re soft tissue content near
(K/DOQI) comp, suitable for all ages bone, Cost, inconvenience
Hydrodensitometry Lean body mass Most accurate in CKD if Difficult for patient
(Underwater Weighing) combined with DEXA and (submersion/exhaling air
volume of TBW. from lungs), special
equipment needed
Bioelectric Impedance Total body water, lean Easy to perform, small May not distinguish
(BIA) body mass, fat-mass time investment, high between changes in LBM
patient acceptance, little versus hydration status.
training needed, portable May be more useful in
populations rather than
individuals
Creatinine Kinetics Lean body mass Relatively easy, similar to Limited research, need to
other procedures such as collect urine/dialysate
UKM
Near Infrared Interactance Body composition, % body Not influenced by state of Limited research in dialysis
fat hydration, consistent patients
measurements, ease of use

References: DeVita MV, Stall S: Dual-Energy X-Ray Absorptiometry: A Review. J Ren Nutr 9(4):178-181, 1999
Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997
Stall S, et al: BIA and DEXA to Monitor Nutritional Status. PD Int 15(Suppl):S59-62, 1995
NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2,
June, 2000.
1-33

SUBJECTIVE GLOBAL ASSESSMENT (SGA)

SGA is the overall evaluation by an experienced clinician of the history and physical exam to rate patients as well
nourished, mild to moderately malnourished, or severely malnourished. The focus of SGA is nutrient intake and body
composition. Both the K/DOQI practice guideline for peritoneal dialysis adequacy and nutrition recommend SGA as a
valid and clinically useful measure of protein-energy status in maintenance dialysis patients. The recommended SGA
uses a 7 point scale (in place of the A-B-C, ratings used in the traditional SGA) with 1-2 ratings for severe malnutrition,
3-4-5 ratings for moderate to mild malnutrition, and 6-7 ratings for well nourished. It uses only four of the main
categories from the traditional SGA: weight change, dietary intake and GI symptoms (anorexia, nausea, vomiting, and
diarrhea), loss of subcutaneous fat, and loss of muscle tissue. The traditional SGA is reviewed here and the K/DOQI-
specific categories are indicated by italics.

SGA is meant to be subjective, based on the clinician’s expertise and experience. Thus, the ratings that follow are only
suggestions. Training and agreement among team members will minimize interrater variability. A one-page rating form
can be used to record observations and the overall rating. The final rating is not an average of the individual category
ratings, but a subjective assessment by the clinician. A number of rating forms have been published for use or
adaptation:

Baxter Healthcare-Renal Division, McGaw Park, IL


Detsky AS: J Parenter Enteral Nutr 11:440-446, 1987
McCann L: Dialysis and Transplantation 25(4):190, 1996
Page C: Nutritional Assessment and Support- A Primer, Williams & Wilkins, Baltimore, 1994
NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl
2, June, 2000.

1-34
Editor’s Note: The use of SGA in the chronic kidney disease population creates the challenge of maintaining the subjectivity of the
tool while trying to maximize interrater consistency. Objective measures of nutrition status are critical to the assessment of CKD
patients, but are only a part of the entire picture. Therefore, we must preserve the intangible value of a clinician’s judgement. Many
professionals have difficulty embracing the SGA tool because it seems too simple. However, SGA has demonstrated its value as a
stand-alone assessment technique, used in conjunction with, rather than combined with, other objective measures. (CAN-USA)

There is also discussion regarding the use of the traditional A-B-C ratings versus the 7 point scale (CAN-USA and K/DOQI).
The 7 point scale allows the clinician to more accurately quantify the status of the patient. Assigning a B rating does not provide the
same level of sensitivity as assigning a rating of 3, (the most negatively significant level of malnutrition in the mild to moderate
category) or a 5 (the least negatively significant level of malnutrition in the mild to moderate category). In addition, the
endorsement of the 7 point scale within the K/DOQI Guidelines for Nutrition in CRF, provides an opportunity to standardize
practice. Standardization of practice allows us to compare populations, to test the long-term validity of the tool in CKD patients, to
observe outcomes of nutrition recommendations, and develop universal clinical performance measures.

While clinical expertise and experience is the most important aspect of SGA, the following tips have been developed from
performing SGA in varying populations around the world. They are put forth for your consideration:

1. Training and a review of technique with colleagues who will be assessing common patients is invaluable.
2. Dietary intake can be the most important early indicator of nutritional risk. Thus, an estimate of current intake compared
to recommended nutrient levels (considering the duration of deficit or excess) is a worthwhile part of SGA.
3. Patterns of muscle wasting or preservation may be inconsistent depending on the physical activity/abilities of the patient.
Patient perspective and insight can be helpful in all aspects of SGA.
4. Tissue loss should be evaluated in relation to weight changes, especially in the baseline assessment.
5. Elderly patients typically have age-related tissue losses that mimic malnutrition. Get the patient’s perspective.
6. With advance planning and instruction, it is possible to observe most or all of the muscle/fat sites toward the end of
dialysis (at or close to dry weight) treatment without compromising the patient’s privacy. Use universal precautions.
7. A majority of patients are able to complete a simple questionnaire to provide some of the information needed for SGA.

1-35

SGA WEIGHT/MEDICAL/NUTRITION HISTORY


Use of standard questions can help improve the accuracy and consistency of SGA ratings. The following questions may
help you gather the information you need for the medical history portion of SGA. Some or most of this information
could also be obtained using a simple, patient-completed questionnaire.

Usual adult weight? Current weight?


Weight six months ago?
Weight 2 weeks ago?
Any signs of fluid overload? Edema? SOB? High B/P?

Current appetite/intake?
Is intake adequate to meet needs and recommendations?
Change in previous six months?
Change in past two weeks?

GI Distress?
Anorexia—frequency/duration of anorexia?
Nausea—frequency/duration of nausea?
Vomiting—frequency/duration of vomiting?
Diarrhea—frequency/duration of diarrhea?

Changes in function or activity related to malnutrition (Activities of daily living, gardening, volunteer work,
household chores, energy levels, etc.)?

Significant metabolic stress other than CKD? (Fever-degrees above normal and duration; use of steroids-dose
dependent, significant infection, etc.)
1-36
SCHEMATIC OF MUSCLE TO GUIDE ASSESSMENT OF WASTING
(Fat store sites are in italics).

1-37

SGA Part I - Review medical record/use specific, detailed questions to assess current status.
(K/DOQI in italics)
Weight
1. Weight change over 6 months (Use rating as listed even in obese patient)
a. <5% = A rating (6 or 7)
b. 5-10% = B rating (3 or 4 or 5)
c. >10% and sustained loss = C rating (1 or 2)
d. 10% but recovery to 5-10% = B rating (3 or 4 or 5)
e. Sustained improvement = one level up from previous
2. Weight change over previous two weeks
a. No change, normal weight = A rating (6 or 7)
b. Increasing or increased = rate one level up from previous rating
c. Decreasing = rate one level below previous rating
Dietary Intake
1. Change in intake (duration and degree)
2. Base ratings on current and prior status:
a. Intake adequate for needs, no change or change is slight/short duration = A (6 or 7)
b. Borderline, decreasing = B (3 or 4 or 5)
c. Unable to eat, starvation = C (1 or 2)
GI Symptoms
1. Nausea, vomiting, diarrhea, anorexia
2. Duration and frequency
a. Symptoms > 2 weeks, almost daily = C (1 or 2)
b. Minor or no symptoms, occasional = A (6 or 7)
c. Degree and frequency of symptoms between A and C = B (3 or 4 or 5) 1-38
Functional Status
1. Decreased strength or stamina due to malnutrition (See page 1-42 for examples)
2. Duration and degree of dysfunction (rate in relation to normal or previous SGA rating)
Metabolic Stress/Disease State/Co-morbidities
1. Low-moderate (infection, skeletal trauma, malignancy)
2. High stress (ulcerative colitis with diarrhea)

Part II Physical Exam (Use universal precautions/protective hand washing)

Exam areas: Tips Severe Mild-Moderate Well Nourished


Malnutrition Malnutrition
Subcutaneous 1 or 2 (C) 3 or 4 or 5 (B) 6 or 7 (A)
Fat
Below the eye View patient Hollow look, Slightly dark circles, Slightly bulged
straight on, depressions, dark somewhat hollow fat pads. Fluid
touch above circles, loose skin look may mask loss
cheek bone with
permission
Triceps/Biceps Arm bent, roll Very little space Some depth to pinch, Ample fat tissue
skin between between folds but not ample obvious between
fingers, do not fingers touch folds of skin
include muscle in
the pinch
1-39

Muscle Wasting Tips Severe Mild-Moderate Well Nourished


Malnutrition Malnutrition
Temple Observe straight on, Hollowing, Slight depression Can see/feel well-
have pt turn head side scooping, defined muscle
to side depression
Clavicle Look for prominent Protruding, Visible in male, Not visible in male,
bone. Make sure pt is prominent bone some protrusion in visible but not
not hunched forward female prominent in female
Shoulder Arms at side, look at Shoulder to arm Acromion process Rounded, curves at
shape joint looks square may protrude arm/shoulder/neck
slightly
Scapula Have patient extend Prominent, visible Mild depression, Bones not prominent,
hands straight out, bones, depressions or bone may show no significant
push against solid between slightly depressions
object ribs/scapula or
shoulder/spine
Interosseous Thumb side of hand; Depressed area Slightly depressed Muscle bulges, could
Muscle pads of thumb/ between thumb- be flat in well-
forefinger touching forefinger nourished person

1-40
Muscle Wasting Tips Severe Mild-Moderate Well Nourished
Malnutrition Malnutrition
Knee (Lower body Have patient sit Bones prominent, Knee cap less Muscle protrudes
is less sensitive to with leg propped little sign of muscle prominent, more bones not
change) up, bent at knee around knee cap rounded prominent
Quadriceps Not as sensitive as Depression/line on Mild depression on Well rounded,
upper body thigh, obviously inner thigh developed
thin
Calf Observe side and Thin, minimal or Not well developed Well-developed
front view no muscle bulb of muscle
definition
Edema - in dialysis, edema is important for quantifying weight loss in view of fluctuating fluid balance.
R/O other causes of View sacrum in Significant Mild to moderate No sign of fluid
edema, patient at activity-restricted swelling swelling accumulation
dry weight patient; ankle in
mobile patient
Reference: McCann L: Subjective Global Assessment as it pertains to the nutritional status of dialysis patients. Dialysis & Transplantation,
25(4):190, 1996

1-41

CRITERIA FOR ESTIMATION OF PERFORMANCE OR FUNCTIONAL STATUS

The scale below is a guide to the assessment of a patient’s functional status. During SGA, look for changes that are
related to malnutrition (difficulty with ambulation secondary to muscle wasting). In the general assessment of renal
patients, look for changes that are related to chronic disease and nutrition. In CKD, compare functional status prior to
kidney disease/dialysis in initial assessment or at last SGA to their current functional status.

Grade Scale Possible SGA Score


0 Fully active, able to carry on all predisease performance without 7
restriction. Fully capable of hard work. (Karnofsky 90-100)
1 Restricted in physically strenuous activity, but ambulatory and 6-5
able to carry out light or sedentary type activities (office).
(Karnofsky 70-80)
2 Ambulatory and capable of all self-care, but unable to work. Up 4-3
and about >50% of waking hours.
(Karnofsky 50-60)
3 Capable of only limited self care, confined to bed or chair more 2
than 50% of waking hours. (Karnofsky 30-40)
4 Completely disabled, confined to bed or chair, no self care. 1
(Karnofsky 10-20)

Reference: Stanley KE: Prognosis Factors for survival in patients with inoperable lung cancer. J Natl Cancer Inst. 65:25-29, 1980

1-42
DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs)
Category/Code Description NDC #
Absence of/Limited Nutrition Service/Prof. Nutritionist Contact D1.001
D1.000 Nutritional Collateral Systems D1.002
Altered/ Body Composition Integrity D2.001
Alteration In Bowel Elimination D2.002
D2.000 Drug Deposition D2.003
Metabolism D2.004
Nutrient Deposition D2.005
Nutritional Biochemistry Integrity D2.006
Conflict In Feeding and Treatment/Diagnostic Schedules D3.001
D3.000
Deficit In Nutrition Education D4.001
D4.000 Nutrition Knowledge D4.002
Dependent On Home Enteral/Parenteral Product Assistance D5.001
D5.000 Home Food Service Assistance D5.002
Home Therapeutic Diet/Product Assistance D5.003

1-43

DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs) (Cont.)

Category/Code Description NDC #


Excessive Calorie Allowance/Intake D6.001
D6.000 Fiber Allowance/Intake D6.002
Protein Allowance/Intake D6.003
Vitamin/Mineral Allowance/Intake D6.004
Water/Fluid Allowance/Intake D6.005
Imbalance Electrolyte D7.001
D7.000 Energy D7.002
Nutrient D7.003
Water/Fluid D7.004
Impaired Activity Performance D8.001
D8.000 Cognition and Behavior D8.002
Fecundity/Fertility D8.003
Growth/Development/Function D8.004
Home Maintenance of Dietary Needs D8.005
Lactation Performance D8.006
Social Performance D8.007
Work Performance D8.008
Inactive Role In Maintaining Adequate Nutrition D9.001
D9.000

1-44
DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs) (Cont.)

Category/Code Description NDC #


Inadequacy Calorie Allowance/Intake D10.001
D10.000 Carbohydrate D10.002
Fat-Essential Fatty Acids D10.003
Feeding Route D10.004
Fiber Allowance/Intake D10.005
Food-Diet Consistency D10.006
Mineral D10.007
Protein-Amino Acid Allowance/Intake D10.008
Vitamin D10.009
Water, Fluids/Fluid Balance D10.010
Treatment Time D10.011
Inappropriate Caloric Distribution D11.001
D11.000 Dietary Habits D11.002
Feeding Route D11.003
Food Role Perception/Food Abuse D11.004
Protein Distribution D11.005
Intolerance Drug/Chemical Substance in Food D12.001
D12.000 Food(s)/Nutrient(s) D12.002

1-45

DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs) (Cont.)


Category/Code Description NDC #
Misinformation Nutrition D13.001
D13.000
Misuse Enteral Product D14.001
D14.000 Nutrient Supplement D14.002
Other Food Substance D14.003
Parenteral Product D14.004
Therapeutic Diet/Product D14.005
Nonacceptance Food Item(s)/Nutritional Products D15.001
D15.000
Noncompliance Nutritional D16.001
D16.000
Possibility A Specific Disease D17.001
of/Possibility of Developing Morbidity, Incr. Duration/Severity of D17.002
D17.000 Illness D17.003
Mortality, Increased Risk of
Potential Consequences of Altered Nutrient Function(s) D18.001
D18.000

1-46
DIETETIC-SPECIFIC NUTRITIONAL DIAGNOSTIC CODES (D-S NDCs) (Cont.)

Category/Code Description NDC #


Prevention, Decreasing, Drug Therapy D19.001
Eliminating Need for/
Use of D19.000
Self Assessment Risk Nutritional D20.001
Factors D20.000
Suboptimal Pregnancy Outcome D21.001
D21.000 Nutritional Resiliency D21.002
Toxicity D22.000 Nutrient D22.001
Undesirable Food/Diag/Tx Schedule Interaction D23.001
D23.000 Med/Food/Nutrient Interaction D23.002
Metabolic Setpoint D23.003
Overweight Status D23.004
Underweight Status D23.005
Weight (e.g. loss/gain) D23.006
Unwellness D24.000 Nutritional D24.001
Reference: (Used with permission) © M.A. Kight and Biodietetic Associates, 1994

1-47

MEDICAL NUTRITION THERAPY (MNT)


Medicare Part B Coverage:
Provides for payment of nutrition services for certain beneficiaries who have diabetes or kidney disease. Kidney
disease is defined as chronic renal insufficiency and post-transplant care provided up to 36 months after transplant. The
IOM defines chronic renal insufficiency as the stage of renal disease associated with a reduction of renal function not
severe enough to require dialysis or transplantation (GFR 13-15 mL/min/1.73m2).

Diabetes mellitus (DM) Type 1 is defined as an autoimmune disease that destroys the beta cells of the pancreas leading
to insulin deficiency. DM Type 2 is defined as familial hyperglycemia that occurs primarily in adults...caused by an
insulin resistance where etiology is multiple and not well understood. Institute of Medicine (IOM) lists the diagnostic
criterion for diabetes as a fasting glucose tolerance test >126 mg/dL.

Current Procedural Terminology (CPT) Codes:


97802 - Medical nutrition therapy; initial assessment and intervention, individual, face-to-face with the patient, billed
in 15 minute intervals
97803 - Reassessment and intervention, individual, face to face with the patient, billed in 15 minute intervals
97804 - Group (2 or more individuals), billed in 30 minute intervals

Fees:
Medicare MNT payment is based on the geographical area in which services are provided.
(Medicare MNT Payment Schedule 2002 by Geographic Area)

References: American Dietetic Association at http://www.eatright.org


Centers for Medicare and Medicaid Services at http://hcfa.gov/stats/cpt/rvudown.htm

1-48
COMMON PHYSICAL SIGNS OF MALNUTRITION
Protective hand washing and other protective precautions, appropriate to the situation, should be taken
prior to any physical contact with patients. (Standard precautions)

Body Signs Description Nutrient


Part
Hair Lack of luster Changes not related to salt Protein
Thin and sparse water/sun/heat/physical Protein/Biotin/Zinc
Dyspigmentation damage, cosmetic treatment, Protein
Easy pluckability or scalp disease Protein/Zinc/EFA
Face Diffuse depigmentation Occurs in dark skinned Protein/calorie
Nasolabial dyssebacia individuals B-Complex
Yellow, greasy appearance
from plugged ducts of
sebaceous glands around
nose/lips
Eyes Conjunctival xerosis Dryness, thickening of bulbar Vitamin A
conjunctiva of exposed eye
Bitot’s spots White-grey foamy plaque Vitamin A
usually laterally to cornea
Corneal xerosis Hazy/opaque appearance of Vitamin A
cornea
Keratomalacia Softening of cornea Vitamin A
Tongue Atrophic papillae Smooth, slick appearance Iron

1-49

COMMON PHYSICAL SIGNS OF MALNUTRITON (Cont.)


Body Signs Description Nutrient
Part
Lips/ Angular Stomatitis Fissuring at angles of mouth Riboflavin
Mucous Cheilosis Red, swollen ulceration of lips B Complex
Membrane Pallor Iron

Gums Spongy, Bleeding Swollen gingival tissue Vitamin C


Bright red Red discoloration of gingiva Vitamin A
Ulceration Inflammation (ulceration/stomatitis) Vit. C, Folate, B12
Skin Xerosis Dryness/scaling Essential FA/Zinc
Follicular Hypertrophy of skin around hair follicles with Vitamin A
Hyperkeratosis formation of plaque
Petechiae Hemorrhagic spots in skin/mucosa Vitamin C, K
Pellagrous Dermatosis Skin hyperpigmentation Niacin
Flaky Paint Dermatosis Scaling skin, leaves hypo-pigmented spots Protein
Nails Koilonychia Spoon shaped deformity of nail Iron
Splinter hemorrhages Semi-circular lattice in nail beds Vitamin C
White spotting Spots/dashes on nail Zinc
Musculo- Epiphyseal Enlargement Enlarged ends of long bones Vitamin C, D
skeletal Beading of Ribs Enlarged cartilage at rib junctions Vitamin D

References: Kight MA: Physical Assessment in Renal Disease. CRN Quarterly 11:9-12, 1987
McLaren DS: A Colour Atlas and Text of Diet-Related Disorders, Mosby-Year Book Europe, 1992
Simko M, et al: Nutrition Assessment: A Comprehensive Guide for Planning Intervention, ASPEN, 1995
1-50
Chapter 10:

ADEQUACY OF DIALYSIS
AND
UREA KINETIC MODELING

GENERAL INFORMATION
The goals of this chapter are to give some simple insight into the components of kinetic modeling, to guide the clinician in
interpreting the Kt/V, and to review the adequacy guidelines that were formulated by K/DOQI. While some simple formulas are
given, it is recognized that access to computer software, on-line, or calculator kinetic modeling programs is widespread and few
people calculate Kt/V, protein equivalent of nitrogen appearance (PNA) by hand. Regardless of how adequacy is measured, targets
below should be interpreted in conjunction with other clinical parameters relating to the individual patient.

K/DOQI SUGGESTED ADEQUACY TARGETS, 2001

Modality Kt/V CrCl/L/1.73 Frequency of Adequacy Testing


2
m
CAPD H/HA 2.0 60 L/wk PET, Kt/V, CrCl, urine at month 1; Kt/V, CrCl, urine at
L/LA* 2.0 50 L/wk months 4 & 6; then: Kt/V, CrCl, urine ≥ every 4 months
NIPD 2.2 66 Include SGA and PNA calculations
CCPD 2.1 63 If there is a discordance in the parameters, use the Kt/V
HEMODIALYSIS (spvv NA Formal spvv urea kinetic modeling is recommended at least
model) monthly. Substitute natural log formula Kt/V or URR, if
Rx ≥ 1.3 formal urea kinetic modeling cannot be performed
Del ≥ 1.2 Other recommendations: Use specific, consistent blood
URR ≥ sampling techniques (pg 10-7) and adequacy testing methods;
65% provide routine error analysis and prompt intervention as
needed to meet adequacy and nPCR targets

*Membrane transport characteristic: H=high, HA=high average, L=low, LA=low average


Low and low average transporters have better survival and technique survival, but without residual urine output may not be able to
achieve a CrCl of 60 L/wk, even when Kt/V is adequate. Thus the CrCl target can be set slightly lower as long as patients are
observed closely for evidence of inadequate dialysis.
10-2
KINETIC MODELING GLOSSARY
Access Recirculation - when the blood flow rate set by the blood pump is higher than the access blood flow, some
outflow blood will recirculate within the access back into the inflow stream. This mixes fresh blood from the arterial
segment and dialyzed blood from the venous segment.
Actual Weight - current body weight expressed in kilograms.
Body Surface Area - total surface area of the body, expressed in square meters/derived from height and weight.
Cardiopulmonary Recirculation - dialyzed blood from the venous outflow of the blood access is recirculated back
into the arterial inflow of the blood access through a circulation loop that includes central veins, right heart, lungs, and
the left heart reducing effective blood clearance.
Clearance (K) - dialyzer urea clearance, expressed as plasma water clearance in ml/min or L/min or the volume of
solution that is cleared or depleted of a solute during a given period of time. It can also mean the rate of mass transport
per unit of concentration gradient. The K in formal urea kinetic modeling includes all clearance including urinary.
Compartmental Disequilibrium - spvv kinetic model assumes solute is distributed in a single, well mixed,
homogenous body and is uniformly removed from the total volume. In reality, solute is removed from the peripheral
compartment and the central compartment lags behind at a higher concentration of solute. At the start of dialysis both
compartments are in equilibrium, but at the end of dialysis, disequilibrium causes a rebound of the solute concentration
into the peripheral compartment after the treatment. Depner T. Sem Dial 5(2):147-154, 1992
Desirable Body Weight - same as ideal body weight.
Direct Dialysis Quantification - direct measurements total effluent dialysate urea or in aliquots of dialysate; may
represent a gold standard for assessing urea removal, but is laborious. Several measurements of dialysate must be taken
to prevent magnification of small errors when results are multiplied by the total effluent dialysate.
dpvv Kt/V = double pool, variable volume Kt/V.
Dry Weight = post dialysis weight at which most or all of the excess body fluid has been removed
Equilibrated Kt/V (eKt/V) = delivered dialysis dose obtained by processing a single pool Kt/V through a formula to
estimate the equilibrated (double pool) Kt/V, or Kt/V calculated with a 30 minute postBUN.
10-3

KINETIC MODELING GLOSSARY (Cont.)

eKdrt/V - total equilibrated Kt/V including urea clearance from both dialysis and residual urine output.
eKdt/V - equilibrated Kt/V from the clearance of urea by dialysis alone. This allows the clinician to observe what
portion of the eKt/V results from the residual urine output.
K - dialyzer urea clearance, expressed as plasma water clearance in ml/min or L/min.
Kdrt/V - total Kt/V that includes clearance from dialysis and residual urine output or KrU.
Kdt/V - Kt/V that includes dialysis clearance only. Allows clinician to observe the prescribed Kt/V for a specific
prescription if the patient’s residual urine output decreases to zero.
Kinetic Volume - determined from the drop in BUN during a single dialysis treatment (can also be called “Current
Volume”). A deviation in kinetic or current volume in a single patient serves as a flag for errors in delivery of dialysis.
Kinetic volume, in a problem free dialysis treatment, should approximate the volume from surface area (VSA).
KoA - overall dialyzer permeability for urea, ml/min (product of the membrane permeability/surface area).
Kt/V - dose of dialysis treatment as determined by the solute clearance-time product normalized to the individual’s
volume of urea distribution or urea clearance (K ml/min or L/min) times the treatment length (T minutes) divided by
urea distribution volume (V) is the total urea clearance provided by the dialyzer and any residual urine output.
Normal Body Weight - median weight of healthy Americans, same age range/height/gender/frame size.
Normalized Protein Catabolic Rate (nPCR) - protein catabolic rate in gm/day normalized as some function of weight
(Recommended: nPCR = PCR/ (V/0.58) to provide gm/kg/day). (More correct terminology is nPNA as below).
Normalized Protein Equivalent of Total Nitrogen (nPNA) - PNA normalized to a function of weight (as above).
Protein Catabolic Rate (PCR) - amount of protein catabolized in grams/d. (More correct terminology is PNA as
below).
Protein Equivalent of Total Nitrogen Appearance (PNA) - expresses total nitrogen appearance in terms of protein in
grams per day (normalized is grams per kilogram per day). The conversion is based on the fact that the nitrogen content
of mixed proteins is approximately 16% and quantitatively, most of the nitrogenous compounds lost from the body are
either metabolites of protein (urea) or actual proteins and peptides (in peritoneal dialysate). See formulas page 10-11
and 10-23 to 10-24.
10-4
KINETIC MODELING GLOSSARY (Cont.)

Relative Body Weight - dry body weight expressed as a percentage of the normal body weight for an individual of the
same gender, height, and frame size. More commonly known as SBW.
Residual Renal Function (RRF) - remaining kidney function in a patient receiving dialysis or in advanced CKD;
GFR expressed in milliliters per minute or liters per day. (Terminology in this chapter has been changed to residual
urine output).
Standard Body Weight = Weight for like individual (gender, frame size, height, age) as determined by NHANES II.
spvv Kt/V = single pool, variable volume Kt/V.
T - dialysis treatment time. (In Kt/V the t also includes frequency of dialysis).
Total Body Water (TBW) - estimated volume of distribution of solute expressed in liters.
Total Nitrogen Appearance (TNA) - the sum of all outputs of nitrogen from the body including dialysate/feces/urine
plus the change in body nitrogen, expressed in grams of nitrogen per day.
Urea Nitrogen Appearance - net appearance of urea nitrogen in body fluids/outputs (urine, dialysate, fistula drainage).
Urea Reduction Ratio (URR) - adequacy measure based on the change in BUN for a single dialysis treatment; does
not account for any urinary clearance of urea, the individual patient volume, ultrafiltration rate, or rebound, thus cannot
be strictly correlated with Kt/V. Has been shown to be significant predictor of mortality in HD patients.
V - urea distribution volume or total body water.
Volume From Surface Area (VSA) - is calculated using a formula (see page 10-9). The VSA is fairly stable unless
there is a significant change in weight such as with acute illness or amputation. VSA may be slightly different from
kinetic volume in the first few modeling sessions if the patient is very lean, very obese or has excessive fluid weight.

Reference: Kopple JD, et al: Proposed Glossary for Dialysis Kinetics. Am J Kidney Dis 26(6):963-981, 1995

10-5

METHODS OF MEASURING HEMODIALYSIS ADEQUACY


Method Advantages Disadvantages
Formal Urea Kinetic -Can be used to develop a prescription -Complex calculations require
Modeling -Provides information to help computer/calculator
identify errors in delivery of dialysis -Assumed parameters of clearance/volume
-Permits calculation of PNA -Accurate data is critical (blood draw
-Has outcome study to identify targets technique, recording of time, BFR)
Kt/V Natural Log -Accounts for volume changes (UF/ -Does not support the calculation of PNA
Formula convective transport) (Nomogram is not well tested)
-Correlates with spKt/V -Does not provide analysis/quantitative Rx
-Best alternative after formal UKM calculation
-Does not provide volume or means of QA
Urea Reduction Ratio -Ease of calculation -Does not provide analysis/quantitative Rx
(URR) -Significant predictor of mortality calculation
-Doesn’t support calculation of PNA
-Doesn’t consider residual urine output
-Much less precise in relation to UKM
Kt/V Derived from -Incorrect in ≥ 20% of patients compared to
Percent Reduction of UKM
Urea (PRU) -Not suitable for routine monitoring of
delivered dose of dialysis
Urea Removal/ Very promising -Lack of clinical experience, patient
On-line Monitor outcomes, targets
-Expense of equipment
Reference: NKF K/DOQI Clinical Practice Guidelines for Hemodialysis Adequacy, Update 2000 Am J Kidney Dis. 37(1) Suppl 1,
January, 2001 10-6
PARAMETERS THAT AFFECT ADEQUACY

Treatment Patient
Blood Flow Rate Height/Weight/Volume
Dialysate Flow Rate Chemistries/Dietary Intake
Dialyzer Capabilities Residual Urine Output
Frequency/Duration

FORMAL UREA KINETIC MODELING (Kt/V) COMPONENTS

K = Total Clearance T = Time V = Volume


Dialyzer efficiency Frequency Body water in which urea is distributed
Blood & dialysate flow Duration
rates
Residual Renal Function

Accurate blood sampling techniques and data recording are necessary for accurate UKM results.
For spvv formal urea kinetic modeling:
PreBUN should be drawn immediately prior to the dialysis treatment, taking care to prevent dilution with saline or
heparin.

PostBUN should be drawn with the slow flow, stop pump technique which prevents sample dilution with recirculated
blood and minimizes confounding effects of urea rebound.

10-7
2-7:

BODY WATER VOLUME


1. Affected by height, weight, age, gender, body fat or muscle stores.
2. Remains relatively constant over time if weight is stable.
3. Can be measured three ways:
a. % Body Weight (50 - 60% male, 50 - 55% female). Inaccurate in approximately 20 - 25% of population.
b. Surface Area (considers ht, wt, gender). Inaccurate in approximately 15% of population.
c. Kinetic or variable volume is determined kinetically from the drop in BUN during a single dialysis treatment;
most accurate, but requires computer assistance. Is skewed when there is an error in the delivery of dialysis.
4. Body water may be low in dialysis patients secondary to low muscle mass, thus what is abnormal in a person
without kidney disease may be normal for a dialysis patient. Expected values for disease-free individuals:
Lean male - 57% Lean female - 52% Obese - 35-40% Very lean - 65%
5. Deviations in kinetic V in a single patient serve as a flag for errors in dialysis clearance.
6. When clearance < expected with a given dialyzer/BFR/DFR/VSA/time/frequency, the kinetic V will be skewed
higher than VSA. The model assumes actual body water is > VSA (calculated) because urea clearance was <
expected (there was a larger body of water from which urea was being cleared).
7. Conversely, when clearance is > than expected with specific treatment parameters, kinetic V will be lower than
VSA. The model assumes that the actual body water is smaller than VSA (calculated) since urea clearance was >
expected (there was a smaller body of water from which urea was being cleared).

10-8
VOLUME FROM SURFACE AREA (VSA) CALCULATION FORMULAS
Hemodialysis: Recommended VSA Formula
BEI Derived Formula:1
Volume (TBW) = -(0.07493713 x age) - (1.01767992 x male) + (0.12703384 x ht) - (0.04012056 x wt) + (0.57894981
x diabetes) - (0.00067247 x wt2) -0.03486146 x (age x male) + 0.11262857 x (male x wt) + 0.00104135 x (age x wt)
+ 0.0186104 x ( ht x wt)
Wt=pt weight/kg Ht=pt height/cm Other factors: Male=1.0 Diabetic=1.0 (if not diabetic/male, values=0)
Peritoneal Dialysis: Recommended VSA Formulas
Watson:
Male: Volume = 2.447-(0.09516 x ageyrs) + (0.1074 x ht cm)+ (0.3362 x wtkg)
Female: Volume = -2.097 + (0.1069 x htcm) + (0.2466 x wtkg)

Hume & Wyers: (J Clin Path 24:234-238, 1971)


Male: Volume = (0.194786 x ht cm) + (0.296785 x wtkg) - 14.012934
Female: Volume = (0.34454 x ht cm) + (0.183809 x wtkg) - 35.270121

Mellits-Cheek Method: Pediatrics


Boys: Volume = -1.927 + (0.465 x wtkg) +(0.045 x htcm) when height is ≤ 132.7 cm
Volume = -21.993 + (0.406 x wtkg) + (0.209 x htcm) when height is > 132.7 cm
Girls: Volume = 0.076 + (0.507 x wtkg) + (0.013 x htcm) when height is ≤ 110.8 cm
Volume = -10.313 + (0.252 x wtkg) + (0.154 x htcm) when height is > 110.8 cm

Reference: NKF K/DOQI Clinical Practice Guidelines for HD Adequacy, 2000 Update, Am J Kidney Dis. 37(1)
Suppl 1, January, 2001
1Chertow GN, et al: Development of a population-specific regression equation to estimate TBW in HD
patients. KI 51:1578-1582, 1997
10-9

DIFFERENCES BETWEEN SINGLE POOL AND DOUBLE POOL KINETICS

Single Pool* Double Pool


Does not account for different rates of urea transfer More accurate in quantifying true intradialytic urea
between body compartments or different blood flow removal and more precise PNA; 30 minute post BUN is
rates to organs. not practical for all patients; formula to calculate eKt/V
from single pool Kt/V:
eKt/V = spKt/V – (0.6)(K/V) +0.03

With increased dialyzer efficiency, urea removal can exceed diffusive transfer rates which creates urea rebound for 30-
60 minutes after treatment. Blood sampling immediately at the end of treatment does not reflect urea that equilibrates
from tissues back into blood, thus BUN is falsely low, and Kt/V is overestimated by about 0.2. Rebound varies from
patient to patient. (One study showed a mean rebound of about 17% at 30 minutes after treatment, some patients as
high as 45% rebound). Rebound begins within minutes of the end of treatment. Most patients equilibrate within 15
minutes, others take up to 60 minutes. Rebound is exaggerated in small patients, cardiac compromised patients, and
treatments complicated by intradialytic hypotension.

*K/DOQI Clinical Practice Guidelines for HD Adequacy recommend the use of single pool variable volume kinetic
modeling because outcome studies are lacking for double pool kinetic modeling.

References: Daugirdas JT, Ing TS: Handbook of Dialysis, 2nd Edition, Little, Brown, & Co., 1994
NKF K/DOQI Clinical Practice Guidelines for HD Adequacy, 2000 Update, Am J Kidney Dis. 37(1) Suppl
1, Jan, 2001

10-10
HEMODIALYSIS FORMULAS FOR UREA KINETIC MODELING (UKM)

1. Measure recirculation using a nonurea-based dilutional or two needle urea-based method. Any recirculation is
abnormal, but recirculation of >10% in the two needle method or >5% with nonurea-based dilutional method
should be investigated. Check needle placement prior to further studies when recirculation exceeds 20%. Perform
the test after approximately 30 minutes of treatment with ultrafiltration turned off.
a. Draw arterial (A) and venous (V) line samples. Immediately reduce blood flow rate (BFR) to 120 mL/minute.
b. Turn blood pump off exactly 10 seconds after reducing BFR. Clamp arterial line immediately above the
sampling port; draw systemic (S) arterial sample from the arterial port line. Unclamp the line, resume dialysis.
c. Measure the BUN in the arterial, venous, and systemic sample and calculate the percent recirculation.
% Recirculation = S - A X 100
S-V
2. PNA (g/pro/day)=PCR (In patients with no significant protein losses) (PNA is the most accurate terminology)
PNA (g/pro/day)=PCR + protein losses (In patients with significant urinary or dialytic protein losses)
3. PNA/PCR calculations are most accurate when calculated with UKM, but following the formulas can estimate PCR:
PNA/PCR (without renal function) GU (mg/min) = (BUN2 x Vu2) - (BUN1 x Vu1) ÷ t
PNA/PCR (gm/day) = 9.35 (GU) + 0.294(V)
PNA/PCR (with renal function) GU (mg/min) = [(BUN2 x Vu2) - (BUN1 x Vu1)/t] + [ KrU x (BUN1 + BUN2/2)
PNA/PCR = (6.49 x UNA) + (0.294 x V) (Borah equation)
4. nPNA = PNA ÷ V/0.58
5. Calculation of Residual Renal Urea Clearance (KrU)
3x wk KrU ml/min = Vu (mL) x Uu (mg/mL) 2X wk KrU mL/min = Vu (mL) x Uu (mg/mL)
t x (0.25 BUN1 + 0.75 BUN2) mg/mL t x (0.16 BUN1 + 0.84 BUN2)
V1 = estimated urea volume V2 = V1 + interdialytic wt gain t = interdialytic time in minutes
Vu = urine volume (mL) during interdialytic period Uu = urine urea nitrogen mg/mL
BUN1 mg/mL = Post-BUN (1st tx of week) BUN2 mg/mL = Pre-BUN (2nd run of week)

References: Jindal KK, Goldstein MB: UKM in Chronic HD. Sem Dial 1:82, 1988
Gee C, Schroeffer C: Urea Kinetics in Nutritional Management of PreESRD, 1997 10-11

SUMMARY OF K/DOQI HEMODIALYSIS ADEQUACY RECOMMENDATIONS

1. Monthly formal urea kinetic modeling.


2. Minimum prescribed Kt/V of ≥1.3.
3. Minimum delivered Kt/V of ≥1.2 for thrice weekly dialysis.
Twice weekly dialysis is not recommended. Although with a GFR >5 mL/min/1.73m2, reduced frequency
may be tolerated, but residual urine output must be monitored diligently and frequency increased as needed to
ensure adequate treatment. (see *Note below)
4. Rigorous blood sampling techniques as outlined in the K/DOQI Clinical Practice Guidelines. (Slow flow,
stop pump)
5. Error analysis with timely modification of treatment parameters to correct underdialysis.
6. Research is needed for alternative methods of adequacy testing; more precise definition of adequate versus
optimal dose of dialysis.

* Note: It has been suggested that at minimum Kt/V of 2.3 be maintained in 2x week patients. Correspondence from
Dr. Frank Gotch, San Francisco, CA, to Satellite Healthcare, March, 1997.

Reference: NKF K/DOQI Clinical Practice Guidelines for HD Adequacy, Update 2000, Am J Kidney Dis. 37(1) Suppl
1, January, 2001

10-12
COMMON CAUSES OF DELIVERED Kt/V ≠ PRESCRIBED
Problem Comment
Access Recirculation Average is 7% (Range 0-100%) can be affected by BFR, needle size, needle placement,
graft placement (more proximal = less prone to recirculation). With transonic
measurements recirculation should be “0.” Potential indicators: high or increasing
venous pressure, black blood syndrome, Kt/V lower than predicted, large increase in
kinetic volume, small needle size. Evaluate: Transonic access evaluation, two needle
urea-based recirculation test, saline recirculation test, hydraulic compression test
Changes in Residual Failure to routinely measure urinary urea clearance results in underestimation of PNA,
Renal Function ignores a significant route of nitrogen elimination. Low preBUN is due to unmeasured
urinary clearance, not low generation/intake. Potential Indicators: nPNA different
than actual pro intake/other protein parameters. Evaluate: 24-48 hr urine collection,
increased ID gain/preBUN as output decreases.
Dialyzer Capabilities Overestimation of clearance capabilities. Clearance can also be reduced by clotting
(decr is not linearly related to loss of volume, 20% loss of volume in a hollow fiber
dialyzer causes approximately a 10% loss of clearance). Potential indicators: Low
Kt/V, high kinetic volume. Evaluate: Check reuse number, total cell volume (should be
≥80%), eliminate other causes of decreased clearance, recheck kinetics with a new
dialyzer.
Excessive ID Weight Patients who cycle on the verge of pulmonary edema pretreatment to volume depletion
Gain posttreatment can have diluted pre-BUN, concentrated/normal post-BUN. Evaluate:
ID weight gain/UF ave.
Double Pooling See page 10-10. Potential indicators: High PNA, high Kt/V, high pre BUN, low
kinetic V Evaluation: 30-minute post BUN, computer calculation of eKt/V.
10-13

STEPS TO ERROR ANALYSIS OF FORMAL HD UKM


Initial analysis:
1. Compare the dialysis prescription to what was actually delivered.
Was the actual BFR = prescribed BFR? Actual time=prescribed? Dialyzer = prescribed? Dialysate flow
rate=prescribed?
If the treatment parameters were not delivered as prescribed, the delivered Kt/V will be different than the prescribed
Kt/V, but the kinetic volume and VSA will not be different unless other problems are also present.
2. Identify the abnormalities/compare: Prescribed Kt/V to delivered Kt/V. Volume from surface area or mean volume
to kinetic (current) volume. nPNA/nPCR to actual protein intake and/or mean nPNA/nPCR.
3. Any significant error (high or low) or a delivered Kt/V < 1.2 should be investigated.

In-depth analysis:
1. Review previous modeling to compare results and parameters. Were pre- and post-BUN levels similar to previous
values? Drawn correctly? Be suspicious of very low post-BUN which may have been drawn from venous line.
2. Look for signs of recirculation (needle placement or size/notations of high or changing venous pressures).
3. Review ID weight gains and dry weight changes. Significant increase in hematocrit can make a small difference.
4. Note dialyzer reuse number, comments on visual inspection of dialyzer, and the tested total cell volume.
5. Clinical difficulties during the run (hypotensive episodes, access problems, off to bathroom, etc.).
6. There may be a combination of problems. When more than one problem is present, the indicators of one problem
may be masked or canceled out by another problem. For example: If a patient has significant rebounding (which
would normally cause a skew downward in kinetic volume) and a concurrent access problem (which would normally
cause a skew upward in kinetic volume), the two might cancel each other out. This would result in the kinetic V
being reasonably close to VSA or mean V and the delivered Kt/V similar to prescribed. Thus neither problem would
be obvious.

10-14
HELPFUL INFORMATION FOR ANALYSIS OF UKM RESULTS:
1. Facility-specific blood sampling techniques. Timing affects values. Sampling should be appropriate for type of
adequacy measure being used and consistent for all patients. (See K/DOQI Clinical Practice Guidelines for HD
Adequacy)
2. Urine handling procedures. Refrigeration retards bacterial growth that can skew urea content in the urine.
3. Machine functions - do they track real treatment time, not just clock time?
4. Type and placement of access for each patient (from the medical record or daily log).
5. Routines for cannulation (distance between needles, orientation of needles).
6. Procedures and average reuse for each patient.
7. Average venous pressures for each patient.
8. Measured (not stated) patient height for accurate VSA calculation.
9. Actual dietary protein intake for comparison to the kinetically generated PNA.
10. Be sure that those who record the treatment parameters are recording actual delivered (time, BFR, DFR, etc.)
treatment parameters, not just what the prescription says.

10-15

ERROR ANALYSIS FOR FORMAL UKM

If Kt/V is < than expected (low clearance) and Kinetic V is > VSA or mean Volume

A. Evaluate Clearance
1. Was blood flow really recorded as delivered? (Turned down or low because of poor access, increased gradually to prescribed
level, but recorded at the prescribed level).
2. Is blood pump calibration correct? (Check other patients using the same equipment).
3. Is the blood pump stroke volume accurate? (Pre pump tubing collapsed with negative pre pump arterial pressure).
4. Clotting of dialyzer? Incorrect dialyzer data (would be consistently off, not just one time)?
5. Access recirculation? (Large increase in kinetic volume, high/changing venous pressures, needles too small).
6. Reuse problem? (Sudden drop in Kt/V, high reuse number, marginal TCV).
7. Was DFR set at the prescribed level and recorded correctly? (May not have been reset after the previous patient).
8. Blood lines or needles reversed?
B. Evaluate Blood Sampling Procedure
1. Was the post BUN drawn too late (BUN begins to equilibrate quickly)?
2. Was the pre BUN sample diluted with saline?
C. Evaluate Volume (V): With spvv UKM, a kinetic volume is determined each time. This kinetic or current volume reflects an
estimate of body water based on the clearance of urea during the individual treatment. If the clearance of urea is less than expected
with a certain dialysis prescription (BFR, DFR, time, frequency, dialyzer, patient VSA), it is assumed that the body of urea-laden
body water is larger than the body water estimate from VSA. These changes indicate an error in the delivery of dialysis. Real
changes in volume (not reflective of an error in the delivery of dialysis) occur if the patient is very muscular, obese, or has had a
significant weight change such as an amputation. In a muscular patient, the kinetic volume may be higher than the anthropometric
volume or VSA since muscle has a higher water content. If the patient has a high level of fat, the actual volume will usually be
lower than the anthropometric volume or VSA because fatty tissue has a lower water content. Most formal kinetic modeling
programs, provide only the VSA to compare to kinetic volume. If the UKM program saves data from session to session, a mean
volume can be calculated. This provides a more accurate volume with which to compare the kinetic volume in those patients with
atypical body composition where legitimate adjustments in body water are averaged into the mean over a few UKM sessions.

10-16
ERROR ANALYSIS FOR FORMAL UKM (Cont.)
If Kt/V is lower or higher than prescribed, but volume is similar to VSA or mean volume

Evaluate Treatment Parameters - because the calculations are based on actual delivered treatment, if the time, BFR,
DFR not delivered as prescribed, but are recorded accurately, formal UKM will use those actual delivered
parameters to calculate the expected Kt/V and the V will not be skewed. The clearance of urea will be
approximately equal to what is expected for the time, BFR, DFR, etc. If the treatment is not delivered as
prescribed but is recorded as if it was, the volume will be skewed.
1. Was treatment time delivered as prescribed? Minor differences (i.e. 5 minutes) don’t impact results that much.
2. Was blood flow rate/dialysate flow rate equal to prescribed? (Same as above)
3. Was the correct dialyzer used?

Monitor urine output:


1. Look for increased ID weight gain which signifies a decrease in output.
2. Look for changes in preBUN (will be higher as output decreases, if protein intake is stable).
3. May see increased albumin if patient has been nephrotic and then urine output drops.

10-17

ERROR ANALYSIS FOR FORMAL UKM (Cont.)


If Kt/V is > than expected and volume is < than surface area or mean volume (clearance better than expected):

A. Evaluate Clearance
1. Was the blood flow rate higher than prescribed? Dialysate flow rate higher than prescribed?
2. Was dialyzer performance better than expected? (Happens often if using in vivo rather than in vitro clearance figures).
3. Is there poor urea equilibration (double pooling)? (Common in small person with high blood flow/short time. Would normally
also see a PNA higher than actual intake, high preBUN if the patient has slow equilibration).
B. Evaluate Recorded Treatment Parameters
1. Were the delivered parameters recorded correctly? Is the machine properly calibrated?
C. Evaluate Blood Sampling Procedure
1. Was the post BUN drawn from the venous line? (Often indicated by abnormally low post BUN, <10 mg/dL).
2. Was the post BUN drawn in accordance with the adequacy method used? Was the post BUN diluted with saline?
3. Was the timing of blood sampling correct?
Immediate = falsely elevated Kt/V, inappropriate timing for any method of adequacy.
15 - 30 seconds after termination of treatment = most appropriate for formal single pool UKM
Slow flow/stop pump technique (angioaccess recirculation resolved, urea rebound beginning)
2 - 3 minutes = low Kt/V/URR because of rebound, cardiopulmonary recirculation dissipated
5 - 10 minutes = low Kt/V or URR because of significant but incomplete urea rebound.
30 minutes = equilibrated for most patients, correlates with double pool model.

Other: Kt/V should be increased in proportion to mean nPNA if protein intake is appropriate or restriction of protein is not
advisable (malnourished patient). Example: In a patient with a mean nPNA of > 1.1, the Kt/V should match the nPNA.
Gotch FA, Keen ML: In Cognan MG: Introduction to Dialysis, Churchill & Livingston, NY, 1991

10-18
DIALYZER CHARACTERISTICS
Type UFR Surface Area
Conventional (refers to 2-6 ml/ mmHg/hr 0.4-1.3 sq. meters
moderate urea clearances, small
pores)
High Efficiency (refers to urea 7-19 ml/ mmHg/ hr 1.3-2.2 sq. meters
clearance)
High Flux (refers to UF 20-60 ml/ mmHg/hr 1.2-1.9 sq. meters
coefficients and pore size)
Membrane Characteristics Names
Cellulose Least expensive; causes the most Cuprophane
complement activation; contact with blood
causes muscle protein catabolism indicated
by aa in efferent blood; less Beta 2
removal *
Modified Cellulose Somewhat more biocompatible because Cuprophane acetate/diacetate/
reactor sites are buffered with aa; less triacetate, cuprammonium rayon
likely to cause aa release secondary to
muscle protein catabolism*
Synthetic Most biocompatible, but to different Polyacrylonitrile (PAN)
degrees; polysulfone membranes are Polymethylmeth-acrylate
endotoxin permeable so there is potential (PMMA)
for inducing endotoxemia.* Polysulfone
*Adverse effects are directly proportional to the amount of complement generated by the membrane, amount of
complement generated is dependent on size and type of the membrane.
Reference: Manufacturers’ Information
10-19

FORMULAS TO ESTIMATE EQUILIBRATED Kt/V

Author Formula
Smye Ceq= Co x EXP (-[T/T-Ts]) x Ln [Cs/Ct]
Ceq = equilibrated post-/ dialysis BUN
Co = pre-dialysis BUN
Cs = mid-dialysis (70 minute) BUN
Ct = BUN at the end of dialysis
T = duration of treatment
Ts = time at which the mid-dialysis BUN is drawn
EXP = exponential of bracketed terms
Ln = natural logarithm of bracketed terms

Daugirdas-Schneditz *arterial post BUN from A-V access:


Rate Adjustment Equation art. eKt/V = art. spKt/V - (0.6 x art. spKt/V/t) + 0.03
venovenous access post BUN:
ven. eKt/V=ven. spKt/V - (0.4 x ven. spKt/V/t) + 0.02
eKt/V = equilibrated Kt/V
spKt/V = single pool Kt/V
t - treatment time in hours
* Mathematical relationship between eKt/V and spKt/V
depends on location of access and blood sampling site.

References: Daugirdas JT, et al: Comparison of models to predict the equilibrated Kt/V in the HEMO study. J Am
Soc Nephrol 6:596, 1995
10-20
FORMULAS FOR OTHER MEASURES OF HD ADEQUACY

Measure Formula Targets


Natural Logarithm Kt/V = -Ln (R - 0.008 X time) + (4 - 3.5 x R) x Same as for formal UKM
Formula ultrafiltration volume in L¸ post dialysis weight in
kg (Where R = post BUN divided by pre BUN)
URR URR = 100 X (1- post-BUN/pre-BUN) ≥ 65%
With significant interdialytic weight gains and (approx. = Kt/V of 1.2)
subsequent ultrafiltration, the URR has variable
correlations to Kt/V.

Reference: NKF K/DOQI Clinical Practice Guidelines for HD Adequacy, Update 2000, Am J Kidney Dis. 37(1)
Suppl 1, January, 2001

10-21

DAILY HEMODIALYSIS

Daily short dialysis has been used by various invesitgators since 1967. It has been consistently associated with marked
improvement in patient well being. Daily short dialysis and slow nocturnal dialysis are both seen as superior standards
of care. The following clinical benefits have been reported:

Increased hematocrit with decreased need for erythropoietin


Enhanced blood pressure control and decreased need for pharmacologic blood pressure therapy
Increased protein intake and body weight (intake went from 1.0 gm/kg to 1.3 gm/kg)
Significantly fewer complications of dialysis (hypotension, headaches, cramps, post-dialysis fatigue)
Increased energy and patient-reported improvement in quality of life
Assumed decrease in mortality
Little or no need for diet restriction (research will help define nutrient losses and replacement needs)
Little or no need for phosphate binders (no patients needed binders, 70% required phosphorus supplementation)
Focus is on long-term healthy eating and activity/exercise as recommended for those without CKD. This becomes
even more important as we are hopeful that these patients will live longer on dialysis therapy.

Adequacy testing for daily short HD and slow nocturnal HD is in development stages. It is possible to modify formal
UKM calcuations to consider the increased frequency of dialysis. Since formal urea kinetic modeling was deemed by
K/DOQI to be the best method of adequacy testing for thrice weekly HD, it is logical that we should apply the same
standard to more frequent dialysis. Some use a simple adaptation of URR, however, the same limitations of URR in
thrice weekly dialysis, would likely apply to its use in more frequent HD therapy (see page 10-6).

Reference: McPhatter LL, Lockridge RS: Nutritional Advantages of Nightly Home HD. NNI16 (3):31-36, 2002
Gotch FA, Levin NW: Daily Dialysis: The Long and Short of It. (Submitted for publication)
10-22
PD ADEQUACY FORMULAS Patient Example:

1. Calculate TBW and BSA (see page 10-9) Urea mg/dL Creat mg/dL Volume mL
2. Calculate residual urea clearance: Urine: 333(Uu) 136 (Ucr) 475 (Uv)
(Uu x Uv)/(1440 x Su) Serum: 60 (Su) 6.91 (Scr)
Dialysate: 52 (Du) 4.5 (Dcr) 12485 (Dv)
3. Calculate residual (urinary) Kt/V: (Total effluent)
(Urea clearance x 1440 x 7)/(V x 1000) 1. BSA = 1.88 m2 Total Body Water or Volume (V) = 40.4
2. Resid. urea clear = (333 x 475)/(60 x 1440)
4. Calculate dialysis Kt/V: (Du/Su x Dv x 7)/(V x 1000) = 158175/86400 or 1.83 mL/min
3. Residual Kt/V = (1.83 x 1440 x 7)/(40.4 x 1000)
5. Calculate total Kt/V: Residual Kt/V + Dialysis Kt/V = 18446.4/40400 or 0.46/wk
4. Dialysis Kt/V = (52/60 x 12485 x 7)/40.4 x 1000
6. Calculate creatinine clearance: (Ucr x Uv )/(1440 x Scr) = 75771.47/40400 or 1.88/wk
5. Total Kt/V = 0.46 + 1.88 or 2.33
7. Calculate mean GFR: 6. Residual CrCl = (136 x 475)/(1440 x 6.91)
(Residual CrCl + Residual urea clearance)/2 = 64600/9950 or 6.49 g/d
7. Mean GFR = 2.33 + 1.83 or 4.16 mL/min
8. Calculate Urinary CrCl: (Mean GFR x 1440 x 7)/1000 8. Urinary CrCl = (4.16 x 1440 x 7)/1000
= 41932.8/1000 or 41.9 L/wk
9. Calculate Dialysis CrCl: (Dcr /Scr x Dv x 7)/1000 9. Dialysis CrCl = (4.5/6.91 x 12485 x 7)/1000
= 0.651 x 12485 x 7/1000
10. Calculate total CrCl: = 56894.2/1000 or 56.9 l/wk
Urinary CrCl + Dialysis CrCl 10.Total CrCl = 41.9 + 56.9 or 98.8 l/wk

11. Normalize to patient BSA 11.Normalized CrCl = 98.8 x 1.73/1.88 or 90.9 l/wk
Total CrCl x 1.73/Pt BSA

10-23

PD ADEQUACY FROMUALS (Cont.) Patient Example: (Same values as 10-23)

1. UNA = (52/100 x 12485)+(333/100 x 475)/1000


1. Calculate UNA UNA = 6492.2 +1581.75/1000
(Du/100 x Dv) + (Uu/100 x Uv)/1000 UNA = 8.07

2. Determine if the patient has protein losses >15 g/d. 2. Obtain 24 hour protein levels from urine and
Potential: Nephrotic patients, those with high dialysate. Sample patient has 117 mg/dL protein in
transport membranes, and those whose clinical dialysate (Dpro) and 107 mg/dL in urine (Upro).
picture doesn’t correspond with chemistries (well Pro loss gm/d =117x(12485/100)+107x(475/100)/1000
nourished, eating well, but low protein parameters.) Pro loss gm/d = (117 x 124.9) + (107 x 4.75)/1000
Obtain 24 hr protein levels for dialysate and urine. Pro loss gm/d = (14613.3 + 508.25)/1000
Convert to gm/day. Total pro loss g/d = 15.1 g
Dpro x (Dv/100) + Upro x (Uv/100)/1000
3. PNA = (6.49 x 8.07) + (0.294 x 40.4) + 24 hr pro loss
3. Calculate PNA if protein loss >15 g/d PNA = 52.4 + 11.8 + 15.1
PCR = (6.49 x UNA) + (0.294 x V) PNA = 64.2 + 15.1
PNA = PCR + Protein losses PNA = 79.3 gm/d

4. Calculate PD PNA (if protein loss <15 gm) 4. PNA = 10.76 x (0.69 x 8.07 + 1.46)(if pro loss < 25 gm)
PNA g/d PNA = 10.76 x 7.031
(Incorporates ave. PD protein loss of 7.3 g/d) PNA = 75.65 gm/d
10.76 x (0.69 x UNA + 1.46)
5. nPNA = 75.65/(40.4/0.58)
5. Calculate Normalized PNA (nPNA) nPNA = 75.65/69.57
nPNA = PNA/(V/0.58) nPNA = 1.09 gm/kg/d

10-24
SUMMARY OF K/DOQI PD ADEQUACY GUIDELINES

1. Initiate dialysis incrementally to maintain a total Kt/V of at least 2.0 and nPNA of at least 0.8 gm/kg.
2. PD adequacy testing should be performed within one month and at least 1 additional time between month 2 and
6 (depends on consistency from initial results), and then q 4 months.
3. PD targets are based on the type of PD therapy with continuous, longer dwell time (CAPD) targets lower than
those for interrupted (NIPD) or shorter dwell therapies (APD). The Kt/V and CrCl L/wk/1.732 targets are:
CAPD 2.0/60 L for high and high average transporter and 2.0/50L for low and low average transporters, NIPD
2.2/66 L, CCPD or APD 2.1/63 L.
4. If total daily creatinine excretion differs from baseline by ≥15%, error analysis should be initiated (patient
compliance, dialysate/urine collection procedures/accuracy, altered peritoneal transport characteristics).
5. Nutritional status of adult PD patients should be assessed at least every 4 months using SGA (1-34 to 1-41) and
PNA (See page 10- 24). Evaluate pediatric patients using PNA and other nutritional assessment techniques that
have been demonstrated as accurate in pediatric patients.
6. Identify and correct patient or staff errors in meeting minimum targets.
7. Regularly measure clinical outcomes (patient survival, technique survival, hospitalization rates, patient-based
QOL, albumin, Hgb/Hct, nPNA, and school attendance/developmental progress in pediatric patients).
8. Indications for PD (pt preference, medical complications/no assistant for home HD). Contraindications for
PD: loss of peritoneal function, inability to perform and no assistant, mechanical defects/leaks, body size, severe
malnutrition, diverticular/bowel disease Reasons to change to HD: consistent adequacy failure, unmanageable
hypertriglyceridemia, recurrent peritonitis/complications, technical/mechanical problems, severe malnutrition.

Reference: NKF K/DOQI Clinical Practice Guidelines for PD Adequacy, Update 2000, Am J Kidney Dis 37(1) Suppl
1, January 2001

10-25

KINETIC MODELING FORMULAS FOR CKD NOT ON DIALYSIS


1. Urea Clearance (KrU) - urine urea x urine volume
BUN time

Creatinine Clearance (CrCl) = urine creatinine x urine volume


serum creatinine time

2. Approximate GFR mL/min = KrU mL/min + CrCl mL/min


2

3. Urea Generation Rate (GU) = KrU x BUN concentration


Creatinine Generation (GCr) = KrCr x Creatinine concentration

4. PNA (PCR) = 9.35 (GU) + 11

5. nPNA (normalized protein equivalent of total nitrogen appearance) = PNA/Lean Body Weight (LBW)
LBW = Total Body Water/0.58 (TBW see 10-9)

6. PNA is the more accurate terminology and:


PNA = PCR (if there are no urinary protein losses)
PNA = PCR + urinary protein losses

Reference: CRN of Northern California/Northern Nevada, Pre-End Stage Renal Disease: A Guide for the Professional
Nutritionist, 1986.

10-26
NUTRITION INTERVENTION BASED ON nPNA

HD nPNA Significance Nutritional Intervention PD


nPNA
>1.4 Excessive intake, excessive Assess dietary intake, decrease protein intake if >1.5
LBV protein, or catabolism excessive and patient is well nourished. Look for other
problems such as catabolism (change in weight/ protein
status).
1.2 Ideal Encourage patient to continue current intake if protein 1.2 - 1.3
status/weight are acceptable
0.7 - 0.9 Inadequate protein intake, Assess dietary intake, counsel patient to increase <1.2
inadequate treatment also protein/calorie intake if appropriate. Look for signs of
increases risk of morbidity/ anabolism (change in wt/protein status). Consider oral
mortality. nutritional supplement. Assess dialysis adequacy.
0.6 - 0.69 Begin oral supplement as tolerated, encourage intake, <0 .8
assess adequacy.
<0.59 Aggressive nutrition support as appropriate. Routinely
assess adequacy at all stages. <0.60

10-27

GLOMERULAR FILTRATION RATE (GFR) CALCULATIONS


MDRD Equation1:
GFR = 170 x serum creatinine -0.999 x SUN -0.17 x Age-0.176 x serum albumin0.318 x 0.762 if female0.762 x 1.18 if black race

Modified MDRD Equation2:


186 x sCR-1.154 x age -0.203 x 0.742 if female x 1.212 if black race

Cockroft-Gault Equation3:
GFR = [(140-age) x body weight (kg) x 0.85 if female] / [72 x serum creatinine (mg/dL)]
1
Reference: Levy AS, Bosch JP, Lewis JB, et al: A more accurate method to estimat GFR from serum creatinine: A
new prediction equation. MDRD Study Group, Ann Intern Med 130:461-470, 1999
2
Levey AS, Greene T, Kusek JW, et al. A simplified equation to predict glomerular filtration rate from
serum creatinine. J Am Soc Nephro 11, 2000
3
Walser M: Assessing renal function from creatinine measurements in adults with chronic kidney failure.
Am J Kidney Dis. 32:23-31, 1998

ESTIMATION OF CREATININE CLEARANCE


Male CrCl = Wt in kg x (140 - age)
72 x serum creatinine (mg/dL)
Female CrCl = Use above formula and multiply by 0.85
Paraplegics = Use above formula and multiply by 0.80
Quadriplegics = Use above formula and multiply by 0.60

References: Schrier R, Ed: Manual of Nephrology, Little Brown and Co., Boston, 1990
Daugirdas JT, Ing TS: Handbook of Dialysis, Little, Brown & Co., 2000

10-28
Chapter 11:

SPECIAL CONSIDERATIONS
FOR THE
PEDIATRIC PATIENT

Notes:

11-2
NUTRITION ASSESSMENT OF THE PEDIATRIC PATIENT

There are a number of clinical issues that may differ in pediatric patients. This chapter is not all inclusive, but
highlights the major differences in assessment parameters for pediatric patients. Notations in this chapter indicate
where additional information is included within the adult assessment chapters. If a specific topic is not addressed, it is
because the pediatric editors determined that there were no significant differences or that the topic was not applicable to
pediatric patients. For more detail on pediatric nutritional assessment, please consult the reference list at the end of this
chapter.

11-3

PRACTICAL STEPS TO NUTRITION ASSESSMENT OF PEDIATRIC PATIENTS


1. Follow-up must be more frequent, depending on age and body needs.
Dialysis patient - Monthly Transplant - Every 1-4 weeks
Pre-dialysis - Monthly, if failure to thrive is an issue
2. Person(s) to Interview: Infant/toddler - primary care giver (parent, grandparent, guardian)
School age children - both child and primary care giver
Adolescent - adolescent with corroboration of primary care giver, as needed
3. Physical assessment to document growth must include routine evaluation of:
Length (laying) or height (standing)
Weight
Head Circumference (age 36 months and younger)
Use standardized measuring techniques
(Queen P: Handbook of Pediatric Nutrition, Aspen Publications, pg. 12, 1993)
Plot results on age and sex appropriate standard or premature growth charts as
applicable to determine percentiles of:
Weight for age Height for age Head Circumference
Weight for height Height age (Age 36 months and below)
Arm anthropometry (Frisancho tables) Mid-arm circumference Triceps Skinfold
Infants (less than 24 months) include: Gestational age Birth weight/length
4. Evaluate current feeding skills/abilities: Sucking (infant)
Chewing/swallowing Self-feeding (finger foods/spoon/bottle/cup)
5. Determine status of toilet training/assess:
Urine output Stool output (frequency, color, consistency)

Note: SGA has not been validated in pediatric patients.


11-4
ASSESSMENT OF PROTEIN/ENERGY STATUS IN PEDIATRIC PATIENTS (K/DOQI)
Initial intense nutritional counseling for appropriate caretakers on individualized plan of care including standard
measurements of growth and physical development. This should be developed early in treatment, reevaluated
frequently, and modified according to progress (minimally every 3-4 months).

Appropriate Methods for Frequency* Frequency* Other


Evaluation of Protein/Energy <2 yrs >2 years
Status
Dietary interview Monthly q 3-4 mo Acid Base Balance:
Serum Albumin Monthly Monthly Maintain serum CO2: ≥ 22 mmol/L
Height/length Monthly q 3-4 mo With administration of alkali
Estimated dry wt Monthly q 3-4 mo therapy or change in dialysate
Weight/Height Index Monthly q 3-4 mo concentration
MAC, MAMC, MAMA q 3-4 mo q 3-4 mo
Skinfold thickness NA q 3-4 mo
Head Circumference (< 3 yrs) Monthly q 3-4 mo to 36 mo
Standard Deviation Score for height
for chronological age Monthly q 3-4 mo
Urea Kinetic Modeling q 3-4 mo PD q 3-4 mo PD PNA not validated

* Frequency of assessment should increase with changes in status such as persistent anorexia or GI symptoms, change in social
structure, decrease in dry weight or height for weight.

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6), Suppl 2,
June, 2000

11-5

MID-ARM CIRCUMFERENCE (MAC) REFERENCE VALUES (cm)

Age Pediatric Male % Standard Pediatric Female % Standard


Years 5 10 25 50 75 90 95 5 10 25 50 75 90 95
1-1.9 142 146 150 159 170 176 183 138 142 148 156 164 172 177
2-2.9 141 145 153 162 170 178 185 142 145 152 160 167 176 184
3-3.9 150 153 160 167 175 184 190 143 150 158 167 175 183 189
4-4.9 149 154 162 171 180 186 192 149 154 160 169 177 184 191
5-5.9 153 160 167 175 185 195 204 153 157 165 175 185 203 211
6-6.9 155 159 167 179 188 209 228 156 162 170 176 187 204 211
7-7.9 162 167 177 187 201 223 230 164 167 174 183 199 216 231
8-8.9 162 170 177 190 202 220 245 168 172 183 195 214 247 261
9-9.9 175 178 187 200 217 249 257 178 182 194 211 224 251 260
10-10.9 181 184 196 210 231 262 274 174 182 193 210 228 251 265
11-11.9 186 190 202 223 244 261 280 185 194 208 224 248 276 303
12-12.9 193 200 214 232 25.4 282 303 194 203 216 237 256 282 294
13-13.9 194 211 228 247 26.3 286 301 202 211 223 243 271 301 338
14-14.9 220 226 237 253 28.3 303 322 214 223 237 252 272 304 322
15-15.9 222 229 244 264 28.4 311 320 208 221 239 254 279 300 322
16-16.9 244 248 262 278 30.3 324 343 218 224 241 258 283 313 334
17-17.9 246 253 267 285 30.8 336 347 220 227 241 264 295 324 350
18-18.9 245 260 276 297 32.1 353 379 222 227 241 258 281 312 325
19-24.9 262 272 288 308 33.1 355 372 221 230 247 265 290 319 345

Reference: Frisancho R: Anthropometric Standards for the Assessment of Growth andNutritional Status, The University of
Michigan Press, Ann Arbor, MI, 1993
11-6
TRICEPS SKINFOLD THICKNESS (mm)

Age Pediatric Male % Standard Pediatric Female % Standard


Years 5 10 25 50 75 90 95 5 10 25 50 75 90 95
1-1.9 6 7 8 10 12 14 16 6 7 8 10 12 14 16
2-2.9 6 7 8 10 12 14 15 6 8 9 10 12 15 16
3-3.9 6 7 8 10 11 14 15 7 8 9 11 12 14 15
4-4.9 6 6 8 9 11 12 14 7 8 8 10 12 14 16
5-5.9 6 6 8 9 11 14 15 6 7 8 10 12 15 18
6-6.9 5 6 7 8 10 13 16 6 6 8 10 12 14 16
7-7.9 5 6 7 9 12 15 17 6 7 9 11 13 16 18
8-8.9 5 6 7 8 10 13 16 6 8 9 12 15 18 24
9-9.9 6 6 7 10 13 17 18 8 8 10 13 16 20 22
10-10.9 6 6 8 10 14 18 21 7 8 10 12 17 23 27
11-11.9 6 6 8 11 16 20 24 7 8 10 13 18 24 28
12-12.9 6 6 8 11 14 22 28 8 9 11 14 18 23 27
13-13.9 5 5 7 10 14 22 26 8 8 12 15 21 26 30
14-14.9 4 5 7 9 14 21 24 9 10 13 16 21 26 28
15-15.9 4 5 6 8 11 18 24 8 10 12 17 21 25 32
16-16.9 4 5 6 8 12 16 22 10 12 15 18 22 26 31
17-17.9 5 5 6 8 12 16 19 10 12 13 19 24 30 37
18-18.9 4 5 6 9 13 20 24 10 12 15 18 22 26 30
19-24.9 4 5 7 10 15 20 22 10 11 14 18 24 30 34

Reference: Frisancho R. Anthropometric Standards for the Assessment of Growth and Nutritional Status, The University of
Michigan Press, Ann Arbor, MI, 1993
11-7
2-7:

ESTIMATED MID-ARM MUSCLE CIRCUMFERENCE

Age Pediatric Male % Standard Pediatric Female % Standard


Years 5 10 25 50 75 90 95 5 10 25 50 75 90 95
1-1.9 110 113 119 127 135 144 147 105 111 117 124 132 139 143
2-2.9 111 114 122 130 140 146 150 111 114 119 126 133 142 147
3-3.9 117 123 131 137 143 148 153 113 119 124 132 140 146 152
4-4.9 123 126 133 141 148 156 159 115 121 128 136 144 152 157
5-5.9 128 133 140 147 154 162 169 125 128 134 142 151 159 165
6-6.9 131 135 142 151 161 170 177 130 133 138 145 154 166 171
7-7.9 137 139 151 160 168 177 180 129 135 142 151 160 171 176
8-8.9 140 145 154 162 170 182 187 138 140 151 160 171 183 194
9-9.9 151 154 161 170 183 196 202 147 150 158 167 180 194 198
10-10.9 156 160 166 180 191 209 221 148 150 159 170 180 190 197
11-11.9 159 165 173 183 195 205 230 150 158 171 181 196 217 223
12-12.9 167 171 182 195 210 223 241 162 166 180 191 201 214 220
13-13.9 172 179 196 211 226 238 245 169 175 183 198 211 226 240
14-14.9 189 199 212 223 240 260 264 174 179 190 201 216 232 247
15-15.9 199 204 218 237 254 266 272 175 178 189 202 215 228 244
16-16.9 213 225 234 249 269 287 296 170 180 190 202 216 234 249
17-17.9 224 231 245 258 273 294 312 175 183 194 205 221 239 257
18-18.9 226 237 252 264 283 298 324 174 179 191 202 215 237 245
19-24.9 238 245 257 273 289 309 321 179 185 195 207 221 236 249
Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6), Suppl 2, June, 2000

11-8
FORMULA FOR MID-ARM MUSCLE CIRCUMFERENCE AND MID-ARM MUSCLE AREA
MAMC = MAC – (3.14 x TSF in cm)
MAMA for males: [MACcm – (3.14 x TSFmm)2 /4 X 3.14] – 10
MAMA for females: [MACcm – (3.14 x TSFmm)2 /4 X 3.14] – 6.5

FORMULAS FOR CALCULATING STANDARD DEVIATION SCORES


SDS = [Pt actual height or weight] – 50th percentile value/standard deviation of control subjects.
SDS for height or weight compares growth rates over specific time intervals.
Note: Approximately 95% of healthy North American children fall within a SDS score of 2 SD
An SDS score of > positive 2.0 or > a negative 2.0 is associated with abnormal ht/wt

LENGTH FOR INFANTS (For calculating SDS Scores)


Boys Girls
Age Length cm SD Length cm Std Dev
0 50.5 2.29 49.9 2.17
0.25 61.1 2.65 59.5 2.49
0.5 67.8 2.69 65.9 2.64
0.75 72.3 2.65 70.4 2.73
1 76.1 2.70 74.3 2.84
1.25 79.4 2.85 77.8 2.95
1.5 82.4 3.04 80.9 3.07
1.75 85.1 3.23 83.8 3.18

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure.Am J Kidney Dis 35(6), Suppl 2, June, 2000

11-9

50 PERCENTILE FOR HEIGHT IN BOYS (For Calculating SDS Scores for Height)
TH

Age 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
2 86.8 87.5 88.2 88.9 89.7 90.4 91.3 92.2 93.1 94.0
3 94.9 95.7 96.6 97.4 98.3 99.1 99.8 100.6 101.4 102.1
4 102.9 103.6 104.4 105.1 105.9 106.6 107.3 107.9 108.6 109.2
5 109.9 110.5 111.2 111.8 112.5 113.1 113.7 114.3 114.9 115.5
6 116.1 116.7 117.3 117.8 118.4 119.0 119.5 120.1 120.6 121.2
7 121.7 122.2 122.8 123.3 123.8 124.4 124.9 125.4 125.9 126.5
8 127.0 127.5 128.0 128.6 129.1 129.6 130.1 130.6 131.2 131.7
9 132.2 132.7 133.2 133.8 134.3 134.8 135.3 135.9 136.4 136.9
10 137.5 138.1 138.6 139.2 139.7 140.3 140.9 141.5 142.1 142.7
11 143.3 143.9 144.5 145.2 145.8 146.4 147.0 147.7 148.4 149.0
12 149.7 150.4 151.0 151.7 152.3 153.0 153.7 154.4 155.1 155.3
13 156.5 157.2 157.9 158.5 159.2 159.9 160.5 161.2 161.8 162.6
14 163.1 163.7 164.3 164.9 165.6 166.2 166.8 167.3 167.9 168.4
15 169.0 169.5 170.0 170.5 171.0 171.5 171.9 172.3 172.7 173.1
16 173.5 173.8 174.2 174.5 174.9 175.2 175.4 175.6 175.8 176.0
17 176.2 176.3 176.4 176.5 176.6 176.7 176.7 176.7 176.8 176.8
18 176.8 176.8 176.8 176.8 176.8 176.8 176.8 176.8 176.8 176.8
Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-10
STANDARD DEVIATION VALUES FOR HEIGHT IN BOYS (For calculating SDS scores)

Age 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
2 3.6 3.63 3.67 3.7 3.74 3.77 3.81 3.84 3.88 3.91
3 3.95 3.99 4.02 4.06 4.09 4.13 4.28 4.43 4.58 4.73
4 4.28 4.31 4.34 4.38 4.41 4.44 4.46 4.49 4.51 4.54
5 4.56 4.58 4.61 4.63 4.66 4.68 4.70 4.73 4.75 4.78
6 4.8 4.82 4.85 4.87 4.89 4.92 4.95 4.98 5.02 5.05
7 5.08 5.10 5.13 5.15 5.18 5.20 5.23 5.26 5.29 5.32
8 5.35 5.39 5.43 5.48 5.52 5.56 5.59 5.63 5.67 5.70
9 5.74 5.78 5.83 5.87 5.92 5.96 6.0 6.06 6.10 6.15
10 6.20 6.26 6.32 6.38 6.44 6.50 6.56 6.61 6.67 6.72
11 6.78 6.86 6.93 7.01 7.08 7.16 7.23 7.3 7.37 7.44
12 7.51 7.58 7.65 7.73 7.79 7.87 7.93 7.99 8.06 8.12
13 8.18 8.23 8.28 8.32 8.37 8.42 8.43 8.44 8.46 8.47
14 8.48 8.46 8.43 8.41 8.38 8.36 8.31 8.26 8.21 8.16
15 8.11 8.04 7.98 7.91 7.85 7.78 7.70 7.62 7.55 7.47
16 7.39 7.32 7.25 7.19 7.12 7.05 7.0 6.95 6.91 6.86
17 6.81 6.79 6.76 6.74 6.71 6.69 6.68 6.68 6.67 6.67
18 6.66 6.66 6.66 6.66 6.66 6.66 6.66 6.66 6.66 6.66

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-11

50 PERCENTILE FOR HEIGHT IN GIRLS (Used to calculate SDS Scores for Height)
th

Age 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
2 86.8 87.4 88.1 88.7 89.7 90.0 90.8 91.6 92.5 93.3
3 94.1 94.9 95.6 97.1 98.3 97.9 99.6 99.4 100.1 100.9
4 101.6 102.3 102.9 104.3 105.9 105.0 105.7 106.4 107.0 107.7
5 108.4 109.0 109.7 110.9 112.5 111.6 112.2 112.8 113.4 114.0
6 114.6 115.2 115.8 117.0 118.4 117.6 118.2 118.8 119.4 120.0
7 120.6 121.1 121.8 122.9 123.8 123.5 124.1 124.7 125.2 125.8
8 126.4 126.9 127.6 128.7 129.1 129.3 129.9 130.5 131.0 131.6
9 132.2 132.8 133.1 134.6 134.3 135.2 135.8 136.4 137.1 137.7
10 138.3 138.9 139.6 140.9 139.7 141.5 142.2 142.8 143.2 144.1
11 144.8 145.5 146.2 147.5 145.8 148.2 148.9 149.5 150.2 150.8
12 151.5 152.1 152.7 151.7 153.9 154.6 155.1 155.6 156.1 156.6
13 157.1 157.5 157.9 158.5 158.6 159.0 169.3 159.6 159.8 160.1
14 160.4 160.6 160.7 164.9 161.0 161.2 161.3 161.4 161.6 161.7
15 161.8 161.9 161.9 170.5 162.0 162.1 162.2 162.2 162.3 162.3
16 162.4 162.5 162.5 174.5 162.6 162.7 162.8 162.9 162.9 163.0
17 163.1 163.2 163.2 176.5 163.3 163.4 163.5 163.5 163.6 163.6
18 163.7 163.7 163.7 176.8 163.7 163.7 163.7 163.7 163.7 163.7
Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-12
STANDARD DEVIATION VALUES FOR HEIGHT IN GIRLS (For calculation of SDS
scores)

Age 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
2 3.65 3.65 3.65 3.65 3.65 3.65 3.67 3.69 3.7 3.72
3 3.74 3.77 3.80 3.83 3.86 3.89 3.92 3.95 3.98 4.01
4 4.04 4.08 4.11 4.15 4.18 4.22 4.26 4.29 4.33 4.37
5 4.41 4.56 4.51 4.55 4.60 4.65 4.69 4.75 4.79 4.84
6 4.89 4.94 4.99 5.04 5.09 5.14 5.19 5.24 5.28 5.33
7 5.38 5.43 5.48 5.52 5.57 5.62 5.67 5.72 5.77 5.82
8 5.87 5.92 5.97 6.01 6.06 6.11 6.15 6.19 6.24 6.28
9 6.32 6.36 6.39 6.43 6.46 6.50 6.54 6.58 6.61 6.65
10 6.69 6.71 6.74 6.76 6.79 6.81 6.83 6.85 6.86 6.88
11 6.90 6.91 6.92 6.94 6.95 6.96 6.96 6.96 6.96 6.96
12 6.96 6.96 6.96 6.96 6.96 6.96 6.96 6.96 6.96 6.96
13 6.96 6.95 6.95 6.94 6.94 6.93 6.92 6.91 6.89 6.88
14 6.87 6.86 6.86 6.85 6.85 6.84 6.83 6.82 6.80 6.79
15 6.78 6.76 6.74 6.73 6.71 6.69 6.67 6.65 6.64 6.62
16 6.60 6.57 6.54 6.50 6.47 6.44 6.42 6.39 6.37 6.34
17 6.32 6.29 6.26 6.23 6.20 6.17 6.15 6.13 6.12 6.10
18 6.08 6.08 6.08 6.08 6.08 6.08 6.08 6.08 6.08 6.08
Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-13

50TH PERCENTILES FOR WEIGHT IN BOYS (For calculation of SDS scores)

Age 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
2 12.34 12.58 12.81 13.05 13.30 13.52 13.74 13.95 14.17 14.38
3 14.60 14.81 15.03 15.25 15.46 15.68 15.88 16.08 16.29 16.49
4 16.69 16.89 17.09 17.29 17.49 17.69 17.89 18.08 18.28 18.47
5 18.67 18.87 19.07 19.27 19.47 19.67 19.87 20.08 20.28 20.49
6 20.69 20.90 21.11 21.32 21.53 21.74 21.96 22.18 22.41 22.63
7 22.85 23.09 23.32 23.56 23.79 24.03 24.28 24.54 24.79 25.05
8 25.30 25.56 25.82 26.08 26.34 26.66 26.95 27.25 27.54 27.84
9 28.13 28.45 28.77 29.09 29.41 29.73 30.07 30.41 30.76 31.09
10 31.44 31.81 32.18 32.56 32.93 33.30 33.70 34.10 34.50 34.90
11 35.30 35.73 36.16 36.59 37.03 37.46 37.92 38.39 38.85 39.32
12 39.78 40.28 40.78 41.27 41.77 42.27 42.81 43.34 43.88 44.41
13 44.95 45.52 46.09 46.67 47.24 47.81 48.40 48.99 49.59 50.18
14 50.77 51.37 51.97 52.56 53.16 53.76 54.35 54.94 55.53 56.12
15 56.71 57.35 57.99 58.63 59.27 59.51 60.03 60.55 61.06 61.58
16 62.10 62.56 63.02 63.47 63.93 64.39 64.77 65.16 65.54 65.93
17 66.31 66.60 66.90 67.19 67.49 67.78 68.00 68.22 68.44 68.66
18 68.88 68.88 68.88 68.88 68.88 68.88 68.88 68.88 68.88 68.88

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-14
STANDARD DEVIATION VALUES FOR WEIGHT IN BOYS (For calculation of SDS
scores)

Age 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
2 1.52 1.54 1.56 1.58 1.60 1.62 1.64 1.67 1.69 1.72
3 1.74 1.77 1.79 1.82 1.84 1.87 1.90 1.93 1.96 1.99
4 2.02 2.05 2.08 2.12 2.15 2.18 2.22 2.26 2.30 2.34
5 2.38 2.42 2.47 2.51 2.56 2.60 2.65 2.70 2.76 2.81
6 2.86 2.92 2.98 3.04 3.10 3.16 3.23 3.29 3.36 3.42
7 3.49 3.59 3.70 3.81 3.91 4.02 4.07 4.13 4.18 4.24
8 4.29 4.38 4.48 4.57 4.67 4.76 4.86 4.96 5.07 5.17
9 5.27 5.38 5.49 5.59 5.70 5.81 5.92 6.03 6.14 6.25
10 6.36 6.47 6.59 6.70 6.82 6.93 7.04 7.16 7.27 7.39
11 7.50 7.61 7.72 7.83 7.94 8.05 8.16 8.26 8.37 8.47
12 8.58 8.68 8.78 8.88 8.98 9.08 9.17 9.26 9.36 9.45
13 9.54 9.62 9.69 9.77 9.85 9.93 10.01 10.08 10.16 10.23
14 10.31 10.38 10.44 10.51 10.57 10.64 10.70 10.76 10.82 10.88
15 10.94 10.99 11.06 11.11 11.17 11.23 11.29 11.34 11.39 11.45
16 11.51 11.57 11.63 11.68 11.74 11.80 11.82 11.84 11.87 11.89
17 11.91 12.01 12.11 12.21 12.31 12.41 12.47 12.53 12.58 12.64
18 12.70 12.70 12.70 12.70 12.70 12.70 12.70 12.70 12.70 12.70

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-15

50 PERCENTILES FOR WEIGHT IN GIRLS (For calculation of SDS scores)


TH

Age 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
2 11.80 12.05 12.29 12.54 12.78 13.03 13.24 13.46 13.67 13.89
3 14.10 14.29 14.49 14.68 14.88 15.07 15.25 15.43 15.60 15.78
4 15.96 16.13 16.30 16.47 16.64 16.81 16.98 17.15 17.32 17.49
5 17.66 17.84 18.02 18.20 18.38 18.56 18.75 18.94 19.14 19.33
6 19.52 19.74 19.96 20.17 20.39 20.61 20.86 21.10 21.35 21.59
7 21.84 22.12 22.41 22.69 22.98 23.26 23.58 23.89 24.21 24.52
8 24.84 25.19 25.54 25.88 26.23 26.58 26.96 27.33 27.71 28.09
9 28.46 28.86 29.26 29.65 30.05 30.45 30.87 31.29 31.71 32.13
10 32.55 32.98 33.42 33.85 34.29 34.72 35.17 35.61 36.06 36.50
11 36.95 37.41 37.86 38.32 38.77 39.23 39.69 40.15 40.61 41.07
12 41.53 41.99 42.45 42.92 43.38 43.84 44.29 44.74 45.19 45.65
13 46.10 46.53 46.96 47.39 47.83 48.26 48.66 49.07 49.47 49.88
14 50.23 50.64 51.01 51.37 51.74 52.10 52.42 52.73 53.05 53.37
15 53.68 53.94 54.19 54.45 54.70 54.96 55.15 55.33 55.52 55.70
16 55.89 56.00 56.11 56.22 56.33 56.44 56.49 56.54 56.59 56.64
17 56.69 56.69 56.70 56.70 56.71 56.71 56.69 56.67 56.65 56.63
18 56.62 56.62 56.62 56.62 56.62 56.62 56.62 56.62 56.62 56.62
Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-16
STANDARD DEVIATION VALUES FOR WEIGHT IN GIRLS (For calculation of SDS
scores)

Age 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
2 1.28 1.33 1.37 1.42 1.46 1.51 1.55 1.59 1.62 1.66
3 1.70 1.74 1.78 1.81 1.85 1.89 1.93 1.96 1.99 2.03
4 2.07 2.11 2.14 2.18 2.21 2.25 2.29 2.33 2.37 2.41
5 2.45 2.49 2.54 2.59 2.63 2.68 2.73 2.79 2.84 2.89
6 2.95 3.01 3.07 3.14 3.19 3.26 3.33 3.41 3.49 3.56
7 3.64 3.73 3.82 3.91 4.00 4.09 4.19 4.29 4.39 4.49
8 4.59 4.70 4.81 4.92 5.03 5.14 5.26 5.37 5.49 5.60
9 5.72 5.84 5.96 6.08 6.20 6.32 6.44 6.56 6.69 6.81
10 6.93 7.05 7.17 7.29 7.42 7.54 7.66 7.78 7.89 8.01
11 8.13 8.24 8.35 8.47 8.58 8.69 8.79 8.89 9.00 9.11
12 9.21 9.30 9.39 9.49 9.58 9.67 9.75 9.83 9.92 9.99
13 10.08 10.15 19.22 10.29 10.36 10.43 10.49 10.55 10.62 10.68
14 10.74 10.79 10.84 10.88 10.93 10.98 11.02 11.06 11.10 11.14
15 11.18 11.21 11.24 11.27 11.30 11.33 11.35 11.37 11.38 11.40
16 11.42 11.43 11.44 11.45 11.46 11.47 11.47 11.47 11.46 11.46
17 11.46 11.45 11.44 11.43 11.42 11.41 11.39 11.37 11.35 11.33
18 11.31 11.31 11.31 11.31 11.31 11.31 11.31 11.31 11.31 11.31

Reference: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-17

PEDIATRIC LABORATORY VALUES THAT ARE DIFFERENT FROM ADULT VALUES


A number of laboratory values differ between children and adults. Of the chemistries commonly monitored in CKD disease, the
following have different normal ranges for pediatrics. These are general, normal ranges, not considering the level of kidney function or
mode of treatment.

Lab Test Newborn Infant Child Adolescent


Serum Albumin g/dL 3.5-5.4 4.4-5.4 4-5.9
Alkaline Phosphatase ImU/mL 85-235 (<2) 65-210 (2-8) 60-300 (9-15)
Blood Urea Nitrogen mg/dL 3-12 5-18 5-18
Serum Cholesterol mg/dL 53-135 70-175 120-200
Serum Creatinine mg/dL 0.3-1.2 0.2-0.4 0.3-0.7 0.5-1.0
CO2 ≥ 22 ≥ 22 ≥ 22 ≥ 22
Ferritin ng/mL 25-200 200-600 (1 mo) 7-142
50-200 (2-5 mo)
Glucose mg/dL 40-90 60-100 (< 2 yrs) 70-105 (>2-adult)
Hematocrit % 44-64 39-59 (2-8 wks) 30-40 (1-6 yrs) 32-44 (6-18 yrs)
35-50 (2-6 mo)
Hemoglobin g/dL 14-24 10-17 (2-6 mo) 9.5-14 (1-6 yrs) 10-15.5 (6-18 yrs)
9.5-14 (6 mo-1 yr)
Iron µmol/L 100-250 50-120
Mean Corpuscular Volume 96-108 80-95 80-95 80-95
Phosphorus mg/dL 4.8-7.4 4.5-6.5

Reference: Pagana KD, Pagana TJ: Mosby’s Diagnostic and Laboratory Test Reference, 4th Ed.1999
Portale A: Blood Calcium, phosphorus, and magnesium. In Favus M (Ed) Primer on Metabolic
Bone Diseases and Disorders of Mineral Metabolism, Lippencott, Williams and Wilkins, 1999. pp 115-118.

11-18
ESTIMATING CALORIE AND FLUID NEEDS OF PEDIATRIC CKD PATIENTS
Holliday-Segar Method or Fluid Method
This is a quick, simple formula that estimates maintenance calorie needs from weight alone. It assumes that for each
100 calories metabolized, 100 cc of water will be required. This method is not suitable for neonates less than 14 days
old, or in conditions associated with abnormal losses.

Calories/kg Water (cc/kg)


1st 10 kg body weight 100 100
2nd 10 kg body weight 50 50
Each additional kg 20 20

Example: 15 kg child will need:


1250 cc fluids per 24 hr (83 cc/kg/day)
1250 calories per 24 hr (83 kcal/kg/day)

Adapted: Johnson KB, Ed: The Harriet Lane Handbook, 14th Ed., St. Louis, Mosby-Year Book, 1996

11-19

GUIDELINES FOR CHOOSING AN INFANT FORMULA

1. Infants (12-24 months or less) may require a formula with lower electrolyte levels (especially potassium and
phosphorus) than found in standard milk or soy-based infant formulas.
2. Commonly suggested formulas include: Enfamil® (Mead Johnson), Similac® and PM 60/40 (Ross
Laboratories), and Good Start® (Carnation).
3. Formulas containing iron are generally required.
4. Infants on peritoneal dialysis may need sodium supplementation to replace dialysis losses.
5. Calories can be concentrated above 20 kcal/oz by adding modular components such as glucose-polymers,
sugar, MCT oil, or vegetable oil.
6. Protein can be supplemented with modular protein powders, as needed.
7. Pediatric and adult enteral formulas (such as Pediasure® or Nepro®, Ross Laboratories) may be considered in
children over 12 months of age.

11-20
PEDIATRIC FORMULAS USED IN CKD (Composition per 100 mL)

Similac® PM 60/40® Enfamil® Good Start® Pediasure®

kcal 67.6 67.6 67.6 67.6 100


Carbohydrate (gm) 7.2 6.9 7.4 7.4 11.0
Protein (gm) 1.45 1.5 1.42 1.62 3.0
Fat (gm) 3.7 3.77 3.6 3.5 5.0
Sodium (mg/mEq) 18.3/0.8 15.6/0.68 18.3/0.8 16.2/0.7 38/1.7
Potassium (mg/mEq) 71/1.8 58/1.49 73/1.9 66.2/1.7 131/3.4
Phosphorus (mg) 38 29.3 36 24.3 80
Calcium (mg/mEq) 49/2.5 75.6/3.78 52.7/2.6 43.3/2.2 97/4.9
Magnesium (mg) 4.1 4.06 5.4 4.5 20
Osmolality (mOsm/kg H2O) 300 280 300 265 365

Reference: Composition of Feedings for Infants and Young Children, Ross Ready Reference, 1996

AVERAGE NUMBER AND VOLUME OF FEEDINGS (INFANT WITHOUT CKD)

Age Number Volume


Birth - 1 week 6 - 10 1 - 3 oz (30 - 90 cc)
1 week - 1 month 7-8 2 - 4 oz (60 - 120 cc)
1 - 3 months 5-7 4 - 6 oz (120 - 180 cc)
3 - 6 months 4-5 6 - 7 oz (180 - 210 cc)
6 - 9 months 3-4 7 - 8 oz (210 - 240 cc)
10 - 12 months 3 7 - 8 oz (210 - 240 cc)

Adapted: Queen PM, Lang CE: Handbook of Pediatrics, ASPEN Publishers, 1993
11-21

NUTRIENT RECOMMENDATIONS FOR PEDIATRIC ACUTE KIDNEY FAILURE (Not


dialyzed)

Nutrient Infant Toddler Child Adolescent


(0-1 year) (1-3 years) (4-10 years) (11-18 years)
Protein* 1-2 gm/kg 1.5-1.8 gm/kg 1.0-1.5 gm/kg .8-1.0 gm/kg
HBV 50 - 65% 50 - 65% 50 - 65% 50 - 65%
Energy Use Holliday-Segar or Fluid Method (pg 11-19)
Sodium Allowances vary considerably. All levels should be monitored closely and
Potassium recommendations adjusted as warranted.
Phosphorus
Calcium
Fluid Assume fluid restriction. Consult with medical team to determine what portion of total
fluid allowance is available for nutrition support.
Vits/Mins Supplement as necessary.

*Goals should be appropriate to kidney function, stage of acute kidney failure, and/or treatment modality.

11-22
NUTRIENT RECOMMENDATIONS FOR PEDIATRIC CKD PATIENTS (Prior to dialysis)
Nutrient Infant Toddler Child Adolescent
Energy 0-0.5 yr: ≥ 108 cal/kg 102 kcal/kg 4-6 yr: 90 kcal/kg 11-14 yr: 47 kcal/kg
0.5-1 yr: ≥ 98 kcal/kg 7-10 yr: 70 kcal/kg 15-18 yr: 40 kcal/kg
11-14 yr: 55 kcal/kg
15-18 yr: 45 kcal/kg
Protein 0-0.5 yr: 2.2 gm/kg 1.2 gm/kg 4-6 yr: 1.2 gm/kg 11-14 yr: 1.0 gm/kg
0.5-1 yr: 1.6 gm/kg 7-10 yr: 1.0 gm/kg 15-18 yr: 0.9 gm/kg
Sodium As tolerated, 1-2 gm/d w/ As tol, 1- As tol, 1-3 gm/day with As tol, 3-4 gm/day with HTN or
hypertension (HTN)/edema 3gm/d HTN or edema edema
w/HTN/edema
Potassium Restriction not usually needed until GFR is below 10% of normal. Most will tolerate ≥ 3 mEq/kg
Calcium* 0-0.5 yr: 400 mg/day 800 mg/day 800 mg/day 1200 mg/day
0.5-1 yr: 600 mg/day
Phosphorus Limit P if serum high, low Usually 600-800 mg/day, when serum levels are elevated
P formula
Fluids Unrestricted unless indicated, then replace insensible losses plus urine output.
Vitamins/ 1 mL MVI drops. * Vit D, Multivitamin or B complex plus C, Vit D, if Multivitamin or B complex plus C.
Minerals if indicated. indicated by Ca++, PTH, alk phos. Vit D, if indicated
Trace Mins Supplement zinc, iron, and/or copper, if needed

* Note: Current practice varies among clinicians regarding the use of standard pediatric multivitamins (MVT) versus B complex
plus any renal formulations have higher vitamin levels than recommended for infants. MVT may be appropriate in the infant
less than 1 year of age to provide sufficient/appropriate vitamins and minerals for growth and development. Adequacy of
vitamin A should be carefully monitored in infants.

Reference: Nelson P, Stover J, Eds: Nutrition Recommendations for Infants, Children, and Adolescents with ESRD. A Clinical
Guide to Nutrition Care in End Stage Renal Disease, 2nd Ed, ADA, 1994
11-23

NUTRIENT RECOMMENDATIONS FOR PEDIATRIC PATIENTS - HEMODIALYSIS

Nutrient Infant Toddler Child Adolescent


Energy kcal/kg 0-0.5 yr: ≥108 cal/kg 102 kcal/kg 4-6 yr: 90 kcal/kg 11-14 yr: % 55/kg & 47/kg
K/DOQI RDA for 0.5-1 yr: ≥98 kcal/kg 7-10 yr: 70 kcal/kg 15-18 yr: % 45/kg & 40/kg
chronological age; 18-21 yr: % 40/kg & 38/kg
monitor response
Protein K/DOQI: 0-0.5 yr: 2.6 gm/kg ≥1.6 gm/kg 4-6 yr: ≥1.6 gm/kg 11-14: %/& 1.4 gm/kg
RDA for 0.5-1 yr: 2.0 gm/kg 7-10 yr: ≥1.4 gm/kg 15-18: % 1.3 & 1.2 gm/kg
chronological age + 19-21: %/& 1.2 gm/kg
0.4 gm/kg
Sodium As tolerated, 1-2 gm/d As tol, 1-3 gm/d w/ As tol, 2-4 gm/day As tol, 2-4 gm/day with
w/ HTN/edema HTN/edema w/ HTN/edema HTN/edema

Potassium 1-3 mEq/kg, if serum levels elevated

Calcium 0-0.5 yr: 400 mg/day 800 mg/day 800 mg/day 1200 mg/day
0.5-1 yr: 600 mg/day
Phosphorus If serum level high, Usually 600-800 mg/day, when serum levels are elevated
use low P formula
Fluids Replace urine, Replace insensible losses plus urine output
insensible losses, +
UF, if possible
Vitamins/ K/DOQI: 100% of Dietary Reference Intake (DRI) for thiamin, riboflavin, pyridoxine, B12, and folic acid.
Minerals 100% of Recommended Dietary Allowance for vitamins A, C, E, K, copper, and zinc.

Reference: Nelson P, Stover J, Eds: Nutrition Recommendations for Infants, Children, and Adolescents with ESRD.
A Clinical Guide to Nutrition Care in End Stage Renal Disease, 2nd Ed, ADA, 1994
NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-24
NUTRIENT RECOMMENDATIONS FOR PEDIATRIC PATIENTS - PERITONEAL
DIALYSIS
Nutrient Infant Toddler Child Adolescent
Energy kcal/kg 0-0.5 yr: ≥108 cal/kg 102 kcal/kg 4-6 yr: 90 11-14 yr: % 55/kg & 47/kg
Include dialysate 0.5-1 yr: ≥98 kcal/kg kcal/kg 15-18 yr: % 45/kg & 40/kg
calories 7-10 yr: 70 18-21 yr: % 40/kg & 38/kg
kcal/kg
Protein gm/kg 0-0.5 yr: 2.9-3.0 gm/kg 1.9-2.0 4-6 yr: 1.9-2.0 11-14: %/& 1.7-1.8 gm/kg
0.5-1 yr: 2.3-2.4 gm/kg gm/kg gm/kg 15-18: %/& 1.4-1.5 gm/kg
7-10 yr: 1.7- 19-21: %/& 1.3 gm/kg
1.8 gm/kg
Sodium gm/d As tol, 1-2 gm/d with As tol, 1-3 As tol, 2-4 As tol, 3-4 gm/d with HTN/edema
HTN/ edema gm/d with gm/d with
HTN/edema HTN/edema
1-3 mEq/kg, if restriction Unrestricted, Generally unrestricted
Potassium mEq/L needed or 1-3
mEq/kg

Calcium mg/d 0-0.5 yr: 400 mg/day 800 mg/day 800 mg/day 1200 mg/day
0.5-1 yr: 600 mg/day
Phosphorus mg Low P formula, if serum Usually 600-800 mg/day, when serum levels are elevated.
level high
Fluids cc Replace all losses Unrestricted, unless signs of fluid overload
Vits/Mins K/DOQI: Same as HD

Reference: Nelson P, Stover J: Nutrition Recommendations for Infants, Children, and Adolescents with ESRD
A Clinical Guide to Nutrition Care in End Stage Renal Disease, 2nd Ed. ADA 1994
NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000

11-25

NUTRIENT RECOMMENDATIONS FOR PEDIATRIC PATIENTS – TRANSPLANT


Nutrient Infant Toddler Child Adolescent
Energy 0-0.5 yr: 102 kcal/kg 4-6 yr: 90 kcal/kg % 11-14 yr: 47 kcal/kg
(After ideal wt to ht ≥ ³108 7-10 yr: 70 kcal/kg 15-18 yr: 40 kcal/kg
is achieved) cal/kg & 11-14 yr: 55 kcal/kg
0.5-1 yr: 15-18 yr: 45 kcal/kg
≥ 98 kcal/kg
Protein 3 gm/kg 2-3 gm/kg initial RDA after 3 1.5-2 gm/kg initially, 1.2-1.5 gm/kg initially,
initial, RDA mo then RDA after 3 mo then RDA after 3 mo
after 3 mo
Sodium 1-3 gm/day 1-3 gm/d initial, Not restricted, 2-3 gm/day initial, 2-4 gm/d initial. Not
initial unless HTN/edema Not restricted unless restricted unless HTN/
HTN/edema edema

Potassium Unrestricted, unless serum levels are high.

Calcium No restriction, supplement to RDA levels as necessary.


Phosphorus May need very high intakes. Supplement as necessary.
Fluids No restriction (>1.5 x maintenance) Unrestricted; high intake encouraged.
Vitamins May not be necessary, unless very Generally unnecessary; Vit D as needed.
Minerals malnour-
ished prior to transplant; Vit D as
needed
Trace Mins Generally unnecessary; supplement iron and magnesium as needed.

Reference: Nelson P, Stover J: Nutrition Recommendations for Infants, Children, and Adolescents with ESRD
in A Clinical Guide to Nutrition Care in End Stage Renal Disease, 2nd Ed. ADA, 1994

11-26
BONE ABNORMALITIES IN PEDIATRIC PATIENTS WITH CKD:
1. The incidence of renal osteodystrophy is greater in infants, children, and adolescents due to the high rate of
bone turnover in the growing skeleton.
2. Radiographic studies of wrists should be performed annually to determine bone age.
3. The maintenance of normal calcium and phosphorus is critical to bone growth. Renal osteodystrophy
significantly contributes to growth retardation.
4. Growing bones are more susceptible to alterations in circulating PTH and Vitamin D.
5. Usual dose of calcitriol: IV = 0.5 - 1.5 µg three times per week ; oral = ≥ 0.25 µg daily.

The dose is dependent on serum calcium, serum phosphorus, alkaline phosphatase, and PTH. Treatment should
be started when the serum intact PTH levels are 400-500 pg/mL and the serum calcium levels are between 9.5-10.5
mg/L. Close attention must be given to the development of adynamic bone lesions in patients who have PTH levels
below 200 pg/mL. Patients with adynamic bone lesions should be managed with low calcium dialysate and Vitamin D
therapy should be withheld.
References: Sanchez C, Salusky IB: The renal bone diseases in children treated with dialysis. Adv in Ren Replacement Ther 3(1):14, 1996

11-27

MALNUTRITION IN PEDIATRIC PATIENTS WITH CKD:

1. Protein-energy malnutrition is the most prominent nutritional disorder in children with CKD. Mild or
moderate under nutrition is also common and is labeled “failure to thrive” (FTT) in younger children.
2. The earlier CKD manifests itself, the more the potential there is for FTT and/or growth retardation.
3. FTT can cause a child to miss developmental milestones including development of feeding skills.
4. A tube feeding (NG or GT) may be necessary if oral intake is insufficient to meet nutrient needs.
5. A variety of formulas can be used depending on the age of the child, level of renal function, and available
fluid volume. (See choosing an infant formula, page 11-21).
6. Oral stimulation is important for development. Begin solid food intake within the normal infant progression
and 4-6 months of age developmentally. Progress to table foods as tolerated.
7. Supplement solids (purees and table food) with modular components of carbohydrate, protein, and fat as needed
to reach recommended levels.
8. Growth hormone can be an important adjunct to nutritional management in treating growth retardation in
patients with compromised renal function.

K/DOQI:
Consider supplemental nutrition support when a patient is not growing normally or fails to consume recommended
levels of calories and/or protein. Oral supplementation is the first choice of therapy, followed by tube feeding.

Recombinant Human Growth Hormone (hGH) should be considered for dialysis patients with growth potential when:
Height for chronological age is more negative than 2 SD or height velocity for chronological age more than negative
2.0 SDS; shows potential with open epiphyses; there are no other contraindications. Protein/energy deficit, acidosis,
hyperphosphatemia, and hyperparathyroidism should be correction prior to hGH therapy.

11-28
GUIDELINES FOR ENTERAL FEEDINGS IN PEDIATRIC PATIENTS WITH CKD

1. Assume the patient will be on a fluid limit.


2. Keep volume as low as possible. Consider 2 kcal/cc formula if electrolyte levels are tolerated. Dialysis may be
required to allow provision of adequate nutrition.
3. Choose formulas that are lower in K+ and P, if possible. Monitor serum levels closely.
4. Infant formulas: Increase calorie density by adding carbohydrate or fat modules, rather than concentrating
the formula.
5. Choose low protein formulas (AminAid) for the child older than 1 year who is not being dialyzed. When
using low protein formulas, monitor electrolytes closely. Low protein formulas may not contain electrolytes,
vitamins, or minerals. These formulas can be given by mouth, but palatability is an issue, especially in children.

11-29

GUIDELINES FOR TUBE FEEDINGS IN PEDIATRIC PATIENTS WITH CKD:


1. The choice of formula depends on the age, diagnosis, renal replacement therapy, and fluid status.
Even 2 kcal/cc formulas can be used in children if the strength, volume and rate of administration are increased
gradually.
2. Feedings are usually given at night with a continuous drip over 8-12 hours. Start slowly and advance
gradually to total volume. Infants may start with 10-20 cc/hour and advance as tolerated.
3. Daytime bolus feedings may be tolerated.
4. The formula concentration and feedings for infants and young children need to be altered frequently in
response to growth and laboratory values.

11-30
GUIDELINES FOR PARENTERAL NUTRITION IN PEDIATRIC PATIENTS WITH CKD

1. Determine available fluid allowance.


2. Use modality specific energy recommendations plus a factor for current medical condition. Obtain indirect
calorimetry measurement if available.
3. Start with a 10% dextrose concentration and advance by 5% daily until the goal is reached. Condense
dextrose as appropriate to keep volume low to minimize the need for dialysis. Try to keep the total volume to
<2 L/day (even lower in smaller patients).
4. Standard amino acid solutions are generally appropriate. Use modality specific protein levels. Children, age 2
or younger, should receive Trophamine. Monitor albumin/prealbumin.
5. Obtain baseline triglyceride levels. If less than 200 mg/dL, begin 20% lipids at 0.5-1.0 gm/kg over 18 hours
daily. Recheck triglycerides 6 hours after completion of the infusion. If less than 250 mg/dL, advance lipids as
necessary to reach desired calorie level. Maximum lipid infusion levels are 3-4 gm/kg in children and lipids
should not exceed 60% of the total calories.
6. Electrolytes:Sodium - individualize as tolerated/appropriate.
Potassium - total should not exceed 50 mEq/L.
Magnesium - decrease standard solution of 10 mEq/L by half (5 mEq/L).
Phosphorus - reduce standard solution of 7.5 mmol/L by ½ of standard.
Do not remove entirely because of the risk for hypophosphatemia.
Calcium - individualize to maintain acceptable serum levels.
MVI - do not add, replace with 1 cc/day of B-complex plus C.
Selenium - renal requirements not clear, limit use. Suggest removing after one week on TPN.
Acetate, Chloride - individualize to maintain acid/base balance.
Zinc, Copper - standard solutions are generally acceptable.

11-31

GUIDELINES FOR UREA KINETIC MODELING IN PEDIATRIC HD PATIENTS:


In theory, urea kinetic modeling (UKM) concepts are the same for children as they are for adults. UKM can provide a
basis for ongoing assessment of dialysis adequacy and protein nutrition. However, the dynamic metabolic activity in
children requires that we recognize special considerations for interpretation and application of urea kinetic
calculations.
1. There are much greater variations in body size (10 kg to 100 kg).
2. Growth factor and metabolic requirements are constantly changing especially in the growing child
requiring at least monthly UKM assessments. Growing children should be in positive nitrogen balance and in
an anabolic state (PNA < dietary protein intake).
3. Total body water is relatively larger in small children (greater volume to weight ratio).
4. The ratio of total body water to weight (volume:weight) can vary as much as 20%, from 0.50 to 0.70, but
should be constant for an individual child.
5. Pediatric patients commonly have a relatively greater interdialytic (ID) weight gain, requiring relatively
greater ultrafiltration (UF).
6. Individualized target PNAs and urea generation rates are needed because of the varied composition of the
diets. (Infant formulas are fairly consistent, toddlers pick at eating, and adolescents may skip meals or eat fast
foods). K/DOQI: PNA not well tested in pediatrics.
7. Double pool kinetics may be more accurate in children because of their low absolute TBW and relatively high
clearances.
8. Suggest PCR targets: Infant/toddler - ≥1.4 Children - 1.2 to 1.4
Adolescents - ≥1.2
9. Target Kt/V = ≥1.4 (K/DOQI Recommendation: Prescribed Kt/V ≥1.3; Delivered ≥1.2)
10. Other recommendations of frequency/method of measurement, blood draw procedures, and problem solving are
the same as for adult HD patients. Most recommendations are based on opinion or adult research.

11-32
GUIDELINES FOR ADEQUACY TESTING IN PEDIATRIC PD PATIENTS
Literature is scant and controversial. Most recommendations are extrapolated from adult data. Special considerations
for interpretation and application of urea kinetic calculations in pediatric PD patients include:
1. Recommended dwell volumes are relatively greater in children. The surface area of the peritoneal membrane is
larger in children than in adults as related to body weight.
2. Dwell volumes of >900 mL/m2 (body size) are recommended for all ages and sizes.
3. In children, CCPD may be more commonly used than CAPD, but this varies from center to center.
4. Initial goals of measured Kt/V and creatinine clearance parallel adult goals.
5. Dietary protein intake must be greater than total protein nitrogen appearance because positive nitrogen
balance is essential for a growing child.
6. PET reference curves for children and evaluations of their application are currently being investigated.
7. K/DOQI Recommendations:
Adults and Children: CAPD: Kt/V 2.0 CrCl: 60 L/week (high/high average transporters)
50 L/week (low/low average transporters)
CCPD: Kt/V 2.1 CrCl: 60 L/week
NIPD: Kt/V 2.2 CrCl: 66 L/week
References: Schleifer CR, et al: The Application of UKM to Peritoneal Dialysis: A review of
Methodology and Outcome. J Ren Nutr 3:2-9, 1993
Kohaut EC: A Simplistic Approach to Kinetic Modeling. Sems Dial 7:398, 1994
Warady BA: The Use of the PET to Modify PD Modality in Children, Sems Dial 7:403, 1994
Harmon WE: Kinetic Modeling of HD in Children. Sems Dial 7:392, 1994
Buur T, et al: Reliability of HD UKM in Children. Pediatr Nephrol 8:574, 1994
NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 37(1) Suppl , June, 2001

11-33

CALCIUM UROLITHIASIS
See notation in Chapter 8, page 8-20.

HYPEROXALURIA
See notation in Chapter 8, page 8-22.

PEDIATRIC REFERENCES:
Barone M, Ed: The Harriet Lane Handbook, 14th Edition, Mosby-Year Book, St. Louis, 1996
Daugirdas J, Ing TS: Handbook of Dialysis, 2nd Edition, Little Brown, & Co., Boston/NY/Toronto/London, 1994
Fine R, et al: Extended recombinant human growth hormone treatment after renal transplantation in children. JASN 12
(Supp3):S274, 1992
Fine R, et al: Five years experience with recombinant human growth hormone treatment in children with CRF. J of
Pediatr Endocrinology 2(1), 1994
Hendricks KM, Walker WA, Eds: Manual of Pediatric Nutrition, BC Decker, Inc., 1990
Holliday MA, et al, Eds: Pediatric Nephrology, 2nd Edition, Williams and Wilkins, 1987
Massie M, et al: Nutritional assessment of children with chronic renal insufficiency. JRN 2(1):2, 1992
Merenstein GB, et al, Eds: Handbook of Pediatrics, 17th Edition, Appleton and Lange, 1994
Queen PM, Lang CE. Eds: Handbook of Pediatric Nutrition, Aspen Publishers, 1993
Sanchez C, Salusky IB: The renal bone diseases in children treated with dialysis. Adv Ren Replace Ther 3(1):14, 1996
Spinozzi N, Nelson P: Nutrition Support in the Newborn Intensive Care Unit, JRN 6(4):188, 1996
Tonshoff B, Fine RN: Recombinant human growth hormone for children with RF. Adv Ren Replace Ther 3(1):37, 1996

11-34
Chapter 2:

LABORATORY VALUES/
DRUG NUTRIENT INTERACTIONS

GENERAL INFORMATION
The information in this chapter may help identify problems with nutritional significance in CKD patients, but it is not
meant to be all inclusive. Some of the signs or symptoms may be present only in the most severe cases. Furthermore,
signs or symptoms may also differ based on the type and stage of kidney disease or the modality of treatment. Critical
judgment and collaboration with the CKD care team should be used to assess the cause(s) of abnormal laboratory
values.

Patient laboratory values will depend also on the analytical method and procedure used by the individual laboratory.
Results can be influenced by a number of factors and must be interpreted in conjunction with clinical assessment.
Reference ranges included in this chapter are as reported in the sources below. There may be minor differences in
normal ranges for the elderly and pediatric patients in some laboratory values. The “CKD ranges” are values that may
be seen in CKD patients, but may not reflect the desired range. Where available, K/DOQI values are noted. Target
ranges vary from clinic to clinic and patient values should be assessed accordingly. A column labeled “Your Lab” has
been provided for notation of laboratory or facility-specific normal ranges.

The information provided on drug-nutrient interactions is very general. The effects of specific medications can differ
from patient to patient. The information is meant to provide a cross reference to patient symptoms. More detailed
information can be obtained from specific drug-nutrient interaction resources, and/or a clinical pharmacist with
expertise in renal pharmacology.

Note: Reference ranges, SI units, and the significance of abnormal values were updated with Mosby’s Diagnostic and
Laboratory Test Reference, 4th edition by Pagana and Pagana, 1999, and Clinical Laboratory and Diagnostic Tests:
Significance and Nursing Implications by Kathleen Treseler, Appleton & Lange, 1995. Where the information was
different from the previous edition of the Pocket Guide, the newest reference was utilized.

2-2
CONVERSION FORMULAS
mg to mEq or mEq to mg “Traditional” to Systeme International (SI) Units
mEq = mg x valence
atomic weight Traditional X Conversion Factor = SI
mg = mEq x atomic weight
valence

Symbol Atomic Wt Valence Traditional Factor SI


Calcium Ca++ 40 2 Albumin g/dL 10 g/L
Chloride Cl- 35 1 BUN mg/dL 0.3570 mmol/L
Iron Fe++ 56 2 Calcium mg/dL 0.2495 mmol/L
Magnesium Mg++ 24 2 Chloride mEq/L 1.0 mmol/L
Phosphorus P 31 2 Cholesterol mg/dL 0.02586 mmol/L
Potassium K+ 39 1 Creatinine mg/dL 88.4 mmol/L
Sodium Na+ 23 1 Ferritin ng/mL 1.0 µg/L
Glucose mg/dL 0.0551 mmol/L
Iron µg/dL 0.1791 µmol/L
Magnesium mEq/L 0.5 mmol/L
Phosphate mg/dL 0.3229 mmol/L
Potassium mEq/L 1.0 mmol/L
Sodium mEq/L 1.0 mmol/L
Total Pro g/dL 10 g/L
Reference: Hunt K: SI Unit Conversion. J Ren Nutr 3(3):146-147, 1993

2-3

LABORATORY TESTS
Test Ref. Range Your Lab CKD Range Significance of Abnormal
Albumin 3.5 - 5.0 g/dL WNL for the High: severe dehydration, albumin infusion
laboratory Low: fluid overload, chronic liver or
SI units:
pancreatic disease, steatorrhea, nephrotic
35 - 50 g/L or >4.0
syndrome, protein-energy malnutrition,
ideal for inflammatory GI disease, infection
CKD
(K/DOQI)

Alkaline 30 - 85 IU/L WNL High: renal osteodystrophy, healing of


Phosphatase fractures, malignancies
SI Units:
Low: congenital hypophosphatemia,
42 - 128 U/L
possibly in kwashiorkor, general debility,
anemia, nephrotic syndrome
Ammonia 15 - 110 WNL High: primary hepatocellular disease,
Levels µg/dL Reye’s syndrome, portal HTN, GI
bleeding/obstruction w/mild liver disease
SI Units: Low: essential or malignant hypertension
47 - 65
µmol/L
LABORATORY TESTS (CONT.)
Test Ref. Range Your Lab CKD Range Significance of Abnormal
B12 100-700 WNL High: leukemia, polycythemia vera, severe
pg/mL liver dysfunction
Low: pernicious anemia, atrophic gastritis,
SI Units: malabsorption syndrome, inflammatory
74-517 bowel disease, Zollinger-Ellison syndrome,
pmol/L achlorhydria, pregnancy, vitamin C or folic
acid deficiency

Blood 10 - 20 mg/dL 60-80 mg/dL High: w/excessive protein intake, GI


Urea (anuric, well bleeding, dehydration, hypercatabolism, CHF
Nitrogen dialyzed, and (a ↓ in cardiac output causes a ↓ GFR),
SI Units:
(BUN) eating adequate transplant rejection, inadequate dialysis
3.6 - 7.1
protein) Low: hepatic failure, over-hydration, acute
mmol/L
low protein intake, malabsorption, ↑
secretion of anabolic hormones

2-5

LABORATORY TESTS (CONT.)

Test Ref. Range Your Lab CKD Range Significance of Abnormal


Serum 9.0 - 10.5 WNL (low end) High: excess vit D/calcium, ↑ GI
Calcium* mg/dL < 9.5 mg/dL absorption, osteolytic disease,
carcinoma, excessive vit A,
SI Units: immobilization, primary
2.25-2.75 hyperparathyroidism, aluminum bone
mmol/L disease, dehydration, prolonged use
of tourniquet
Low: insufficient Vitamin D,
malabsorption, during bone building,
post-parathyroidectomy, long term
Dilantin therapy, hypoparathyroidism
*Adjust for low with low albumin (lack of carrier),
albumin see
formula page 8-16
but ionized is usually WNL
Ceruloplasmin 23-43 mg/dL WNL High: acute inflammatory response
(Cp) cancer, biliary cirrhosis, pregnancy,
copper intoxication
Low: Nephrotic Syndrome,
kwashiorkor, sprue,
hyperalimentation, infants

2-6
LABORATORY TESTS (CONT.)

Test Ref. Range Your Lab CKD Range Significance of Abnormal


100 - 106 mEq/L WNL High: excess salt, dehydration
Chloride (concentration), some forms of
SI Units:
metabolic acidosis, excessive use of
98 - 106 mmol/L
meds containing chloride, primary
hypoparathyroidism
Low: diabetic acidosis, K+ deficiency,
metabolic alkalosis, excessive
sweating, starvation, GI losses
(vomiting), chronic pyelonephritis,
dilution due to fluid excess, serum
chloride is affected by the same
conditions that affect serum sodium
and moves in the same direction as
sodium
Carbon 23 - 30 mEq/L WNL ≥ 22 High: metabolic acidosis
Dioxide (K/DOQI) Low: metabolic alkalosis
(Total) SI Units:
23 - 30 mmol/L
< 200 mg/dL WNL High: high cholesterol/saturated fat
Cholesterol < 150-180 mg/dL diet, hereditary disorders of lipid
SI Units: Evaluate for metabolism, nephrotic syndrome,
< 5.2 mmol/L nutrient glucocorticoid therapy
deficit Low: acute infection, starvation,
(K/DOQI) protein-energy malnutrition
2-7:
2-7

LABORATORY TESTS (CONT.)

Test Ref. Range Your Lab CKD Range Significance of Abnormal


Creatinine 0.5-1.1 mg/dL (F) 2-15 mg/dL High: muscle damage, catabolism, MI,
0.6-1.2 mg/dL (M) muscular dystrophy, ARF/CKD, use of
cephalothin/cimetidine, excessive
SI Units: protein intake, inadequate dialysis,
44-97 µmol/L (F) transplant rejection, relates to muscle
53-106 µmol/L mass, muscle turnover, and GFR
(M) Low: in chronic dialysis <10 may
indicate P-E malnutrition and wasting
of muscle

C- <0.8 mg/dL WNL High: arthritis, Crohn’s disease, lupus


Reactive erythematous, tissue infarction or
Protein SI Units: NA damage, acute MI, kidney or bone
marrow transplant rejection, soft tissue
trauma, bacterial infection,
postoperative wound infection, UTI,
TB, malignant disease

Fecal Fat <5 gm/24 hr WNL High: cystic fibrosis, malabsorption,


short-gut syndrome, maldigestion due
SI Units: NA to obstruction of pancreatic or biliary
tree, pancreatic insufficiency or
fibrosis
2-8
LABORATORY TESTS (CONT.)

Test Ref. Range Your Lab CKD Range Significance of Abnormal


Ferritin 12 – 300 ng/mL (M) ≥100 ng/mL High: iron overload, many
10 - 150 ng/mL (F) but no known transfusions, dehydration, can be
benefit with altered in inflammatory state, falsely
SI Units: >800 elevated in active liver disease
12 - 300 µg/L (M) (K/DOQI) Low: iron deficiency
10 - 150 µg/L (F)
Folic 5-20 µg/mL WNL High: pernicious anemia,
Acid vegetarianism, recent massive blood
SI Units: transfusion
14-34 mmol/L Low: folic acid deficiency, hemolytic
anemia, malnutrition, malabsorption
syndrome, malignancy, liver disease,
pregnancy, alcoholism, anorexia
nervosa
Globulin 2.3 - 3.4 g/dL WNL High: infection, liver disease,
leukemia, hyperlipidemia
SI Units: Low: malnutrition
23 - 35 g/L

2-9

LABORATORY TESTS (CONT.)


Test Ref. Range Your Lab CKD Range Significance of Abnormal
Glucose 70 - 105 mg/dL WNL High: DM, chronic hepatic dysfunction,
(Fasting) hyperthyroidism, malignancy, acute
SI Units: <200 stress, emotional distress, burns, diabetic
3.9 - 5.8 non-fasting acidosis, pancreatic insufficiency, glucose
mmol/L before dialysis; intolerance
influenced by Low: hyperinsulinemia, ETOH abuse,
dietary intake pancreatic tumors, liver failure, pituitary
dysfunction, malnutrition, extreme
exercise

Hematocrit 42 - 52 % (M) 33 - 36% High: polycythemia, dehydration


37 - 47 % (F) (K/DOQI) Low: anemias, blood loss (endogenous &
SI Units: dialysis), CKD, insufficient EPO
0.42-0.52 (M)
0.37-0.47 (F)
volume fraction

2-10
LABORATORY TESTS (CONT.)
Test Ref. Range Your Lab CKD Range Significance of Abnormal
Hemoglobin 14 - 18g/dL (M) Variable High: dehydration
12 - 16g/dL (F) 11-12 g/dL Low: over-hydration,
(K/DOQI) prolonged iron deficiency,
SI Units: mmol/L anemias, blood loss, CRF
8.7-11.2 (M)
7.4-9.9 (F)
Hemoglobin Adult: 4 - 8% WNL High: newly diagnosed/poorly
Alc “Good” control <7% controlled DM, splenectomy,
(Glycosolated “Fair” control 10% pregnancy, non-diabetic
hemoglobin hyperglycemia
GHb, GHB) SI Units: NA Low: hemolytic anemia,
chronic blood loss, early CKD

2-11

LABORATORY TESTS (CONT.)


Test Ref. Range Your Lab CKD Range Significance of Abnormal
Iron 60-175 µg/dL (M) WNL High: Fe overload, sideroblastic
50-170 µg/dL (F) anemias, estrogen/oral
contraceptives, hemolysis, ↑ for 1-2
SI Units: wks after IV iron-dose dependent
13-31 µmol/L Low: iron deficiency, low iron
intake, long term blood loss, during
rapid growth. Diurnal/day-to-day
variations are common, but
minimized if sample taken w/in same
time frame. Varies by lipid fraction
that is elevated/low.
Lipoproteins HDL:>45 mg/dL (M) WNL High: HDL (familial
>55 mg/dL (F) lipoproteinemia, excessive exercise)
LDL: 60-180 mg/dL LDL/VLDL (familial
VLDL: 25-50 mg/dL lipoproteinemias, nephrotic
syndrome, hypothyroidism, chronic
SI Units: mmol/L liver disease, poor glycemic control)
HDL: >0.75 mmol/L (M) Low: HDL (familial
>0.91 mmol/L (F) hypoliproteinemia, hepatocellular
LDL: <3.37 mmol/L disease, hypoproteinemia from
VLDL: NA malnutrition or nephrotic syndrome)
LDL/VLDL (familial
hypolipoproteinemia,
hypoproteinemia from
malabsorption, severe burn or
malnutrition)
2-12
LABORATORY TESTS (CONT.)

Test Ref. Range Your Lab CKD Range Significance of Abnormal

Lymphocyte 1500 - 4000 mm3 High: acute viral infections, collagen


WNL
Count disease, hyperthyroidism, high altitude
(total = % SI Units: NA Low: malnutrition (synthesis requires
lymphocytes x Investigate adequate calories/protein), adds power to
WBC) <1200 - 1500 significance of ↓ albumin, stress
Magnesium 1.2 – 2.0 mEq/L WNL High: w/excess intake of Mg+ in water,
dialysate, Mg+ containing parenteral
SI Units: infusion or OTC medications,
0.6-1.0 mmol/L dehydration
Low: w/some diuretics, ketoacidosis,
hypercalcemia, ETOH abuse, refeeding
syndrome, diarrhea/malabsorption,
malnutrition
Mean 80 - 95 µm3 WNL High: folic acid/B12 deficiency, cirrhosis,
Corpuscular reticulocytosis, chronic alcoholism
Volume SI Units: NA Low: chronic iron deficiency, anemia of
(MCV) chronic disease (MCV levels indicative of
anemias: pernicious >120; microcytic
<78; often seen with iron deficiency <64)

2-13

LABORATORY TESTS (CONT.)


Test Ref. Range Your Lab CKD Range Significance of Abnormal
Phosphorus 3.0 - 4.5 mg/dL 3.5 - 6.0 High: CKD, osteodystrophy, vit D
mg/dL intoxication, diurnal rhythm-evening or
SI Units: afternoon as much as 2x the am level,
0.97 - 1.45 excessive intake, inadequate P binder
mmol/L Low: vit D deficiency, low intake, excess P
binding, malabsorption/diarrhea/vomiting,
alkalosis, diabetic acidosis, diuretic therapy,
alcoholism, refeeding syndrome, post
parathyroidectomy, osteomalacia
Potassium 3.5 – 5.0 mEq/L 3.5 - 6.0 High: CKD, tissue destruction, shock,
mEq/L acidosis, dehydration, hyperglycemia,
SI Units: aldosterone antagonistic overuse, diuretics,
3.5 - 5.0 mmol/L falsely ↑ w/tourniquet, excessive oral intake,
inadequate dialysis, or inappropriate
dialysate K+, compression/fist clenching
prior to sample
Low: diuretic therapy, ETOH abuse, stress
response, vomiting/diarrhea/laxative or
enema abuse, malabsorption, correction of
diabetic acidosis

2-14
LABORATORY TESTS (CONT.)
Test Ref. Range Your Lab CKD Range Significance of Abnormal
Prealbumin/ 15 – 36 mg/dL ≥30 mg/dL High: administration of corticoids
Transthyretin (K/DOQI) Low: neonate, liver disease,
SI Units: malnutrition, inflammation
150 - 360 mg/L

Protein, Total 6.4 – 8.3 g/dL WNL High: dehydration, acute/chronic


infectious disease,
SI Units: leukemia/multiple myeloma
64 - 83 g/L Low: malnutrition, malabsorption,
cirrhosis, steatorrhea, edema,
nephrotic syndrome
Intact Intact: 150 – 300 pg/mL High: hyperparathyroidism, non-
Parathyroid 10 - 65 pg/mL (Target for iPTH) PTH producing tumors, lung or
Hormone kidney cancer, hypocalcemia,
(iPTH) N terminal: malabsorption syndrome, vitamin
8 - 24 pg/mL D deficiency, rickets
Low: hypoparathyroidism,
C terminal: hypercalcemia, metastatic bone
50 - 330 pg/mL tumor, sarcoidosis, vitamin D
intoxication, hypomagnesemia
SI Units: NA

Editorial Note: Reference and appropriate CKD ranges for 3rd generation PTH are currently being determined. Variance between
third and second generation iPTH depends on the patient-specific level of PTH fragment (7-84) that is measured by the second
generation iPTH. Concurrent measures of 2nd and 3rd generation iPTH may be helpful, especially where previous (second
generation) values and the clinical picture are inconsistent with current (third generation) PTH measurements. In research done at
Satellite Laboratory Services, Redwood City, CA, (368 patients), the 3rd generation PTH values were from 0.47 to 0.53 lower than
2nd generation PTH values in most (97-98%) patients.
2-15

LABORATORY TESTS (CONT.)


Test Ref. Range Your Lab CKD Range Significance of Abnormal
Reticulocyte 0.5% - 2% Variable in Index of bone marrow activity;
Count response to EPO reflects early change in RBC
production

High: hemolytic anemia, acute


bleed
Low: certain anemias due to
ineffective erythropoiesis (defic. of
iron, B12, folic acid, B6) or anemia of
chronic disease

RBC Count million/mm3 WNL High: high altitude, temporarily


Multiply auto- 4.7 - 6.1 (M) w/strong emotion, diurnally, cold
matic counter 4.2 - 5.4 (F) shower, reduced plasma volume,
values X 1 mil- dehydration
lion for total #) SI Units: NA Low: anemia, hemorrhage,
infectious disease, iron deficiency
Sodium 136-145 mEq/L WNL High: dehydration, diabetes
insipidus, often masked by water
SI Units: retention
136-145 mmol/L Low: over hydration, inappropriate
ADH diuretic use, burns, starvation,
adrenal insufficiency, nephritis,
hyperglycemia, diabetic acidosis,
hyperproteinemia
2-16
LABORATORY TESTS (CONT.)

Test Ref. Range Your Lab CKD Range Significance of Abnormal


TIBC 250-420 µg/dL WNL High: chronic iron deficiency,
Transferrin = Varies with pregnancy, alcoholism, acute hepatitis
(0.8 x TIBC)-43 SI Units: iron stores Low: cirrhosis, malnutrition, collagen or
45-73 µmol/L chronic disease/infection, iron overload,
inflammation
Transferrin Adult: mg/dL WNL High: chronic iron deficiency,
215-365 (M) pregnancy, alcoholism, acute hepatitis
250-380 (F) Low: cirrhosis, malnutrition, collagen or
chronic disease/infection, iron
SI Units: NA overload,inflammation
Transferrin 20 - 50% (M) ≥20% but no High: iron overload, pregnancy,
Saturation 15 - 50% (F) benefit to >50% alcoholism, acute hepatitis
(K/DOQI) Low: cirrhosis, malnutrition, collagen or
SI Units: NA chronic disease/infection, iron deficiency

Triglycerides 40-160 mg/dL (M) WNL High: liver disease, gout, pancreatitis,
35-135 mg/dL (F) < 200 mg/dL ETOH abuse, MI, diabetes, PD, use of
steroids, nephrotic syndrome
SI Units: Low: malnutrition, malabsorption
0.45-1.81 mmol/L
0.40-1.52 mmol/L

2-17

LABORATORY TESTS (CONCLUSION.)


Test Ref. Range Your Lab CKD Range Significance of Abnormal
Uric Acid 2.1-8.5 mg/dL (M) WNL High: gout, early CKD, thiazide diuretics,
2.0-6.6 mg/dL (F) starvation
SI Units: (mmol/L) Low: with high salicylate doses, hepatic failure
0.15 - 0.48 (M)
0.09 - 0.36 (F)
WBC Count 5000–10,000 mm3 WNL High: leukemic neoplasia, acute infection or
SI Units: inflammation, fever, anemia, tissue necrosis,
5-10 x 109/L trauma, stress
Low: radiation, chemotherapy, bone marrow
failure, dietary deficiencies, overwhelming
infection, autoimmune diseases
Zinc 85 - 120 µg/dL WNL High: contaminated sample, hemolysis
Low: low intake or absorption / increased loss
or needs, alcoholism, cirrhosis of the liver

References: Pagana KD, Pagana TJ: Mosby’s Diagnostic and Laboratory Test Reference,1999
Treseler, K: Clinical Laboratory and Diagnostic Tests, Appleton & Lange, 1995
Ravel R: Clinical Laboratory Medicine. Yearbook Medical Publishers, 1984

2-18
POSSIBLE NON-DIETARY CAUSES OF HYPERKALEMIA IN KIDNEY DISEASE
Mild to moderate renal insufficiency: primary cause is a defect in distal tubular K+ secretion with or without distal
renal tubular acidosis.
Laboratory error: hemolysis caused by improper blood sampling or specimen handling
Acidosis: each 0.1 decrease in arterial pH may increase serum potassium by 0.6 to 1.0 mEq/L
High serum glucose: shift between cell and serum
Insulin Deficiency: in diabetics
Inadequate dialysis: poorly functioning vascular access, too little time, insufficient blood flow, inappropriate dialyzer.
Other chemistries are usually elevated in conjunction with potassium
Dialysate potassium concentration too high
Drug Interactions: K-penicillin, beta blockers, angiotensin-converting enzyme inhibitors, muscle relaxants,
non-steroidal anti-inflammatory agents, steroids, cyclosporin, other OTC medications
Tissue destruction: rhabdomyolysis, burns
Catabolism/starvation: cell breakdown with release of potassium into serum, usually in combination with significant
weight loss
Concomitant disease: Addison’s disease, sickle cell anemia
Decreased gut excretion: severe, long term constipation

Adapted: Beto J: Hyperkalemia: Evaluation of Dietary and Non-Dietary Etiology.


J Ren Nutr 2:28-29, 1992

2-19

SIGNS AND SYMPTOMS OF ABNORMAL SERUM POTASSIUM

System Hypokalemia Hyperkalemia


Laboratory < 3.5 mEq/L > 6.0 mEq/L
Clinical Finding Frequently none until serum potassium levels are very high or low.
Skeletal/Muscle General muscle weakness, cramps, Usually no symptoms; could have
difficult respiration general weakness, tingling,
difficult speech, respiration, and
ambulation
Cardiac Effects Tachycardia with cardiac Bradycardia, cardiac block or
dilation/block/arrest, presence of U waves, arrest, low pulse rate, prolonged
flattened T and U waves PR interval, widened QRS, tall T-
waves, flattened P-waves
GI/Smooth Muscle Decreased peristalsis, early nausea/ Decreased peristalsis leading to
vomiting, constipation, abdominal nausea and diarrhea
distention, anorexia
Nervous System Listlessness, lethargy Irritability, mental confusion

References: Tisher C, Wilcox C: Nephrology for the House Officer, Williams & Wilkins, 1993
Treseler K: Clinical Laboratory and Diagnostic Tests, Appleton & Lange, 1995

2-20
ACIDOSIS/ACIDEMIA
Acidemia – abnormally increased hydrogen ion concentrations in the blood.
Acidosis, metabolic - disturbance where the acid-base status of the body shifts toward the acid side due to changes in
the fixed acids and bases in the body. Acidosis refers to the existence of one or more conditions that promote acidemia.

Acid production in dialysis patients is a function of the net rate of protein degradation (protein equivalent of total
nitrogen appearance) and is estimated to be 0.77 x PNA. The estimated alkali needed per dialysis treatment is 240
mmol and is usually delivered in the dialysate solution, usually as bicarbonate or acetate. While serum bicarbonate
levels are often low in maintenance hemodialysis patients, direct plasma pH provides a more absolute confirmation of
acidosis or acidemia. There is evidence that acidosis causes loss of lean body mass and may increase protein
catabolism. Several studies have shown that metabolic acidosis blocks the ability of CKD patients to adapt to a low
protein diet. Others suggest that muscle protein degradation is higher in patients with lower serum bicarbonate levels.
Conversely, treatment with NaHCO3 decreases protein degradation. Some studies suggest that acidosis may also cause
negative nitrogen balance and inhibit albumin synthesis. While future research may elicit the full clinical impact of
acidosis in CKD patients, current recommendations suggest maintaining serum bicarbonate levels at ≥22mEq/L
(KDOQI). Supplementation of bicarbonate in dialysate or orally may be needed to maintain acceptable bicarbonate
levels throughout the interdialytic period. Dialysate concentrations of >38 mmol/L have been shown to safely increase
predialysis serum bicarbonate levels as have oral doses of sodium bicarbonate (usually 2 – 4 g/d or 25 to 50 mEq/d).

References: NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, Am J Kidney Dis
35 (6) Suppl 2, p S38-S39, June, 2000
Mitch WE: Mechanisms Causing Muscle Wasting in Uremia, J Ren Nutr 6(2):75-78, 1996
Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997

2-21

ACIDOSIS/ALKALOSIS

Type HCO3 Blood pH PCO2 Causes


Metabolic Decreased Decreased Normal Diarrhea, uncontrolled diabetes or diabetic
Acidosis ketoacidosis, shock, starvation, large chloride
infusion, CKD, sepsis or severe infection,
excessive protein intake, intestinal fistula
Metabolic Increased Increased Normal Most common cause in dialysis patients is
Alkalosis vomiting, reduced protein intake, intensive dialysis

Respiratory Normal Decreased Increased Chronic lung disease, depression of ventilation rate
Acidosis
Respiratory Normal Increased Decreased Hyperventilation (emotions, pain, respirator over-
Alkalosis ventilation) hypoxia

Reference: Daugirdas JT, Ing TS: Handbook of Dialysis, Little, Brown & Co., Boston, 1994
Schrier R (Ed): Manual of Nephrology, Little, Brown, & Co., Boston, 1990
Pagana KD, Pagana TJ: Mosby’s Diagnostic and Laboratory Test Reference, 4th Ed. 1999

2-22
Na+/ K+ CONTENT OF SALT AND SALT SUBSTITUTES (Per ¼ tsp.)

Brand Na+mg K+mg


Iodized Salt 590 Trace
Adolph’s Salt Substitute+ 0 550
Adolph’s Seasoned Salt-Free+ 2 226

Durkee’s Low Sodium Salt 0 480


Substitute+
Durkee’s Seasoned Salt Lite+ 135 0
Lawry’s Seasoned Salt Free+ 2 226
Morton Lite Salt 280 350
Morton Salt Substitute 0 600
Morton Seasoned Salt Substitute 0 480
Natures Seasonings (Morton) 380 tr
NoSalt, Seasoned Alternative+ 0.5 333
NoSalt Alternative 0 650
NuSalt 0 663
Papa Dash Salt Lovers+ 240 tr
Papa Dash Light, Light, Light+ 90 tr
Savorex, Loma Linda+ 80 53
Sterling Lo-Salt+ 115 150

References: Pennington, J. Food Values of Portions Commonly Used, 17th Ed, 1998
Product Update, J Ren Nutr 5(2):91-92, 1995
Manufacturers’ Labels
+ Unable to obtain updated information on these products.
2-23

DRUGS THAT MAY IMPAIR ABSORPTION OR UTILIZATION OF NUTRIENTS

Drug-nutrient interactions depend on the drug dose and timing of administration. Multiple drugs may have simultaneous and
compounding effects.Phosphate binders/calcium supplements can affect and/or be affected by many drugs and should be taken away
from other medications if at all possible. Bicarbonate administration reduces folate and iron absorption.

Drug Nutrient
Alcohol Increased excretion of Mg++, K+ zinc, impaired utilization of folic acid
Antibiotics: Cycloserine Decreased levels of B12 B6, folic acid
Neomycin Decreased absorption: fat, lactose, protein, vit A, D, K, B12, Ca++, K+, Fe++
Isoniazid Pyridoxine deficiency
Tetracycline Ca++, Mg++, iron, zinc
Tobramycin Increased urinary loss of K and Mg, Hypokalemia
Antacids* Decreased absorption of Phosphorus, Fe++
Anticoagulants Decreased Vitamin K-dependent coagulation factors
Anticonvulsant: B12, folic acid, Ca++, Mg++, Pyridoxine, Vitamin K & D
Phenobarbital Pyridoxine may increase drug effect,
Anti-Gout Incr excretion of K+, Na+, Ca++, Mg++, P, Mg++, amino acids, Chloride, vit B2
Anti-inflammatory Folic acid, Na+, K+, fat, vit C, nitrogen, B12
Corticosteroids Incr protein catabolism/decr synthesis; decr absorption of Ca++, P, K+; incr need
for B6, Folate, vits C, D, zinc
Diuretics Incr urinary excretion of Mg++, zinc, K+, thiamin
Hypocholesterolemics Decr absorption: fat, carotene, vit A, D, K, B12, Fe
Laxatives Increased fecal loss of fat, Ca++, K+, Mg, fluids, most vitamins, carotene,
Mineral Oil Decr absorp vit A, D, E, K, Ca++ May not be clinically significant.

References: Mosby’s Nursing Drug Reference, Mosby 2000


Moore MC: Nutritional Care 4th Ed. Mosby’s Pocket Guide Series, 2001
Alpers DH, et al: Manual of Nutritional Therapeutics. Lippincot Williams & Wilkins, 2002
2-24
DRUG-NUTRIENT INTERACTIONS

Medications can alter absorption or enzyme systems; damage intestinal mucosa/alter normal flora; alter cellular
metabolism; or cause excess excretion (urine/stool). They can also cause a myriad of symptoms including diarrhea,
N & V constipation, anorexia, GI distress, dry mouth, altered taste, change in appetite, change in GI secretion and/or
transit time. In addition, some foods can affect drug actions as indicated below.

Diet Factor Drugs Affected Actions


Caffeine, Sodium restriction Lithium Increases drug toxicity
Potassium deficiency Digitalis
Grapefruit juice Cyclosporin, nifedipine, calcium Decreases first pass extraction and
channel blockers causes increased drug levels
Natural licorice Thiazides Excessive K+ loss, cardiac
dysrhythmia
Salt Substitutes ACE inhibitors Elevation of potassium levels
Tyramine/dopamine sources: MAO inhibitors Heachache, hypertensive crisis,
(liver, hard salami, pickled or potential intracranial hemorrhage
aged proteins, aged cheese,
yogurt, fava beans, raisins,
figs, banana, etc)

Reference: Moore MC: Nutritional Care. 4th Ed. Mosby’s Pocket Guide Series, 2001

2-25

POTENTIAL NUTRITION EFFECTS OF COMMON IMMUNOSUPPRESSIVE DRUGS


Drug Nutrition -related side effects

Azathioprine - Imuran Nausea, vomiting, stomatitis, esophagitis, pancreatitis, muscle


wasting
Basiliximab - Simulect Vomiting, nausea, diarrhea, constipation, abdominal pain

Corticosteroids/Prednisone Diarrhea, nausea, abdominal distension, GI hemorrhage,


Deltasone, Liquid prednisone, increased appetite, pancreatitis, osteoporosis, poor wound
Meticorten, Orasone healing, fluid retention, hyperglycemia
Cyclosporin Nausea, vomiting, diarrhea, oral candida, gum hyperplasia,
Sandimmune, Neoral pancreatitis, hepatoxicity, nephrotoxicity, hyperkalemia

Muromonab-CD3/Orthoclone OKT3 Nausea, vomiting, stomatitis, muscle wasting, peripheral edema


Mycophenolate GI bleeding, abdominal pain, hypophosphatemia,
CellCept hypercholesterolemia, hyperglycemia
Sirolimus - Rapamune Hyperlipidemia
Tacrolimus N & V, diarrhea, constipation, albuminuria, proteinuria,
Prograf hematuria, hyper-/hypokalemia, hypomagnesemia,
hyperglycemia, nephrotoxicity
Tymo Globulin Diarrhea, gastritis, hyperkalemia
(Anti-thymocyte Globulin)

Reference: Skidmore-Roth L: 2000 Mosby’s Nursing Drug Reference, 2000


Kopple JD, Massry S, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997
Simon & Schuster Interactive: The Pill Book on CD-ROM, 1996

2-26
HERBAL SUPPLEMENTS
Alternative medical therapies are prevalent in the US, both in generally healthy individuals and in those with various diseases /
illnesses. Clinicians must create an environment of openness for CKD patients to report information regarding the use of alternative
therapies. In general, use of medicinal herbs can be dangerous and inadvisable for those with CKD. Medical herbs can have
potent pharmacological activity, questionable chemical components, microbial contamination, and effects that interfere with
conventional medications. In addition, research on efficacy and safety is lacking, especially in CKD. Common categories of herbs
are women’s or men’s health, cold/flu, memory/concentration, sleep, cardiac/cholesterol, weight loss, anxiety/depression, and
headache.

Commonly Used Herbs in the US

Herb Use Comments/Effects


St. Johns Wart Anxiety/depression Interacts with many drugs, including immunosuppressant drugs,
hidden K+
Echinacea Cold/flu symptom relief Could worsen autoimmune disease/Type I DM, interact
w/antirejection drugs
Garlic Cardiac/reduce lipid levels Side effects: Bad breath, gastritis, diaphoresis, light headedness,
impaired blood clotting, can affect insulin and oral antidiabetics
Ginseng Multiple: stress, B/P, Can create anxiety, increased B/P, insomnia, headaches, asthma
depression, memory attacks, hypoglycemia, decreased anticoagulant activity. Do not
use in CKD
Ginko Biloba Memory, concentration Headache, anxiety, restlessness, incr risk for bleeding, N & V,
diarrhea, anorexia
Valerian Insomnia Headache, excitability, uneasiness, cardiac disturbances, N & V,
anorexia, hepatotoxicity, insomnia, vision changes, may negate
warfarin
Feverfew Headaches, migraine Mouth ulcers, incr heart rate, limits iron absorb, N & V, anorexia,
muscle/joint pain

2-27

CKD AND HERBAL MEDICINES


Classification Herbs Reported Effects
Potentially Rheum rhaponticum (Chinese rhubarb), Improved proteinuria, delayed
Beneficial Epimedium sagittatum, Man Shen Ling, progression, improved protein
Rhizome wheat starch, Acacia senegal (Gum status, improved kidney
Arabic) function/edema/anemia, increased
diuresis.
Potentially Mixture: (C. Magnolia officinalis, R. stephaia, Polyuria resulting in dehydration,
Detrimental Tetrandra, R. Aristolochia, Fanchi) Artmisia ARF, CKD, and stone formation,
asbinthium (wormwood plant), Glycyrrhiza potassium imbalance
glabra (licorice), Chuifong tuokuwan (Black
Pearl), Tung sheuh (Cow’s Head Brand)

References: Geraghty ME: Herbal Supplements for Renal Patients: What do we know? NNI, March 2000
Skidmore-Roth L: Mosby’s Handbook of Herbs and Natural Supplements. Mosby, Inc. 2001

2-28
Chapter 3:

NUTRIENT
CALCULATIONS

GENERAL INFORMATION

Nutrient recommendations in this chapter are compiled from a number of sources as noted and reflect the
K/DOQI nutrition practice guidelines where available. While the information here is appropriate for a majority of
patients, each patient should be assessed individually and thoroughly. Base nutrient recommendations on the findings
in the nutrition assessment, clinical expertise, and common sense. Do not restrict the diet above what is necessary to
maintain clinical, nutritional, and metabolic status.

Editorial Comment:
Methods of patient instruction vary widely within renal nutrition practice. Patients should be given written instruction
on appropriate food choices based on their level of kidney function, treatment modality, clinical status, and biochemical
profile. Instruction should also be appropriate for the patient’s level of education and literacy skills. Providing a
written meal pattern or guide serves several purposes. It can prove that a patient has received instruction and written
guidance in the event of a medical-nutrition crisis or significantly abnormal laboratory values. Verbal follow-up with
the patient can refer the patient back to the previously provided written information. Failure to provide written
instruction based on the patient’s individual needs may put the dietitian at risk of legal accountability for an event such
as hyperkalemia. With the focus on preventing malnutrition and maintaining or improving the nutrition status of our
patients, we have moved toward much more liberal meal plans. Provision of written and verbal nutrition guidance for
patients and/or their support persons is of utmost importance. Failure to provide verbal and written guidance is
unacceptable renal nutrition practice. The ability to provide quality nutrition care depends on adequate staffing.
According to the K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure, “There appears to be a
general sense among renal dietitians, based on experience, that an individual dietitian (full time) should be responsible
for the care of approximately 100 maintenance dialysis patients, but almost certainly no more than 150.” Other
documentation (NKF-CRN Staffing Guidelines, CRN of Northern California/Northern Nevada) suggests that staffing
should be based on total number of patients with additional time for higher acuity levels (language barrier, diseases,
lack of economic/social resources, advanced age) within the patient population and new patients (usually 80-100
patients per FTE). Those patients with higher acuity levels and new patients require additional intervention and
dietitian time over stable MD patients.
3-2
DAILY NUTRIENT RECOMMENDATIONS FOR CKD

Nephrotic
CKD PD Transplant
Acute1 Syndrome HD
Post-op Chronic
Protein 0.6-0.8 K/DOQI: 0.8-1.0 K/DOQI: K/DOQI: 1.3-2.0 0.8-1.0
gm/kg3 Based on renal GFR <25 mL/min Replacing urine ≥1.2 ≥ 1.2-1.3
function/treatment /1.73 m2 loss is ≥ 50% HBV ≥50% HBV
0.60-0.75 gm/kg controversial
>50% HBV
Energy 35-50 K/DOQI: 35 unless pt is K/DOQI: K/DOQI: 30-35
kcal/kg3 depends on 30-35 >60 yrs obese; high 30-35 >60 yrs 30-35 >60 yrs Maintain SBW, limit fat to
stress/status 35 <60 yrs complex CHO; 35 <60 yrs 35 <60 yrs 30% kcal, < 300 mg
of nutrition low cholesterol; including cholesterol/day
<30% fat dialysate
calories
Na+ 1-2 Varies from 1-3 1-2 1-3 2-4 2-4 2-4
gm/day Based on B/P, to no added salt Monitor
edema; replace fluid balance
diuretic phase
K+ 2 Usually Usually 2-3 3-4 Unrestricted, unless serum
gm/day Maintain serum unrestricted unless unrestricted Adjust to serum Adjust to serum level high, may need diet
<5 mEq/L serum level is high levels levels restriction with cyclosporin
Replace loss
diuretic phase
1
TPN recommendations are in Chapter 9.
2
Editorial Note: A 1 gm Na+ (sodium) restriction on HD or PD is generally difficult to achieve in an outpatient setting and seldom needed with
dialysis.
3
Based on standard or adjusted body weight

3-3

DAILY NUTRIENT RECOMMENDATIONS FOR CKD (CONT.)

Nephrotic Transplant
CKD
Acute1 Syndrome HD PD
Post-op Chronic
Phosphorus Maintain 10-12 mg/gm ≤ 12 mg/kg/day 10-12 mg/gm protein 10-12 mg/gm RDA - RDA
mg/gm pro serum value protein or < 900 mg/day adjust for protein or supplement
or mg/day WNL 10 mg/kg/day pro < 900 mg/day, as needed
adjust for pro

Calcium Maintain 1.0-1.5 Same as < 2.0-2.5 < 2.0-2.5 0.8-1.5 0.8-1.5
gm/day serum WNL < 2-2.5 incl predialysis Include Include
(adjusted for binder load binder load binder load
low albumin)
Fluid Output plus No restriction Maintain Output plus 1000 cc Maintain Unrestricted, unless
cc/day 500 cc balance balance overloaded

Vitamins/ RDA: adjust RDA: B- Same as CKD C: 60-100 mg B6 - 2 mg Same as HD RDA, may need
Minerals to degree of complex & C; Research Folate - 1 mg B12 – but may need additional Vitamin D
(Daily) catabolism, Individualize needed to 3 µg/d 1.5 to 2 mg of
TPN - may Vit D, Fe, Zinc quantify needs. RDA others B1 due to
require May need Vit E-15 IU/d dialysis loss
multivitamin Vitamin D Zinc-15 mg/d
& minerals Individualize Fe, Vit D

Fiber Increased dietary fiber may be beneficial for CKD patients, however, optimal dose, source, and long term clinical benefits have
not yet been established. 20-25 gm/day has been suggested.

References: Kopple JD and Massry SG Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997
rd
Mitch WE and Klahr S Eds: Handbook of Nutrition and the Kidney, 3 Ed, Little, Brown & Co., 1998
NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000
3-4
NUTRITION RECOMMENDATIONS FOR CKD PATIENTS NOT ON DIALYSIS
Stage Description GFR (mL/min/1.73 m2)
1 Kidney damage with normal or increased GFR ≥ 90
2 Kidney damage with mild decrease in GFR 60-89
3 Moderate decrease in GFR 30-59
4 Severe decrease in GFR 15-29
5 Kidney Failure < 15 (or dialysis)

Individuals with GFR <60 mL/min/1.73 m2 (stages 3, 4, 5) should undergo assessment of dietary protein and energy
intake and nutrition status. Status should be monitored at regular intervals. (Nutrition Guidelines 23, 26)

Nutrient recommendations (Nutrition Guidelines 24, 25) for individuals with GFR <25 mL/min/1.73 m2: 0.6-0.75 gm
protein/kg SBW or ABW and 35 kcal/kg SBW or ABW for those <60 years of age and 30-35 for those >60 years of
age.

Reference: NKF K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation Classification, and
Stratification. Am J Kidney Dis 39 (Suppl 1):S1-266, 2002

3-5

L-CARNITINE SUPPLEMENTATION IN MD PATIENTS


Area of Impact Potential Benefits Reported by Some Investigators in their Research
Findings
Lipid abnormalities Results variable
Intradialytic complications Lower incidence of intradialytic hypotension/muscle cramps
Patient well-being Patient/staff report significant improvement of patients’ sense of well-being
Muscle/cardiac function Lower rate of arrhythmia, improved cardiac function, decreased
cardiomegaly/cardiomyopathy
Exercise tolerance Reported improvement in muscle function and oxygen consumption
Protein/muscle metabolism Decr serum urea nitrogen/Cr/phosphate due to decr in protein/muscle
catabolism; Incr albumin/BW
Anemia Increased hematocrit/hgb and lower EPO dose, L-carnitine is found in
phospholipids that make up the red cell membrane, w/ supplementation the red
cell membrane is more stable w/ less cell fragility and longer cell life span;
may help clear toxins that hinder erythropoiesis
Supplement IV dose: 10-20 mg/kg/day Oral Carnitine is not indicated for CKD patients.
Recommendations: Maintenance Dose: Undetermined, dialysis losses are significant and ongoing;
no known harm

Deficiency is multifactorial: inadequate intake of carnitine-rich foods, lack of kidney production, dialysis removal (70% of serum carnitine is
cleared in a 3 hour treatment). Serum carnitine is preserved at the expense of muscle carnitine with the potential of creating significant
carnitine deficiency over time in CKD patients treated with dialysis. K/DOQI Clinical Practice Guidelines for Nutrition in CRF
note:supplementation of L-carnitine in MD patients may improve subjective symptoms (malaise, muscle weakness, intradialytic cramps,
hypotension, quality of life) and be most helpful in the treatment of EPO-resistant anemia.

Reference: Brass EP, Adler S, Sietsema E, et al: Intravenous L-Carnitine Increases Plasma Carnitine, Reduces Fatigue, and May Preserve
Exercise Capacity in HD Patients. Am J Kidney Dis 37(5):1018-1028, 2001
NKF K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35(6) Suppl 2, June, 2000
Kletzmar J, Mayer G, Legenstein E, et al: Anemia and carnitine supplementation in HD patients. KI 55(Suppl 69):S93-106, 1999
Vesela E, Racek J, Trefil L, et al: Effect of L-Carnitine Supplementation in HD Patients. Nephron 88:218-223, 2001
3-6
NUTRIENT RECOMMENDATIONS FOR THE PREGNANT DIALYSIS PATIENT
Nutrient Recommendation Goals
Protein* 1 gm/kg + 20 gm/day Meet increased needs, BUN <45-50 mg/dL
Calories* Rec. dialysis level + 100-300 kcal Dry weight gain per prenatal normals
Sodium** Individualize BP control, euvolemia
Potassium Depends on RRF/serum levels Serum level: 3.5-5.5 mEq/L
Calcium 1000-1600 mg/day Serum level: WNL
Phosphorus Balance of diet/binders Serum level: 4.5-5.5 mg/dL
Magnesium As needed to prevent Serum level WNL
hypomagnesemia
Fluid** Individualize to RRF, BP, hydration ID gain < 1 kg, minimal fluid shift
Fiber Encourage increased dietary fiber Prevent constipation
Vitamins/ Supplement as for dialysis with Replace losses, meet additional needs,
Minerals additional on individual basis plus maintain serum ferritin >100 µg/L
zinc. Vitamin C <150 mg/day. Other: CO2 WNL, creatinine 5-8 mg/dL

* Based on pre-pregnancy SBW or ABW.


** Hypertension and hypotensive episodes are common and dangerous complications. Increased dialysis (by at least
50%, 5-7 days a week) is recommended to minimize fluid shifts and prevent build up of uremic toxins. Dialysate
bicarbonate concentration may need to be decreased to prevent metabolic alkalosis with daily dialysis.

References: Levy DP, Giatras I, Jungers P: Pregnancy and end stage renal disease-past experience and new insights.
Nephrol Dial Transplant 13:3005-3007, 1998
Wilkens K, Schiro K: Suggested Guidelines for Nutrition Renal Patients. ADA, 1992
Grossman S, et al: Nutrition in the Pregnant Dialysis Patient. J Ren Nutr 3(2):56-66, 1993
Hou S: Pregnancy and birth control in dialysis patients. D & T 23:22-26, 1994

3-7

NUTRIENT RECOMMENDATIONS FOR AIDS

Nutrient AIDS AIDS and Dialysis


Protein 1.5-2.5 gm/kg actual or usual body weight 1.4-2.0 gm/kg actual or usual body
weight
Calories 35-45 calories/kg actual or usual BW 45-50 kcal/kg actual or usual body
weight
Fat < 30% of kcal/modify type of fat < 30% of kcal/modify type of fat
based on fat malabsorption based on fat malabsorption
Sodium Estimated safe/adequate amount; 1.1-3.3 gm/day 2 to 4 gm/day
Potassium Estimated safe/adequate amount; 1.9 -5.6 gm/day 2-3 gm/day
May need supplement if diarrhea is present PD may need supplements
Calcium 2 times RDA 1-1.5 gm/day
Phosphorus 2 times RDA 10-12 mg/gm protein
Fluid No restriction Urine output plus 1000-1200 cc
Iron Individualize Individualize
Zinc Twice RDA (30 mg) especially with significant Individualize
diarrhea is present
Vitamins 2 times RDA Same as non-AIDS dialysis patient

Reference: Plourd D: Nutritional Management of the Dialysis Patient with AIDS. J Ren Nutr 5(4):182-193, 1995

3-8
HARRIS-BENEDICT FORMULA FOR DETERMINING BASAL ENERGY
EXPENDITURE*

Female (kcal) = 655 + (9.6 x Body Weightkg) + (1.8 x Heightcm) - (4.7 x Ageyrs)
Male (kcal) = 66 + (13.7 x Body Weightkg) + (5.0 x Heightcm) - (6.8 x Ageyrs)
* May overestimate calorie needs/reported to overestimate resting metabolic rate by 10-15%.

Resting Energy Requirements During Acute Illness = BEE x Adjustment Factor


Acute KD Energy Requirements = Estimated BEE x Adjustment for Illness x 1.25

SUGGESTED ADJUSTMENT FACTORS FOR ENERGY NEEDS DURING ACUTE ILLNESS*

Bone Fractures 1.2-1.25


Burns (% burned) 0-20%/21-40%/41-100% 1.0-1.5/1.5-1.85/1.85-2.05
Elective Surgery - Day 1-4/Day 18-21 1.0/0.95
Fever x 7% for 1o F/ x 13% for 1o C > normal
Infection, Mild/Moderate/Severe 1.0/1.2-1.4/1.4-1.6
Maintenance Hemodialysis 1.0-1.05
Malnutrition (Chronic, severe) 0.70
Multiple Organ Failure 1.2-1.4
Nondialyzed CKD 1.0
Peritonitis, Soft Tissue Trauma 1.15
Postoperative (no complications) 1.0
1.2 - 1.25

* Even in hypermetabolic conditions, energy requirements rarely exceed 130% of BEE.


Reference: Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins,1997
Page CP, et al: Nutritional Assessment and Support, 2nd Ed.Williams & Wilkins, 1994

3-9

ESTIMATED BODY WEIGHT AND ENERGY NEEDS IN PARA- AND QUADRIPLEGIA

STEP
Determine SBW or ABW
1
STEP Modify weight for paralysis
2 Paraplegia=subtract 5-10% from SBW/ABW
Quadriplegia=subtract 10-15% from SBW/ABW
STEP To estimate energy expenditure in paraplegia or
3 quadriplegia:
Use reduced SBW/ABW in Harris-Benedict
Formula

SBW = Standard body weight


ABW = Adjusted body weight

Note: Weight was changed from Hamwi IBW to SBW or ABW for consistency with the NKF K/DOQI guidelines.

References: Peiffer SC, Blust P, Leyson JFJ: Nutritional Assessment of the Spinal Cord Injured Patient. J Am
Dietetic Assoc 78:501, 1981

3-10
ESTIMATES OF CALORIES ABSORBED FROM PERITONEAL DIALYSATE

The most accurate method of determining the caloric load from peritoneal dialysate is to measure the grams of glucose in the effluent
and compare that to the grams of glucose that were infused. Several formulas have been published:

Reference Formula Example Comment


Grodstein, et al. Glucose absorbed = 4 L of 1.5% (1.36) + 4 L of Developed before significant
KI, 19:564-567, 1981. (11.3 x – 10.9) times 4.25% (3.8) solution = average differences in membranes
L inflow times 3.4 2.6% were recognized, but gives a
where x = the average glucose (11.3 x 2.6) – (10.9 x 8 liters) = rough glucose absorption/kcal
concentration infused. 29.4 – 10.9 x 8L = 18.5 x 8L estimate.
18.5 x 8 L = 148 gms glucose
148 X 3.4 = 503 calories
Bodner, et al. Adv in PD, (1-D/Do) xi where D/Do is the Infused = 4 L of 38 gm/L + 4 L of This considers dialysis
9:114-118, 1993 fraction of glucose remaining 13.6 gm/L=152 + 54.4 = 206 gm modality and transport
and the xi is the initial glucose Measured remaining glucose = characteristics.
infused. 1200 mg/dL in 10 liters effluent
or 1200 x 10,000 mL/100,000
which = 1200 X 0.1 = 120 gm
D/Do = 120/206 = 0.58
1–0.58 x 206 = 86.5gm x 3.4 =
294 kcal

3-11

ESTIMATES OF CALORIES ABSORBED FROM PERITONEAL DIALYSATE (cont.)

Reference Formula Example Comment


Podel, et al. With acute peritoneal dialysis in the critical care setting the mean total glucose absorbed was
J Ren Nutr 43% ± 15%, suggesting that the Grodstein formula overestimates glucose absorption with 4.25%
10:93-7, 2000 APD exchanges and underestimates glucose absorption with 1.5% APD exchanges.
Simple Glucose infused x 40% (CCPD) or 60% absorption 4 L, 1.5% = 124 Rough estimate;
estimate (CAPD) 4 L, 4.25% = 346 doesn’t consider
Total kcal = 470 membrane transport
1.5% 1L=15 gm x 3.4 = 51 x 60%=31 kcal/L characteristics or
PD modality.
2.5% 1L=25 gm x 3.4 = 85 x 60%=51 kcal/L

4.25% 1L=42.5 gm x 3.4=144.5 x 60%=86.7 kcal/L

3-12
NATIONAL RENAL DIET FOOD CHOICE LISTS (CKD Not on Dialysis)
(In development at press time)

Food Group Choices Protein Calories Sodium Potassium Phosphorus


High Protein 6-8 50-100 20-150 50-150 50-100
+High P 6-8 50-100 20-150 50-150 100-300
+High Na+ 6-8 50-100 200-400 50-150 50-100
Vegetable- Low K+ 2-3 10-100 0-50 20-150 10-70
Med K+ 150-250
High K+ 250-550
Breads/Starches 2-3 50-200 0-150 10-100 10-70
+ High Na+, P 2-3 50-200 150-400 10-100 100-200
Fruit – Low K+ 0-1 20-100 0-10 20-150 1-20
Med K+ 150-250
High K+ 250-550
Calorie 0-1 100-150 0-100 0-100 0-100
Flavor 0 0-20 250-300 0-100 0-20
Vegetarian Protein 6-8 70-150 10-200 60-150 80-150
+High Na+ / K+ /P 6-8 70-150 250-400 250-500 200-400

3-13

NATIONAL RENAL DIET FOOD CHOICE LISTS (CKD on Dialysis)


(In development at press time)

Food Group Choices Protein Calories Sodium Potassium Phosphorus


High Protein 6-8 50-100 20-150 50-150 50-100
+High Na, K+, P 6-8 50-100 200-500 250-450 100-300
Dairy/Phosphorus 2-8 100-400 30-300 50-400 100-120
Breads/Cereal/Grain 2-3 50-200 0-150 10-100 10-70
+High Na+, P 2-3 50-200 200-400 10-100 100-200
Fruit/Vegetables – Low K+ 0-3 100-100 1-50 20-150 0-70
Med K+ 150-250
High K+ 250-550
Calories 0-1 100-150 0-100 0-100 0-100
Flavor 0 0-20 250-300 0-100 0-20
Vegetarian Protein 6-8 70-150 10-200 60-150 80-150
+High Na+ /K+ /P 6-8 70-150 250-400 250-500 200-400

3-14
VITAMINS FORMULATED FOR CKD PATIENTS

Product Vit C B1 B2 Niacin B6 B12 Folic B5 Biotin Fe Zinc


(mg) (mg) (mg) (mg) (mg) Acid (mg) (mcg) (m (mg)
g)
Dialyvite 100 1.5 1.7 20 10 6 mcg 1 mg 10 300 -
Dialyvite 800 60 1.5 1.7 20 10 6 mcg 800 mcg 10 300 -
Diatx* 60 1.5 1.5 20 50 1 mg 5 mg 10 300 -
Nephrocaps 100 1.5 1.7 20 10 6 mcg 1 mg 5 150
Nephron-FA 40 1.5 1.7 20 10 6 mcg 1 mg 10 300 66
Nephrovite-Rx 60 1.5 1.7 20 10 6 mcg 1 mg 10 300 -
Nephrovite 60 1.5 1.7 20 10 6 mcg 1 mg 10 300
NephPlex-RxR 60 1.5 1.7 20 10 6 mcg 1 mg 10 300 - 12.5
TM
RenaPlex 60 1.5 1.7 20 20 6 mcg 800 mcg 10 300 - 12.5

*(DiatxFe is also available and is comparable to Diatx plus 100 mg elemental iron.)

References: Internet-Manufacturers’ Information

3-15

CONSIDERATIONS FOR A KOSHER DIET

There are three basic concepts in Jewish dietary law:

1. The main concept governs the selection, preparation, and slaughtering of animal foods.
a. Animals must chew a cud and have cloven hooves. Only the forequarters of these animals are acceptable.
b. Eating of the blood (including arteries, veins, and muscle tissue) is forbidden.
c. Turkey, chicken, goose, pheasant, and duck are kosher. Birds of prey are not kosher.
d. Eggs from kosher birds are kosher, others are not.
e. All kosher animals must be slaughtered in a specific way as described by the Torah.
f. Fish with fins and scales are kosher; crustaceans, shellfish, and fish-like mammals are forbidden.
2. The second basic concept is the koshering of meat and poultry foods.
a. Koshering removes all the blood through soaking and salting. Liver must be broiled.
b. Koshering is done prior to cooking the food.
3. The third concept of the rules of kashrut is the separation of meat and dairy products.
a. Meals either have a meat or a dairy focus. Fish is considered neutral and can be eaten with either.
b. It is customary to wait 6 hours (Orthodox) after eating meat before ingesting dairy products.
(1-5 hours for reformed conservative).
c. Meat products can be eaten within a half hour to an hour after a dairy meal if the mouth is rinsed.
d. Two sets of cookware, dishes, utensils, and drain boards are kept, one for dairy and one for meat.
e. There are three categories of kosher food: meat, dairy, and pareve. Pareve are neutral foods that can
be served with meat or dairy. Examples are fruits, vegetables, grains, beans, legumes, and their derivatives.
Margarine is considered dairy unless marked “pareve.”

Note: A Rabbi can be consulted for information about exceptions for medical conditions.
Reference: Nichols D: What is a Kosher Renal Diet? J Ren Nutr 5(3):144-147, 1995

3-16
AVAILABLE FIBER, POTASSIUM, AND PHOSPHORUS IN COMMON HIGH FIBER
CEREALS

Cereal Serving Size Fiber (gm) K+ (mg) Phos


(cup)
Cracklin’ Bran ¾ 6.5 255 187
Bran Flakes, Post ¾ 5.3 185 152
All Bran, Kellogg’s Extra Fiber ½ 15.0 300 287
Grape-Nuts ½ 5.0 178 138
Multi-Bran Chex, General Mills 1 6.4 191 173
Quaker Oat Bran 1¼ 6.0 257 306
Shredded Wheat-n-Bran 1¼ 7.9 248 235
100% Bran, Post 1/3 8.3 274 236
Oat Bran, Cooked 1 5.7 201 261

Reference: Internet: U.S. Department of Agriculture, Agricultural Research Service, 1999


Database for Standard Reference, Release 13. Nutrient Data Laboratory Home
Page: http://www.nal.usda.gov/fnic/foodcomp

3-17

COMPOSITION OF MILK AND SUBSTITUTES (1 fluid oz serving unless indicated)

Product kca CHO PRO FAT Na+ K+ P Ca++


l (gm) (gm) (gm) (mg) (mg) (mg) (mg)
Coffee Rich 44 4.4 0.0 3.2 22 12 10 0
Coffee-Mate 40 4.0 0 2.0 0 50 14 0
DariFree Beverage Mix (4 oz) 181 42.2 0 0 231 N/A 0.1 150
Farm Rich 36 2.2 0 3.0 14 28 18 0
Half & Half, 1 Tbsp. 20 0.6 0.4 1.7 6 19 14 16
Light Cream, 1 Tbsp. 29 0.5 0.4 2.9 6 18 12 14
Milk, 2% 15 1.5 1 0.5 15 47 29 37
Milk, 1% 12 1.5 1 0.3 15 48 29 37.5
Milk, Skim 11 1.5 1 0.05 16 51 31 38
Milk, 3.25% 19 1.5 1 1 15 46 28 36
Mocha Mix 38 2.4 0.2 3.2 14 38 16 2
Mocha Mix Frozen Dessert 148 17.9 0.6 7.6 81 105 NA NA
Polyrich 44 4.4 0 2.6 14 24 10 0

References: Internet: U.S. Department of Agriculture, Agricultural Research Service, 1999


Pennington JAT: Food Values of Portions Commonly Used, 17th Ed. Lippencott, 1998
Manufacturers’ Information

3-18
Chapter 4:

SPECIAL CONSIDERATIONS
FOR THE
DIABETIC PATIENT

COMMON SYMPTOMS OF DIABETES COMMON TREATMENTS OF DIABETES


Type I Type II Type I Type II
Frequent urination* Drowsiness* Insulin (often use Diet modification
Abnormal thirst* Itching multiple shots) Exercise
Unusual hunger Blurred vision* Diet modification Oral Agent/Insulin
Rapid weight loss Excess weight Exercise Blood sugar tracking
Irritability Tingling in feet* Frequent BG tracking Education
Obvious weakness Easily fatigued* Education
Fatigue Skin infections*
Nausea and vomiting Slow healing*
15-20% inherited Family history of DM

*Common to both types

DEFINITIONS OF DIABETES:

Type I: Type I diabetes (formerly insulin dependent) is characterized by insulin deficiency that results from the
destruction of beta cells of the pancreas, usually by an autoimmune process.
Type II: Type II (formerly non-insulin dependent) is more common and is characterized by insulin resistance or
decreased tissue glucose uptake in response to insulin. There is an insulin secretory defect that makes it impossible for
them to release enough insulin to compensate for the insulin resistance.
Gestational Diabetes Mellitus: This type of diabetes is one that is characterized by any glucose intolerance that first
occurs or is recognized during pregnancy.
Impaired Glucose Tolerance: Impaired glucose tolerance and impaired fasting glucose (IFG) are not considered as
absolute diabetes but they are risk factors for later development of diabetes and cardiovascular disease. IFG is defined
as a glucose concentration of >140 but <200 mg/dL 2 hours after ingestion of a 75 g glucose load or when fasting
plasma glucose is >110 but <126 mg/dL.
4-2
STAGES OF DIABETIC NEPHROPATHY
Stage 1: Hyperglycemia leads to increased kidney filtration due to osmotic load and toxic effects of high blood
glucose. There is increased GFR with enlarged kidneys.

Stage 2: Clinically silent phase, but continued kidney hyperfiltration and hypertrophy.

Stage 3: Microalbuminemia (defined as 30-300 mg/day (20-200 mcg/min) loss of albumin in urine.
With microalbuminemia 20% develop nephropathy within 5 years on standard care, 50% do not progress.
Microproteinemia is a better predictor of progression in Type I than Type II.
Microalbuminuria is a predictor of increased macrovascular disease.
Microalbuminuria is associated with higher than recommended HbA1c levels (> 8.1%)

Stage 4: Overt Nephropathy


Almost always with hypertension, > 300 mg/day of albumin in the urine, about 10% have nephrotic range
of proteinuria; GFR is decreased.

Stage 5: CKD needing renal replacement therapy


Over 30 years, >25% of patients with Type I DM progress to this stage.
Over 25 years, about 8% of patients with Type II progress to this stage.

Treatments to Slow Progression:


ACE inhibitors (reduce microalbuminuria and the progression, independent of hypertension).
Angiotensin II blockers may also be effective
Mild protein restriction (0.6-0.75 gm/kg) (Some recommend up to 0.8 gm/kg)

4-3

RECOMMENDED DIETARY MODIFICATION IN DIABETIC NEPHROPATHY


Stage of Disease % Calories as CHO % Calories as Fat % Calories as Protein
Pre-clinical 50 - 60% ≤30% total calories as fat ~12 - 15% *
nephropathy Up to 40 gm fiber ≤10% saturated fat
Stage 1-2-3 Achieve and maintain 6-8% polyunsaturated fat
desirable body weight < 300 mg cholesterol/day
Progressive 55 - 65% ≤30% total calories as fat ~ 10% (50% HBV);
nephropathy Up to 40 gm fiber ≤10% saturated fat replacement of urinary losses
Stage 4 Achieve and maintain < 300 mg cholesterol/day or 0.8 - 1.0 gm/kg if not
desirable body weight replacing urinary losses)*
Liberalize during periods of
catabolic stress

Hemodialysis 50 - 60% ≤30% total calories as fat ~12 - 20% *


Low glycemic index ↑ ≤10% saturated fat
fiber
Peritoneal Dialysis ~35 - 40% oral ≤30% total calories as fat ~12 - 20% *
~15% dialysate
*Liberalize protein allowance to 1.2 - 1.5 during catabolic stress.

K/DOQI Recommendations for CKD not on dialysis: See page 3-5

Reference: Mitch WE, Klahr S, Eds: Nutrition and the Kidney Little, Brown and Co., 1993
Kaysen G: Nutritional Management of Nephrotic Syndrome. J Ren Nutr 2:50, 1992
Stover J Ed: Clinical Guide to Nutrition Care in End-Stage Renal Disease, ADA 1994

4-4
TYPES AND ACTIONS OF INSULIN
Type Onset Peak Duration Names
Crystalline zinc, 30-60 min 2-4 hours SC: 6-8 hours Pork Regular Insulin and Iletin II,
unmodified, regular IV: 30-60 min Beef/Pork: Regular Iletin I
insulin Human: Humulin R, Novolin R, Velosulin
Concentrated Regular For people who need more than 200 units of insulin
Iletin II U 500 per day; not for IV use
Insulin glargine 2 hours 6-8 hours 24 hours Lantus - Given at bedtime provides better blood
glucose control throughout the day
Insulin lispro 15 min 30-90 min 5 hours or less Humalog (rDNA origin)
Insulin zinc suspension 1-2½ hr 7-15 hours About 22 hours Beef: Lente Insulin Pork: Lente Iletin II, Lente L
Beef/Pork: Lentin Illetin I Human: Humulin
L/Novolin L
Insulin zinc suspension 4-8 hours 10-30 >36 hours Ultralente Humulin U
extended (Ultralente) hours

Insulin zinc suspension, 1-1½ hours 5-10 hours 12-16 hours Beef: Semilente Insulin
prompt (Semilente) Beef/Pork: Iletin I Semilente
Isophane insulin 1-1½ hours 4-12 hours Up to 24 hours Beef: NPH Insulin; Pork: NPH-N, Pork NPH Iletin II
suspension (NPH) Beef/Pork: NPH Iletin I Human: Humulin N,
Novalin N
Isophane insulin 30-60 min 4-8 hours 24 hours Human: Humulin 50/50, Humulin 70/30, Novalin
suspension/Injection 70/30

NOTE: Time of onset/peak/duration may vary greatly among patients and is affected by dose/source/site of injection/exercise of the injection area
(arm, leg)/insulin antibodies. Because the kidney is the site of insulin degradation, the onset, peak and duration may be altered in CKD.

References: PDR Nurses Handbook, 3rd Edition, Medical Economics Company, 1998
4-5

ORAL HYPOGLYCEMIC AGENTS


Type Onset Duration Other
Acarbose: Precose 2-hour half-life Delays CHO digestion, does not incr insulin. Taken w/
meals, excreted in urine/stool. Treat low blood sugar
carefully
Acetohexamide: Dymelor 1 hour 12-24 hours Excreted through kidneys
Chlorpropamide: Diabinese 1 hour 60-72 hours Long duration; caution in aged/CKD; hyponatremia
potential
Glimepiride: Amaryl 1 hour 24 hours Taken 30 minutes before meals.
Glipizide: Glucotrol 10-30 min 24 hours Metabolized in liver; excreted in urine; low toxicity;
Glucotrol XL caution in elderly
Glyburide: Diabeta, Micronase 2-4 hours 16-24 hours Metabolized in liver; 50-200 X more potent than other
Glynase PresTab 1 hour 12-24 hours agents; ↓ toxicity; caution in elderly
Metformin HCL: Peak 1-3 hr 9-17 hours Onset/duration not clearly defined; food delays
Glucophage half-life 1½-5 onset/peak; given w/ meals; decr insulin resistance. Not
for CKD
Pioglintazone: Actos 2 hours 24 hours Takes 3 months to reach steady state.
Repoglinide: Prandin 30 min 4 hours Take 15-30 minutes before a meal, good for erratic meals
Rosiglitazone: Avandia 1 hr 24 hour Takes 3 months to reach steady state.
Tolazamide: Tolinase 4-6 hours 12-24 hours Absorbed slowly, possibly fewer side effects
Tolbutamide: Orinase 1 hour 6-12 hours Most benign; totally inactivated; useful in CKD

Reference: On the Cutting Edge: Diabetes Care and Education 10, November, 1989 (ADA)
Campbell: How Oral Agents are Used in Treatment of Type II Diabetes. Pharm Times 53:32-40, 1987
Skidmore-Roth L: 2000 Mosby’s Nursing Drug Reference, Mosby, 2000
Hodgson BB, Kizior RJ: Saunder’s Nursing Drug Handbook, 1999

4-6
GLYCATED HEMOGLOBIN (HbA1c)
Glycation is the non-enzymatic addition of a sugar residue to the amino groups of protein, specifically the hemoglobin
protein. The formation of glycated hemoglobin is irreversible and is unaffected by exercise and sudden shifts in blood
glucose (BG) levels. Because the erythrocyte is freely permeable to glucose, the rate of glycation is proportional to the
concentration of glucose. The life span of the average blood cell is 120 days and HbA1c is formed by the attachment of
glucose to the N-terminal end of each β chain of the hemoglobin molecule. The amount of HbA1c, therefore, represents
the integrated values of glucose over the previous 100-120 days. Obviously, any factor that reduces the life span of the
erythrocytes, also reduces the glycated hemoglobin. The Diabetes Control and Complications Trial (DCCT) research
group reports the following relationship between glycated hemoglobin (% A1c) and average blood glucose (BG) during
the previous 2-3 months: a 1% change in HbA1c = a 30 mg/dL change in average BG.

In the past, the clinical utility of glycated hemoglobin measurements in CKD was controversial. Early studies showed
no correlation between glycated hemoglobin and other indicators of blood glucose control in uremic subjects. The lack
of correlation is attributable, in part, to analytical interferences of altered hemoglobin found in uremic blood. Using
ion-exchange chromatography, HbA1c values are often more directly correlated to urea and creatinine than to glucose.
Measurement of HbA1c with the use of analytically specific methods can accurately reflect plasma glucose control in
uremic patients as long as the HbA1c values are interpreted in view of the potentially shortened erythrocyte survival
time.

Reference: Bruns DE, et al: Specific Affinity-Chromatography Measurement of Glycated


Hemoglobin in Uremic Patients. Clinical Chemistry 30(4):569-571, 1984
Mosby’s Diagnostic and Laboratory Test Reference, 4th Ed, 1999

4-7

HYPOGLYCEMIA
Causes: Excess circulating insulin, inadequate food intake, physical activity, drug interactions, glucose-free dialysate.
Symptoms: Blood pressure may increase or decrease by 20-30 mmHg, pulse may fluctuate, sweating, cool/pale/moist skin,
dizziness, fainting progressing to coma, slurred speech, tremor progressing to convulsion, headache, nervousness, restlessness,
irritability, diminished mentation, weakness (similar symptoms are present in hypotensive episodes on dialysis except that systolic
blood pressure drops below 100 mmHg).

Hypoglycemic Protocol - Outpatient


1. If the blood glucose is <70 mg/dL, give 15 grams of CHO:
½ cup of regular soda
½ cup apple juice
5 lifesavers
3 sugar cubes or 3 packets of sugar
3 glucose tablets
1 tube Glutose 15
2. Recheck blood glucose in 15 minutes, if <70 mg/dL, repeat steps above.
3. Follow-up with a more substantial snack or meal containing CHO, pro, fat,
especially if the next meal is more than 2 hours away.

NOTE: Patients on Precose and oral sulfonylureas or insulin must be treated with glucose. Precose inhibits the breakdown of sugar
(sucrose) to glucose and slows the absorption of sucrose or fructose (found in sodas or fruit juices) making them less effective in
treating hypoglycemia.

References: Moore MC: Nutritional Care. Mosby’s Pocket Guide Series, 4th Ed, 2001
Robels F: On the Cutting Edge: Diabetes and Care and Education, ADA, 10:2, 1989

4-8
MODIFICATIONS FOR ACUTE ILLNESS IN INSULIN DEPENDENT DM
General Goals Suggested 15 gram CHO Sick Day Foods
1. Check blood glucose frequently, q 2-4 hrs ½ cup regular gelatin
2. Ingest 10-15 gm CHO every 1 to 2 hours. ½ cup sherbet or sorbet
3. If symptoms of diarrhea, vomiting, or fever, 1 Frozen juice bar
take small amounts of fluids every 15-30 min 6 unsalted top crackers
4. Contact the MD if unable to ingest and retain 4 pieces of melba toast
CHO-containing foods and fluids for more than 1 cup reduced-salt chicken noodle/rice/pasta soup
4 hours, if BG is fluctuating widely, or illness ¼ cup regular pudding or custard
lasts more than 24-48 hrs. ¾ cup ginger ale
½ cup regular lemon-lime soda
½ cup apple juice
⅓ cup cranberry juice cocktail or grape juice
5 lifesavers
References: Moore MC: Nutritional Care. Mosby’s Pocket Guide Series, 4th Ed, 2001
Hands, ES: Nutrients in Foods. Lippencott Williams & Wilkins, 2000

4-9

FOOD GLUCOSE EQUIVALENT TO 15 GM CARBOHYDRATE

Source Amount Glucose (gm) CHO (gm) KCAL Fluid Potassium (mg)
Gelatin, Reg ½ cup 6 17 71 ½ cup 30-110
Honey 1 Tbsp. 7.1 17.3 64 - -
Orange ½ cup 6.6 12.8 54 ½ cup 230-250
Juice 1 cup 5.8 15.2 60 1 cup 37
Gatorade 3 Tabs 15* 15 60 -
BD Tablets 5 Tabs 14* 14 56 -
Dextrosol 40 gm 16* 16 64 -
Glutose

* Preferred choices, all available as glucose.

DO NOT USE fruit or soft drinks that contain only high fructose corn syrup to treat hypoglycemia.
The major carbohydrate source should be glucose, dextrose, or sugar.
Reference: McKinley H: On the Cutting Edge: Diabetes Care and Education, ADA, 14(4):23, 1992

Acceptable food equivalents for renal patients include: 2 tsp sugar or jelly, 6-8 jelly beans or lifesavers (chewed),
½ cup apple, grape juice, or cranberry juice.

Reference: Levine S: On the Cutting Edge: Diabetes Care and Education, ADA, Winter, 1985

4-10
DIABETIC GASTROPARESIS
Diabetic gastroparesis and delayed gastric emptying are linked to unpredictable nutrient absorption and poor food
intake causing wide fluctuations in blood sugar by compromising the effects of oral agents and exogenous insulin.
Small, frequent feedings, medications, and interventions as listed below, may ease the symptoms of gastroparesis.
Gastroparesis is characterized by vomiting of undigested food several hours after ingestion. Common symptoms
include vague abdominal distress, heartburn, nausea, vomiting, early satiety, abnormal food digestion and absorption,
increased fluctuations in blood sugar.

Intervention Effect
Frequent, small meals Helps minimize symptoms. Low fat may help. Advise pt to chew foods well
Metoclopromide HCL Stimulates motility of upper GI tract w/out increasing gastric, bilary or pancreatic
secretions. May help diarrhea. High incidence of CNS side effects
Loperamide HCL Increases gastric contractions, relaxes pyloric sphincter, anti-emetic actions
Cisapride: Propulsid Reduces gastric retention in some diabetic patients.
(Not recommended in CKD due to potentially fatal dysrhythmias)
Jejunostomy Tube Overcomes gastric stasis, can provide symptomatic relief
Erythromycin Systemic treatment of gastropariesis
Domperidone Prokinetic GI motility drug, blocks dopaminergic receptors in upper alimentary tract,
stimulating the motility of the esophagus, stomach, & upper small intestine
Motilin antagonist Same as Domperidone
References: Daugirdas JT, Ing TS: Handbook of Dialysis, 2nd Edition, Little, Brown, & Co., 1994
Beaven K. Gastroparesis and Jejunal Feeding. J Ren Nutr 9(4):202-205, 1999
Skidmore-Roth L: 2000 Mosby’s Nursing Drug Reference, Mosby, 2000

4-11

OTHER NUTRITION ISSUES FOR DIABETICS


Standard calorie-specific meal patterns have traditionally been used for diabetic patients. The current American Diabetes
Association (ADA) recommendations suggest that “consistent carbohydrate meal plans” may be the most appropriate method for
maintaining metabolic control. These meal plans are based on a consistent carbohydrate (CHO) content for each meal rather than
specific calorie levels for each meal. The CHO content for each specific meal would be consistent from day to day (breakfast =
breakfast, lunch = lunch, dinner = dinner, snack = snack) although the CHO content could differ between breakfast, lunch, and
dinner. It is also suggested that the use of “ADA diet” terminology be discontinued since the ADA no longer endorses a single meal
plan or absolute percentages of macro nutrients. Further, meal plans such as “no added sugar,” “low sugar” and “no concentrated
sweets” are no longer appropriate. These general meal plans do not reflect current diabetes nutrition therapy. They unnecessarily
restrict sucrose and may falsely imply that simple restriction of sucrose sweetened foods will improve blood sugar control.
Clear or Full Liquid Diet – Initiate 200 gm CHO per day in equally divided amounts at meal and snack times using regular,
sweetened liquids and adjust diabetic medications as needed.
Post-Surgery - Initiate oral intake quickly, as tolerated, with rapid progression to solid foods.
Catabolic Illness - Continuous, careful monitoring of nutritional and glycemic status is critical in addition to providing adequate
nutrition without exacerbating hyperglycemia or overfeeding the patient.

Reference: Schafer, R.G. et al. Translation of the diabetes nutrition recommendations for health care institutions: Position Statement. JADA
97(1):43-53, 1997

4-12
Chapter 5:

SPECIAL CONSIDERATIONS
FOR THE
ELDERLY PATIENT

EDUCATION CONSIDERATIONS FOR THE ELDERLY


1. Be considerate. Start by asking the patient to tell you if they get tired or overwhelmed.
2. Include family members or caretakers in the diet instruction as permitted by the patient.
3. Speak directly to the patient in a strong, clear voice.
4. Keep the instructions simple and short. Then, ask questions to ascertain the patient’s understanding
before moving on.
5. Limit the time you spend each session and present only 2-3 points at each session.
6. Review the previous session briefly before moving on to the next area of instruction.
7. Use large print materials, pictures, and food models to illustrate your points.
8. Give written materials to back up verbal information. If changing medications such as binders,
calcium, or vitamins, provide written follow-up to a verbal instruction.
9. Because of a tendency to decrease intake (both in CKD and aging) it is critical to be as liberal as
possible with the meal plan.
10. Recognize that you will probably not change a lifetime of eating patterns and include the foods the
patient has always eaten.
11. Recognize the decrease in taste/smell, and allow the patient as much flavor enhancement as possible.

5-2
D-E-T-E-R-M-I-N-E: A NUTRITION CHECKLIST FOR THE ELDERLY

D Disease - physical or emotional issues that change the way the patient eats.
E Eating poorly - too little or too much can cause nutrition problems.
T Tooth loss/mouth pain - are teeth and gums healthy, do dentures fit?
E Economic hardship - many elderly persons have poverty level incomes.
R Reduced social contact – 1/3 live alone; social contact influences morale/intake.
M Multiple medicines - means greater chance for nutritional side effects.
I Involuntary weight loss or gain - an important warning sign.
N Needs assistance in self-care - 1 in 5 needs help (shopping/cooking/walking).
E Elder years above 80 - as age increases, generally so do the problems.

This acronym was developed by The Nutrition Screening Initiative. (Nutrition Interventions Manual for
Professionals Caring for Older Americans, Washington, D.C.; Nutrition Screening Initiative, 1992) The
original was written for patient self assessments, but was adapted to provide a checklist of risk factors for
interviewing elderly patients. Leung and Dwyer adapted this tool for CKD patients.
Reference: Simko M et al: Nutrition Assessment: A Comprehensive Guide for Planning Intervention, ASPEN Publications, 1995
Leung J, Dwyer J: Renal DETERMINE Nutrition Screening Tools for the Identification and Treatment of Malnutrition, J Ren Nutr 8(2):
95-103, 1998

5-3

POTENTIAL INFLUENCES ON NUTRITION STATUS IN THE ELDERLY

Physical Psychological Social


Dental problems Depression Financial constraints
Swallowing disorders Anorexia Inconvenient food preparation
Excretion problems Personal taste preferences Difficult adaptation to change
Decreased activity Lifetime eating patterns Erroneous dietary beliefs
Physical weakness/limits Lack of socialization Susceptibility to fad claims
Loss of sensations Dementia
Lactose intolerance Loss of spouse
Drug interference
Abnormal digestion
Chronic disease
Thyroid dysfunction
Nutrient deficiencies
Alcohol consumption

References: Chernoff R: Meeting the Nutritional Needs of the Elderly in the Institutional Setting. Nutrition Reviews 52(4): 132, 1994
Grodner M, Anderson S, DeYoung S: Foundations And Clinical Applications of Nutrition: A Nursing Approach Mosby, 2000

5-4
PHYSIOLOGICAL CHANGES IN THE ELDERLY
Area Change Result
Mouth Mouth pain, ill-fitting dentures Pt uses soft/liquid foods with limited nutrients

Sensory Loss of taste and smell, Loss of papillae/taste buds on tongue, difficulty with ↓ salt diet,
especially sweet and salty foods taste bitter

Digestive Decreased esophageal motility Dysphasia, pain, and regurgitation


Tract Decreased peristalsis Slow movement through GI tract, sense of fullness, constipation
Bowel muscle atrophy Coupled with inactivity, causes constipation
Decreased thirst sensation Dehydration

Organs Decreased hepatic function Decreased protein synthesis


Decreased kidney function Can advance to CKD with a health crisis

Muscle Decreased skeletal muscle mass Difficult ambulation, inactivity can lead to negative nitrogen
balance, decreased ability/strength to prepare meals

Skeleton Osteoporosis, bone mineral loss Easy fractures compounded by further muscle loss from inactivity

Mental Decreased alertness, confusion Difficulty with activities of daily living; target for fad foods/OTC
medications

Reference: Simko M, et al:. Nutrition Assessment: A Comprehensive Guide for Planning and Intervention, ASPEN Publications, 1995

5-5

BODY COMPOSITION CHANGES IN THE ELDERLY


Age % Fat % Cell Mass % Bone Mineral Other
25 yrs 20% 47% 6% 27%
70 yrs 36% 36% 4% 24%

Reference: Gregerman RI, Bierman EI: Textbook of Endocrinology, RH Williams, Ed. WB Saunders Co., 1974

DECREASE IN PHYSIOLOGICAL FUNCTION AT 80 YEARS OF AGE

Physiological Function % Decrease From Age 30


Nerve Conduction Velocity 15 - 20%
Basal Metabolic Rate 20%
Standard Cell Water Content 20%
Cardiac Index 30%
Standard GFR 45%
Standard Renal Plasma Flow 53%

This information is included to help differentiate normal changes of aging from those changes that could
indicate disease or malnutrition.

Reference: Tobin JD: Normal Aging - The Inevitable Syndrome, The Quality of Life, The Later Years, Brown LE, Ed. Publishing Sciences Group,
Inc. 1975

5-6
INCIDENCE OF MALNUTRITION IN THE ELDERLY
Reference Population Parameters Incidence
Mowe, et al. 311 elderly, hospital Albumin, body mass index, 52.9% undernourished (M)
1994 admission MAMC, TSF, intake record 60.6% undernourished (F)
Low intake-65% (M) 69% (F)
Abbasi, et al. 2,811 skilled nursing Albumin, weight 11.8% underweight
1993 facility (SNF) -VA 27.5% hypoalbuminemic

Mowe, et al. 121 elderly, acute Albumin, weight, MAC, 54.5% undernourished
1991 care facility MAMC, TSF
Thomas, et al. 61 elderly, ECF/ Albumin, wt, TSF, MAC, 54% malnourished on admission,
1991 rehab hospital MAMC, Hgb, TLC, 37% still malnourished at 2 months
nutrition index
Pinchofsky, 227 elderly, ECF Albumin, wt, TSF, MAC, 52% PE malnutrition
et al. 1987 MAMC, prealbumin, 24% adult kwashiorkor
retinol binding protein, 19% mixed
TLC, Hct/Hgb 9% marasmus
Reference: Simko M, et al: Nutrition Assessment - A Comprehensive Guide for Planning Intervention. Aspen Publishers, 1995

5-7

SUBJECTIVE GLOBAL ASSESSMENT


(SGA information can be found on page 1-34 to 1-41)

Editorial Note: It is critical to assess tissue (fat and muscle) loss objectively in the aged. The tissue loss seen in the
aging patient mimics the tissue loss seen in malnutrition. In view of this, some of the other parameters of SGA may
become more important in elderly patients. Pay special attention to weight changes, gastrointestinal symptoms,
alterations in food intake, and a comparison of actual nutrient intake to recommended levels. Question the patient
carefully to get his/her views on the significance of changes and their duration. Some research indicates that SGA can
overestimate malnutrition in as many as 20% of elderly patients.
Reference: Ek AC, et al: Interrater variability and validity in subjective nutritional assessment of elderly patients. Scand J Caring Sci 10(3):163-168,
1996

5-8
Chapter 6:

HYPERLIPIDEMIA
IN
CHRONIC KIDNEY DISEASE

GENERAL PATTERNS OF HYPERLIPIDEMIA IN CKD

Pattern Distribution of lipid/apolipoproteins in CKD: CKD/HD: mild to moderate hypertriglyceridemia,


low to mildly elevated cholesterol/LDL, low HDL PD: triglycerides (TG) may be very elevated,
HDL often normal, cholesterol WNL to high Transplant: High LDL/cholesterol especially with
cyclosporin, HDL often normal, TG may be very high Nephrotic syndrome: low to normal HDL,
high cholesterol/LDL, high triglyceride levels are common.

Mechanism Mechanisms probably include both increased hepatic production and impaired removal of
circulating triglyceride-rich lipoproteins (VLDL, LDL). Altered carbohydrate metabolism with
concurrent hyperinsulinemia, and peripheral insulin resistance may also contribute.

Treatment Moderate diet modification as outlined for the general population. Weight control and reduced
(See pages intake of carbohydrate can minimize the overproduction of LDL/triglycerides. Exercise, as
6-4 to 6-5) tolerated, may help. Diet modifications for maintaining acceptable nutrition status takes priority
over diet for hyperlipidemia. It may be difficult to limit fat to < 30% of total calories when protein
levels are dictated and calorie needs are high. Nephrotic Syndrome: low fat, high complex
carbohydrate, salt restricted with other nutrients as described in Chapter 3. Long term use of
pharmacologic lipid lowering agents requires careful consideration/monitoring in CKD.

References: Mitch WE, Klahr S, Eds: Nutrition and the Kidney, Little, Brown & Co., 1993
Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997

6-2
PATIENTS AT RISK FOR DEVELOPING CARDIOVASCULAR COMPLICATIONS

High serum lipids and LDL cholesterol have been shown to be important risk factors for coronary heart disease.
Extrapolation of general risks and guidelines to the CKD population are not clear; however, the lipid disorders of CKD
may contribute to the high incidence of atherosclerosis and CV disease in this patient population. A conservative
treatment approach for dyslipidemia in CKD patients results from the lack of evidence that aggressive treatment makes
a significant difference. Further studies are being undertaken to establish appropriate treatment parameters. In addition
,research is under way to elucidate the role of homocysteine in aggravating cardiovascular complications.

1. Patients with established coronary artery disease


2. Patients with diabetes mellitus
3. Patients with LDL cholesterol > 60 mg/dL (100-160 mg/dL depending on risk factors-see pg.6-5)
4. Patients with markedly elevated triglycerides (>500 -1000 mg/dL)
5. Young/middle-aged male patients w/significant hyperlipidemia/prospect of long term dialysis
6. Patients with nephrotic syndrome. Every effort should be made to decrease proteinuria since hyperlipidemia
correlates with proteinuria and is inversely related to serum albumin. Pharmacologic therapy is almost always
necessary. A soy-based vegetarian type diet with fish oil has been shown to decrease total cholesterol, LDL
cholesterol, and triglycerides

Reference: Kopple JD, Massry SG, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997

6-3

NATIONAL CHOLESTEROL EDUCATION PROGRAM (NCEP), 2001


Focus on Multiple Risk Raises persons with DM without CHD to risk level of CHD risk equivalent
Factors Uses Framingham projections of 10 years CHD risk to identify those who need more
intensive treatment
Identifies pts w/multiple risk factors (metabolic syndrome) for intense Theraputic
Lifestyles Changes (TLC)
Intensity of risk reduction therapy adjusted to person’s absolute risk
Modifications of Identifies LDL cholesterol as primary target of therapy
Lipid/Lipoprotein Identifies HDL <40 mg/dL as the at risk level (up from <35 mg/dL)
Classification Lowers TG classification cutpoints to focus on moderate elevations
Support for implementation Recommends complete lipoprotein profile (LDL, HDL, TG) as initial test
Encourages use of plant sterols and viscous fiber as diet options for lowering LDL
Provides strategies for promoting adherence to TLC and drug therapy
Recommends treatment beyond LDL lowering for TG ≥200 mg/dL
LDL Goals depend on risk CHD and CHD Equivalents (DM) <100 mg/dL
factors Multiple (2+) risk factors <130 mg/dL
Zero to one risk factor <160 mg/dL
Major Risk Factors that Modify LDL Goals: Cigarette smoking, hypertension, HDL
<40 mg/dL, Family history of CHD (men-1st degree relative <55 years; women -1st
degree relative <65 years), age (Men >45; women >55); DM; life habit risk factors
(obesity, physical inactivity, atherogenic diet); emerging risk factors (lipoprotein -1,
homocysteine, prothrombiotic and proinflammatory factors)

6-4
TARGET LIPID LEVELS
Cholesterol Optimal Borderline High Very High
Total < 200 mg/dL 200-239 mg/dL > 240 mg/dL
LDL < 100 mg/dL 130-159 mg/dL 160-189 mg/dL >190 mg/dL
HDL > 60 mg/dL

Fasting levels for adults, >20 years. Panel should be obtained q 5 years. If non-fasting, only total/HDL will be usable.

THERAPEUTIC LIFESTYLE CHANGES (TLC)


Diet Total Sat. Polyunsat. Monounsat. CHO Protein CHOL Fiber Total Kcal
Fat* Fat* Fat* Fat* (mg/day) (g/day)
TLC 25-30% <7% up to 10% up to 20% 50-60% 15% <200 20-30 To maintain
desirable BW

* Percentage of total calories.

TLC: enhancing LDL lowering actions (use of plant stanols/sterols), increased soluble fiber (10-25 gm/day), weight
reduction as appropriate, and increased physical activity. After 12 wks, if LDL goal not met, consider drug therapy.

Major Risk Factors that Modify LDL Goals: Cigarette smoking, hypertension, low LDL, family history of CHD
(men-1st degree relative <55 years; women-1st degree relative <65 years), age (Men > 45; women > 55), DM
Reference: Adult Treatment Panel III - National Cholesterol Education Program (NCEP), NIH, National Heart, Lung, and Blood
Institute, NIH Publication #01-3670, May 2001

6-5

ANTIHYPERLIPIDEMIC DRUGS

Drug Action Adverse Effects* Dietary Needs


Bile Acid Sequestrants Works in bowel, does not Gastrointestinal Balanced diet ,
Cholestyramine Resins enter blood stream. distress, constipation, ↑ fiber,
Questran Removes bile acids from decreased absorption ↓ fat/cholesterol.
Cholestipol biliary system, uses of nutrients and other
Cholestid cholesterol to make bile drugs.
Colesevelam acids. ↓ LDL by ~15-30% Do not use if TG are
0−↑ TG, ↑ HDL 3-5% >400.

Fibric Acids Interferes with hepatic Most common: ↓ fat/cholesterol,


Clofibrate-Αtromid-S synthesis of dyspepsia, gallstones, maintenance of
Gemfibrozil-Lopid cholesterol/TG, myopathy. desirable body
Fenofibrate-Lipidil ↑ rate of removal. weight; Taken with
↓ TG by ~ 20-50%, Do not use in severe food/milk eases GI
↓ LDL by ~ 5-20% kidney or liver effects.
↑ HDL by 10-20%. disease.
Avoid in CKD - risk for
myopathy/rhabdomyolysis

* Incomplete list, most common and/or are nutrition-related side effects.

6-6
Drug Action Adverse Effects* Dietary Need
HMG-CoA Reductase Inhibits early rate-limiting step Myopathy, ↑ liver enzymes. ↓ fat/cholesterol, weight
Inhibitors (Statins) in cholesterol synthesis. Levels Do not use in active or control
Atorvastatin-Lipitor decrease within 1-2 weeks, chronic liver disease. Do not
Cerivastatin-Baycol reaches lowest in 4-6 weeks. use with cyclosporin,
Lovastatin-Mevacor macrolide antibiotics,
Fluvastatin-Lescol ↓ LDL by ~18-55%, antifungal agents,
Pravastatin-Pravachol ↓ TG by ~ 7-30%, cytochome P-450 inhibitors.
Simvastatin-Zocor ↑HDL by ~ 5-15% Use caution with niacin and
fibrates.

Nicotinic Acid Not well understood. Flushing, hyperglycemia/ Adjust CHO intake, ↓
Nicolar, Nicobid Estimated to glucose intolerance, upper purines, limit alcohol,
Niacor, NiaBid ↓ LDL by ~ 5-25%, GI distress, give with meals, liberal
Nico400, Nicotinex ↓ TG 20-50% hyperuricemia/gout, bland diet with antacid
SloNiacin, Niaspan ↑ HDL by ~15-35%. Individual activates peptic ulcers,
response depends on severity hepatotoxicity. Do not use in
and etiology of lipidemia. chronic liver disease or
severe gout. Caution: DM,
peptic ulcer, hyperuricemia.

* Incomplete list, most common and/or are nutrition-related side effects.

References: Nursing Drug Handbook, Springhouse Corp, Pennsylvania, 1997


Physicians Desk Reference, Medical Economics Company, New Jersey, 1994
Simon & Schuster Interactive, The Pill Book on CD ROM, 1996
Adult Treatment Panel III - National Cholesterol Education Program (NCEP), NIH, National
Heart, Lung, and Blood Institute, NIH Publication #01-3670, May 2001

6-7

APPROXIMATE CHOLESTEROL CONTENT OF COMMON FOODS*

Food Source CHOL Food Source CHOL


(mg) (mg)
Bacon, 1 strip 5 Mayonnaise, 1 Tbsp. 7
Beef, lean, 1 oz 25 Milk, whole, 1 cup 33
Bologna, beef, 1 slice 13 2% 18
Butter, 1 tsp. 11 1% 10
Chicken, white, 1 oz 24 Skim 4
Dark, 1 oz 26 Buttermilk, cultured 9
Cheese, Cheddar, 1 oz 30 Pork, 1 oz 28
Cottage Cheese, 4 oz 17 Peanuts, ½ oz 0
Egg, 1 large 272 Shellfish: Shrimp, 1 oz 43
Frankfurter, beef (8/lb) 35 Crab, Lobster, 1 oz 20
Halibut, 1 oz 12 Soybean Oil, 1 tsp. 0
Ice Cream, 10% fat, ½ cup 30 Tuna, light, in water, 1 oz 10
Lamb, lean, 1 oz 20 Turkey, white, 1 oz 12
Liver, beef, 1 oz 111 Dark, 1 oz 24
Margarine, 1 tsp. 0 Veal, 1 oz 25

* Does not address levels of saturated fat. Values are calculated from data in reference.
Reference: Pennington JAT: Food Values of Portions Commonly Used, Harper & Row, New York, 1998

6-8
Chapter 7:

ANEMIA IN CHRONIC
KIDNEY DISEASE

ANEMIA

Anemia is described by the relationships between the number, size, and hemoglobin content of red blood cells
(RBC). Normochromic, normocytic anemia is present in most patients with chronic kidney disease.

TERMINOLOGY USED TO DESCRIBE CELL ALTERATIONS IN ANEMIA

Term Cell Characteristics


Normochromic Normal hemoglobin content per cell

Hypochromic Decreased hemoglobin content per cell


Hyperchromic Increased hemoglobin content per cell
Normocytic Normal cell size
Microcytic Smaller than normal cell size
Macrocytic Larger than normal cell size

Reference: Ravel R: Clinical Laboratory Medicine: Clinical Application of Laboratory Data, 4th Edition. Year Book Medical
Publishers, Inc. Chicago-London, 1984

7-2
TYPES AND CHARACTERISTICS OF ANEMIA

Anemia Classification Characteristics


Hypochromic Iron deficiency anemia, most common anemia in CKD especially with
Microcytic EPO therapy
Normochromic Usually due to acute loss of red blood cells from hemorrhage or
normocytic hemolysis. Anemia of chronic disease
Megaloblastic Folic acid/B12 deficiency usually due to long term inadequate dietary
intake or deficient absorption/utilization. Responds to replacement of
nutrients. Blood cells are larger than normal.
Other Protein deficiency anemia is rare even in cachexia. Copper/heavy metal
deficiency anemia is rare. Anemia is common in patients with low serum
albumin for a variety of reasons.
Reference: Ravel R: Clinical Laboratory Medicine: Clinical Application of Laboratory Data, 4th Edition Year Book
Medical Publishers, Inc. Chicago-London, 1984

7-3

LABORATORY VALUES USED TO DIAGNOSE ANEMIA


Initiate Evaluation (K/DOQI)
Hgb <11 g/dL, Hct <33% premenopause (F) or prepubertal (M); Hgb <12 g/dL, Hct <37% adult (M) or postmenopausal (F)

Value Definition
Hematocrit (Hct) Volume of packed cells/100 mL blood (40% means 40 mL of red blood cells
(RBC)/100 mL blood).
K/DOQI Targets with EPO therapy: 33-36%
Hemoglobin (Hgb) Oxygen carrying protein of RBCs gm/100 mL (15.5 means 15.5 g Hgb/100 mL
blood)
K/DOQI Targets for EPO therapy: Hgb 11-12 g/dL
Mean Corpuscular Volume (MCV) Describes red cells in terms of volume per cell. Normal is 81-100 µm3*
Mean Corpuscular Hemoglobin Measures concentration of hemoglobin in 100 mL of RBCs. Normal is 32-35%
Concentration (MCHC)
Mean Corpuscular Hemoglobin (MCH) The hemoglobin content of each red blood cell. Normal is 27-31 pg/cell*
Reticulocyte Count Most sensitive indicator of red cell production/bone marrow activity; responds
before hematocrit. Reported as a % of the total RBCs. Normal is 0.5 - 2%
Reticulocyte Index Indicates erythropoetic response in anemic or low Hct patients calculated as RI =
Reticulocyte count (IU%) x patient Hct. normal Hct.If the RI is < 1.0 even with
high reticulocyte count, marrow response is inadequate.
Iron Monitoring Parameters Serum iron, serum ferritin, TIBC, % transferrin saturation (K/DOQI)

Test for Occult Blood Test stool for occult blood


* Normal values are laboratory specific. The above values are general ranges.

Reference: Treseler KM: Clinical Laboratory and Diagnostic Tests, 3rd Edition, Appleton Lange, 1995
NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001

7-4
INTERPRETATION OF IRON STATUS PARAMETERS

Parameter Iron Deficiency Inflammation* Combination


Serum Iron Decreased Decreased Decreased
Transferrin Saturation Decreased Decreased Decreased
TIBC Increased Decreased Normal
Ferritin Decreased Increased Normal to increased
(1 ng/mL = 8-10 mg stored iron)

*Suspect inflammation when serum iron is decreased, transferrin saturation is decreased, and serum
ferritin is increased. Ferritin is an acute phase reactant; therefore, synthesis is increased, independent
of iron stores, in chronic or acute inflammation, fever, or liver disease.

References: Foxen L: Monitoring for Infection and Inflammation During EPO Therapy. Presentation, 1993
Stivelman J: Optimization of Iron Therapy in HD Pts Treated with rHuEPO. Sem Dial 7:288,1994

7-5

IRON BALANCE IN CKD PATIENTS (K/DOQI)

1. Deficiency of erythropoietin in CKD causes anemia which is further aggravated by iron deficiency.
EPO therapy increases the rate of erythropoiesis and the demand for iron.
2. Maintain transferrin saturation (TS) ≥20% and serum ferritin ≥100 ng/mL during EPO therapy. Better response or equal
response with lower doses may be achieved with higher iron stores (up to 50% TS or 800 ng/mL serum ferritin).
3. Measurement of iron parameters: Individual IV iron dose ≥1000 mg-wait 2 weeks after last iron administration; iron dose
< 100-125 mg/week-no interruption of therapy needed; IV iron doses of 200-500 mg-wait at least 7 days.
4. Iron absorption is thought to be normal in CKD patients, but losses of up to 6 mg/day from blood testing, dialyzer/tubing
waste, GI bleeding, and leakage of vascular access, exceed the amount of iron that can be absorbed from oral sources. In
addition, inconvenient dosing and side effect may limit the use of oral iron.
5. CKD-prior to initiation of dialysis and PD, patients have minimal iron losses and many may be able to maintain iron
stores by taking oral iron (≥ 200 mg elemental iron per day, divided into 2-3 doses in adults and 2-3 mg/kg/day in the
pediatric patient). Absorption is inversely related to body iron stores and may decrease when ferritin >200 ng/mL and TS
>20%.
6. Ionic iron salts (ferrous fumarate, sulfate, or gluconate) are inexpensive and provide known amounts of elemental iron.
Other iron supplements have not been shown to be more effective or to have fewer side effects and they are generally
more costly. K/DOQI opinion: Oral iron is not indicated when using IV iron.
7. Oral iron supplements should be ingested away from other medications and ≥2 hours before or ≥1 hour after meals.
Vitamin C, in doses safe for CKD patients, does not enhance ferrous iron absorption.
8. Enhance compliance and avoid side effects of oral iron by using smaller, more frequent doses, increasing the dose slowly,
changing the compound/product, or prescribing iron at bedtime.
9. A trial of oral iron is acceptable in HD, but most HD patients will require IV iron to maintain iron stores and Hgb/Hct
especially on EPO. (See page 7-8)

Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001

7-6
LABORATORY VALUES USED TO DIAGNOSE IRON DEFICIENCY IN CKD (K/DOQI)

Total iron binding capacity, transferrin saturation (TS) and serum ferritin are the best indicators of iron
stores and available iron for erythropoiesis, but do not absolutely define iron deficiency or iron overload.

Lab Test Indication Normal Indication of Iron Deficiency*


Serum Ferritin Reflects iron stored in liver, 12-300 µg/L <100 µg/L
spleen, bone marrow
reticuloendothelial cells
Transferrin Saturation Reflects iron that is readily 35±10% <20%
available for erythropoiesis

*In chronic kidney disease it has been suggested that iron stores must be sufficient (as above) to maintain a hemoglobin
of 11-12 g/dL and a hematocrit of 33-36%. Some patients are able to sustain erythropoiesis and an acceptable
hematocrit in spite of ferritin and TS levels less than above. In contrast, some patients are functionally iron deficient
(respond to higher doses of iron) with laboratory levels greater than those above. Both serum ferritin and TS are most
accurate in predicting iron deficiency or iron overload when they are extremely high or low. They are not perfectly
sensitive or specific. The levels above are suggested guidelines for identifying CKD patients who may be iron
deficient. Other laboratory tests that have traditionally been used to diagnose iron deficiency do not seem to increase
the diagnostic specificity or sensitivity over the two parameters recommended above. Administration of IV iron can
falsely alter serum ferritin and TS levels for 1-3 weeks post administration depending on the dose administered. The
levels of ferritin or TS that indicate iron overload are not well defined but there does not seem to be any benefit
(increased response to EPO or ability to use lower doses of EPO) in maintaining ferritin at >800 ng/mL or TS at >50%.
Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001
7-7

ESTIMATION OF IRON NEEDS: Recommendations for Repletion


1. To increase the hematocrit from 25% to 35%, the amount of supplemental iron needed in the first 3 months of EPO
therapy is approximately 1000 mg. Storage iron in the body is 800-1200 mg and 400 mg of iron are needed just to
replace losses. The other 600 mg are needed to support the production of red blood cells to achieve the target
Hgb/Hct.
2. After reaching target Hgb/Hct, 400-500 mg every 3 months is needed to maintain stores.
3. Oral iron alone is usually insufficient to meet these needs. 100-125 mg of IV iron at each HD treatment for 10-8
weeks is recommended to correct functional iron deficiency. A second course should be given if iron parameters
remain low.
The administration schedules of IV iron therapy range from three times per week to once every two weeks with the
goal of giving 250-1000 mg of iron within a 8-12 week period.
4. Obtaining accurate measurement of TS and ferritin depends on the dose of IV iron:
IV iron dose of <100-125 mg/week - no interruption of therapy is needed.
Individual IV iron dose of ≥ 1 gram - wait at least 14 days after the last IV iron administration.
IV iron dose of 200-500 mg - wait at least 7 days after the last IV iron administration.
5. Prevention of functional or absolute iron deficiency with maintenance doses of IV iron improves erythropoiesis.
Maintenance doses of IV iron range from 25-100 mg/week for HD.
6. Iron supplementation should be temporarily withheld (up to 3 months) if iron stores are high (no known benefit
from increasing TS >50% and/or ferritin >800 ng/mL). Once TS and ferritin drop back into target range,
maintenance IV iron should be restarted at a dose reduced by 1/3 to 1/2.

Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001

7-8
IRON SUPPLEMENTS
There are a variety of iron supplements, many of which have added nutrients which may not be appropriate or
needed in CKD patients. This list is not all inclusive. It contains iron compounds that do not contain added nutrients.

Iron Source % Examples Elemental Dose Side Effects


Elemental
Ferrous 12% Fergon® 35 mg/300 6-7/day GI symptoms, N & V, constipation
Gluconate Ferralet® mg
O
tablet
R Ferrous 33% Hemocyte® 106 mg 2/day Same as above
Fumarate Nephro-Fer® 116 mg 2/day
A Ferrous 20% Slow-Fe® 50 mg 3-4/day Same as above
Sulfate 30% dried Feosol® 65 mg 3/day
L Polysaccharide 100% Niferex 150® 150 mg 1-2/day Same as above
NuIron 150® 150 mg 1-2/day
Heme Iron Proferrin® 7 mg/capsule 2-4/day “No adverse reactions” per
Polypeptide manufacturer.
Iron InFed® 50 mg/mL 100 to Altered/metal taste, N/V, ↓ BP,
Dextran DexFerrum® 1000 mg flushing, myalgia/arthralgia, rash,
urticaria/anaphalaxis/tachycardia
I
Ferrous Ferrlecit® 12.5 mg/mL 62.5 to 125 mg Rarely-hypotension, flushing,
V Sodium cramps, N/V, malaise, agitation,
Gluconate fatigue. No reported deaths.
Iron Sucrose Venofer® 20 mg/mL 5-10 ml, 2-3 Hypotension, cramps/leg cramps,
times/wk nausea

Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1, Jan, 2001
Saunders Nursing Drug Handbook, 1999, WB Saunders Company

7-9

REASONS FOR INADEQUATE RESPONSE TO EPO THERAPY

Inflammation/Infection (access, surgical inflammation, AIDS)


Iron deficiency/Inadequate EPO dose
Folic acid/B12 deficiency*
Aluminum toxicity
Malnutrition
Significant chronic blood loss
Hemolysis/shortened erythrocyte survival
Multiple myeloma
Osteitis fibrosa
Hemoglobinopathies (Sickle cell disease)
Angiotensin-converting enzyme inhibitors (potential)

*It may be prudent to monitor folic acid and B12 levels on a regular basis.

Reference: NKF K/DOQI Clinical Practice Guidelines for Anemia of CKD, 2000 Update, Am J Kidney Dis 37, Suppl 1,
Jan, 2001

7-10
Chapter 8:

BONE METABOLISM AND


DISEASE IN CKD/
UROLITHIASIS

MANAGEMENT OF OSTEODYSTROPHY IN CHRONIC KIDNEY DISEASE


It has been suggested that one cannot be dogmatic in the management of osteodystrophy in CKD. Therapeutic
approaches must be tailored to meet individual needs and parallel constant changes in dialytic therapy. Osteodystrophy
in CKD is a complex disorder of bone and mineral metabolism where correction of one abnormality can often lead to
the aggravation of another. A number of protocols have been developed for the management (prevention and treatment)
of bone disease in CKD. Protocols must be updated on a regular basis and reflect the changing profiles of CKD-related
bone disease as well as current research. In addition, patient responses must be monitored to guide changes in protocols
and ensure the best possible outcomes. Historically, each new bone disease therapy that has evolved in CKD has
created new problems. From aluminum toxicity to hypercalcemia to soft tissue calcification, the quest for balance in the
area of minerals and CKD-related bone disease continues.
Bone and mineral abnormalitites in CKD include: hypocalemia, secondary hyperparathyroidism,
hyperphosphatemia, defective absorption of calcium from the gut, abnormal bone mineral content, altered vitamin D
metabolism, bone disease, soft tissue calcification, altered kidney handling of calcium/phosphorus/magnesium,
pruritus, proximal myopathy, skin ulceration, and soft tissue necrosis. Risk factors that can impact the type of bone
lesion include: prolonged aluminum exposure, glucocorticoid therapy, DM, beta-2 microglobulinemia amyloidosis,
metabolic acidosis, hypophosphatemia secondary to aggressive dietary or binder control, or chronic low intake.
The K/DOQI Bone Metabolism and Disease Work Group is developing practice guidelines for the management of
bone disease in CKD. These guidelines, scheduled to be published in 2002, will objectively and critically elicit an
evidence-based approach to bone disease in CKD. Watch for these guidelines from the National Kidney Foundation to
update your knowledge on the topic of this chapter.

8-2
OSTEODYSTROPHY IN CKD: TYPES AND CHARACTERISTICS
Type Attributes Incidence Usual Lab Profile Response
Ca++ P Alk PTH AL++ to Calcitriol
Phos
HYPERPARA- Excess PTH, Common ↓ ↑ M-↑ ↑ N-M Good
THYROID high bone
Early turnover,
osteitis
fibrosa
HYPERPARA- As above Less ↑ ↑ ↑ ↑↑ N Varied to poor
THYROID common
Late
ADYNAMIC Low bone Non- N-↑ N- N-↓ N-↓ N-↑ Poor, can
OR turnover aluminum ↑ <100 aggravate
APLASTIC PTH Over- related pg/mL condition
suppression common,
may play role aluminum
related rare
MIXED Combination Increasingly ↓ ↑ M-↑ N-↑ N-↑ Good, if
UREMIC of mixed rare predominately
signs hyperparathyroid
OSTEO- Low bone Increasingly ↑ N- N-↓ N-↓ N-↑ Poor
MALACIA turnover rare ↓

N-Within normal limits M-moderate ↑ Increased, above normal ↓ Decreased, below normal ↑↑ Very high
Reference: Antonsen JE, Sherrard DJ: Renal Osteodystrophy: Past and Present. Sem Dial 9(4):296-302, 1996
8-3

NEGATIVE EFFECTS OF HYPERPHOSPHATEMIA

Removal of phosphorus (P) during hemodialysis depends on pre-dialysis serum level and dialyzer used. Phosphorus removal can
range from 250-1000 mg per HD treatment. In contrast, about 250-300 mg of phosphorus is removed per day with peritoneal
dialysis. An estimate of P that must be controlled by binders is equal to the amount of P absorbed (approximately 50-60% of intake)
minus the amount of P removed during dialysis. Adequate dialysis delivery, moderation of dietary P and adequate binder therapy
are all necessary to control serum P. Consequences of hyperphosphatemia, in addition to osteodystrophy in CKD, include:

1. Contributes to the calcium x phosphorus product, metastatic calcifications, and calciphylaxis.


2. Combines with low calcium as a stimulant to PTH secretion; impairs the feedback inhibition of PTH production and secretion.
3. Suppresses the effect of phosphate loading on renal tubular production of calcitriol.
4. Inhibits the action of 1-alphahydroxylase and, thereby, decreases Vitamin D activation in the kidneys.
5. Stimulates PTH secretion/parathyroid gland hyperplasia.
6. Induces resistance to calcitriol (PTH reduction) when a serum P >8 mg/dL .
7. Contributes to myocardial fibrosis, heart, and valve calcification, as well as cardiovascular sudden death.

HYPERPHOSPHATEMIA DUE TO RELEASE OF PHOSPHORUS FROM BONE


As much as 300 mg of phosphorus per day can be released from the bone in severe hyperparathyroid bone disease. P (released
directly into the blood) is not accessible to phosphate binders in the gut. The following may indicate that high serum P is, at least in
part, due to release of P from the bone:

1. The patient is compliant with binders and tending toward hypercalcemia with minimal or no calcium load.
2. The PTH has been elevated for a significant time and/or there are signs of increased bone resorption.
3. The patient is getting a significant dose of vitamin D or analog without response.
References: Daugirdas JT, Ing TS: Handbook of Dialysis, Little, Brown and Co., 1994
Antonsen J, Sherrard D: Renal Osteodystrophy: Past and Present. Sem Dial 9(4):296-302, 1996
Block GA, Port FK: Re-evaluation of Risks Associated with Hyperphosphatemia and Hyperparathyroidism in
Dialysis Patients: Recommendations for Change in Management. Am J Kidney Dis 35:1226-1237, 2000
8-4
PHOSPHORUS DENSITY OF COMMON FOODS
Food Measure Phos (mg) Pro (gm) mg Phos/gm Pro
Beans, Dried 1 cup 209-251 14-16 14.9-15.7
Beer 12 oz 43 1 43
Chocolate 1 miniature 95 3 31.7
Coffee, Brewed 1 cup 2.3 0 -
Cola 12 oz 44 0 -
Egg 1 large 86 6 14.3
Cheese, Cheddar 1 oz 145 7 20.7
Cheese, Cottage 1 cup 151-297 14-28 10.6-10.8
Cheese, Cream 2T 30 2 15.0
Fish 3 oz 214-282 21-23 10.2-12.3
Liver, Beef 3 oz 392 23 17
Milk 1 cup 209-247 8 26.1-30.9
Nuts 1 oz 98-147 4-8 18.4-24.5
Peanut Butter 2T 101-118 8 12.6-14.8
Pork, Poultry 3 oz 146-210 22-28 6.6-7.6
Oysters 3 oz 196 13 15.1
Red Meats 3 oz 189-203 22-25 8.1-8.6
Shellfish 3 oz 116-175 17-19 6.8-9.2
Soybeans, Boiled 1 cup 421 29 14.5
Soybeans, Roasted 1 cup 624 61 10.2
Sunflower Seeds 1 oz 322 6 53.7
Tofu 100 gm 52-76 4-6 12.7 - 13.6
Yogurt 4 oz. 162-177 6 27-29.5

Note: If dairy products, nuts, beans, and seeds are eliminated, average mg P per gm of protein is approximately 10 to 11.
Reference: US Department of Agricultrue, Agriculture Research Service, 2001. USDA Nutrient Database for Standard
Reference, Release 14, Nutrient Data Laboratory Home Page, http://www.nal.usda.gov/fnic/foodcomp
8-5: 8-5

PHOSPHATE BINDING AND CALCIUM SUPPLEMENTATION


Any product used for phosphate binding should be taken with meals for optimum binding. Calcium products meant to be used as a
calcium supplement should be taken between meals. The K/DOQI bone disease work group is evaluating the literature regarding
calcium supplementation and calcium load. Their findings are not available for this edition of the Pocket Guide, however, there is an
increasing trend toward maintaining low normal serum calcium and lower calcium times phosphorus product. It has been strongly
suggested that efforts to reduce PTH with high calcium levels should be abandoned. These changes in practice should be kept in
mind when recommending the dose and source of phosphate binders. Iron supplements should NOT be taken with binders or
calcium supplements (limits iron absorption and reduces the binding of phosphorus). Below are steps to phosphorus control:

1. Limit dietary P as much as possible within adequate protein levels.


2. Evaluate patient for calcium load and calcium status. Current opinion suggests that we must take care in dosing binders so
that we do not add to the risk of soft tissue calcification (<2000 mg elemental Ca++/day). If serum Ca++ >9.5 mg/dL,
consider adding or substituting a non-aluminum, non-calcium binder.
3. Evaluate the actual P intake to plan the initial and subsequent binder doses.
4. Titrate the binder dose to the meal or snack.
5. Recommend taking binders during or immediately before or after meals. Some research indicates it may help to take
binders regardless of timing, if forgotten at meal time; however, this could increase calcium absorption.
6. Prescribe binders with consideration of medical needs, serum chemistries (including Ca x P product), patient preference
for source and form as well as efficacy, availability, and cost.
7. Use the most concentrated form and check compliance before increasing the dose.
8. Consider binder change if source or form of binder isn’t tolerated, results are unsatisfactory, or other problems are created
or exacerbated (like hypercalcemia and soft tissue calcification).
9. Avoid aluminum-containing binders unless all other therapies fail. Limit the use of aluminum to minimal, short term
dosing in patients with uncontrolled hyperphosphatemia. Do not use aluminum and citrate together.

8-6
CALCIUM COMPOUNDS

Source % Elemental Ca++ mg Ca++/g Compound


Calcium Acetate* 25% 250
Calcium Carbonate** 40% 400
Calcium Citrate*** 22% 220
Calcium Gluconate 9% 90
Calcium Glubionate 6.5% 66

*Estimated in vitro binding power: 40-60 mg P bound per 1 gram calcium acetate
Reference: Slatopolsky E: Kidney International 27:173, 1985

**Estimated in vitro binding power: 39 mg P bound per 1 gram of calcium carbonate


Reference: Schiller L: N Engl J Med 320:1110-1113, 1989

POTENTIAL SIDE EFFECTS OF CALCIUM-BASED BINDERS/SUPPLEMENTS:

1. Hypercalcemia (symptoms page 8-17).


2. Added calcium load (varies by compound) that can elevate Ca x P product and increase the risk for
metastatic calcification.
3. GI intolerance (bloating, gas, nausea, vomiting, constipation).
4. May be limited by hypercalcemia (>9.5-10.2 mg/dL) or high calcium x phosphorus product (>55 mg2/dL2).
5. Calcium citrate is not recommended because it enhances aluminum absorption, especially when combined with
aluminum-based binders.***

8-7

COMMON NAME BRAND CALCIUM-BASED BINDERS/SUPPLEMENTS


Compound Name Brands Compound Elemental Ca++ Manufacturer
Calcium PhosLo 667 mg 169 mg Braintree Laboratories
Acetate
Calcium Hil-Cal 670 mg 170 mg Hillstad (Calcium Supplement)
Acetate
Calcium Calci-Chew 1250 mg 500 mg Watson Pharmaceuticals
Carbonate Calci-Mix 1250 mg 500 mg Watson Pharmaceuticals
Caltrate 600 1500 mg 600 mg Whitehall-Robins
Chooz (Gum) 500 mg 200 mg Schering-Plough
Nephro-Calci 1500 mg 600 mg Watson Pharmaceuticals
Oscal 500 1250 mg 500 mg Whitehall-Robins
TUMS 500 mg 200 mg Glaxo Smith Kline
TUMS E-X 750 mg 300 mg Glaxo Smith Kline
TUMS Ultra 1000 mg 400 mg Glaxo Smith Kline
TUMS 500 1250 mg 500 mg Glaxo Smith Kline

Combination Binders with Calcium


Mg/Ca++ Product Composition/ 1 Tab Elemental Manufacturer
Magnesium MagneBind™ 200 magnesium carbonate Mg = 57 mg Nephro-Tech
carbonate combined 200 450 calcium acetate Ca++= 113 mg
with calcium acetate. 300 magnesium carbonate Mg = 85 mg
Magnesium is MagneBind™ 300 calcium acetate Ca++= 76 mg
dialyzable. 300

References: Saunders Nursing Drug Handbook, WB Saunders, 1999


Internet: Manufacturers’ Web Sites, 2001

8-8
OTHER PHOSPHATE BINDERS
Calcium-free/Aluminum-free Binders

These binders are indicated for reduction of serum phosphorus in CKD without the addition of a calcium load. They
can help prevent or correct hypercalcemia, elevations of calcium x phosphorus product, and the risk for soft tissue
calcification. These binders also reduce total and LDL cholesterol, and may increase HDL cholesterol. Reported side
effects are minimal, primarily GI distress such as nausea, constipation, diarrhea, bloating, and indigestion.
Compound Name Brand Description Forms Manufacturer
Sevelamer Renagel® Ca++- free, aluminum-free cationic Renagel® Tablets 400/800 mg Genzyme
hydrochloride polymer; not absorbed Renagel® Capsules 403 mg

Aluminum-based Binders
Not appropriate for long term therapy but can be used (<4 weeks) in patients with significant hyperphosphatemia
(>7.0 mg/dL) and when other methods of phosphate control fail. Avoid doses >2.5 gm aluminum hydroxide per day
and any source of citrate. Common side effect include constipation, potential for other toxic side effects if used
excessively or for long periods of time. Long term side effects can include CNS (dementia, encephalopathy) and bone
effects (aluminum bone disease/osteomalacia); bone mineralization may also be impaired due to aluminum deposition.

Compound Name Form Manufacturer


Brands
Aluminum Carbonate Baseljel Liquid Axcan Pharma, Inc.

Aluminum Hydroxide AlternaGEL Liquid Johnson & Johnson, Merck


(In vitro binding power is estimated Alu-Cap Capsule 3M Pharmaceuticals
to be: 22 mg P bound per 5 ml Alu-Tab Tablet 3M Pharmaceuticals
liquid, 15 mg P bound per tablet). Amphojel Liquid Axcan Pharma, Inc.
Balsa RW Nephron 45:16-21, 1987

References: Internet, Manufacturers’ Information, 2001


8-9

AVAILABLE VITAMIN D AND VITAMIN D ANALOGS – ORAL/IV

Product Source Forms Peak Action Sites Manufacturer


Calcijex® Calcitriol, synthetic vitamin IV Rapidly available, Intestine, bone, Abbott Labs
(calcitriol)* D3 3-5 day pharmacologic kidney, and
Active Vitamin D hormone activity parathyroid
Hectorol® Prohormone metabolized in IV, 11-12 hrs Intestine, bone, and Bone Care
(doxer calciferol) the liver to Oral (Half life is 32-37 parathyroid Intl.
1∝25-(OH)2 D2 and hours)
1∝24(OH)2 D2
Not active at ingestion or
injection/activated in liver
Rocaltrol® Synthetic vitamin D3 Oral 3-6 hours following Intestine, bone; acts Roche Pharm.
(calcitriol) 1,25-dihydroxyvitamin D3 0.25-1mcg dose on parathyroid and
Active Vitamin D hormone intestinal tissue

Zemplar® Paricalcitol sodium, IV 5 minutes, decreases Parathyroid gland, Abbott Labs


(paricalcitol) synthetic-vitamin D2 analog; within 2 hours. Half- bone
Active Vitamin D hormone life is about 15 hrs

*Generic calcitriol is also available.

8-10
USE OF ACTIVE VITAMIN D OR VITAMIN D ANALOGS - ORAL/IV
Parameters Criteria for Initiation Therapy Goals Common Monitoring*
Serum Ca++, Adjusted* Low normal (8.5-9.5 WNL* Prevent hypercalcemia/ Weekly to monthly
(formula pg. 8-16) mg/dL)* soft tissue calcification
Serum P (WNL for CKD, no dialysis) 3.5 - 5.5 mg/dL* Weekly to monthly
Ca-P Product ≤ 5.5 mg/dL* (3.5-5.5 Prevent soft tissue calcification Weekly to monthly ↓ freq. when
Serum iPTH (intact mg/dL) 2-3x upper non-uremic normal; stable
parathyroid hormone) ≤ 55 mg2/dL2* ↓ PTH/bone demineralization* At least quarterly
Aluminum Bone ≥ 300 pg/mL* Normal bone mineralization
Disease (2nd gen. iPTH) WNL * (Signif. drop toward Aluminum, biannually
Alkaline Phosphatase Absent* normal=potential for hyper Ca+) Monthly
ΝΑ
Steps to Initiation: (* Acceptable values may vary by facility/MD. Ca++, P, and product targets may be liberalized slightly with
higher iPTH)
1. Obtain baseline chemistries including iPTH and stop other Vitamin D forms.
2. Control serum P to <5.5 mg/dL*; adjust binders and/or dietary intake. (might consider up to 6.5 mg/dl if PTH very high)
3. Control serum calcium to WNL* or ≤9.5 mg/dL (adjust oral intake and/or dialysate level).
4. See manufacturer’s information for dosing guidelines; most recommend higher initial doses for higher iPTH.
5. Monitor response/trends. Change dose accordingly based on iPTH/Ca++/P/product/alkaline phosphatase; allow adequate time
for physiologic response before changing. Monitor Ca++/P/product at least weekly w/ dose changes.
6. Modify dose, hold, or discontinue Vitamin D/analog if Ca x P product >55 mg2/dL2*, Ca++> normal*, P ≥5.5 mg/dL*, PTH ≤
100 pg/mL.
7. Restart when above values are within desired levels. If held for hypercalcemia or low PTH, restart at lower dose. If held for
hyperphosphatemia or high product, counsel patient on diet/binders, continue same dose or decrease.

References: Coburn J: Calcitriol in the Management of Renal Osteodystrophy. Sem Dial 9(4):316-326, 1996
Kates D: Control of Hyperphosphatemia in CRF: Role of Aluminum. Sem Dial 9(4):310-315, 1994
Block GA, Port FK: Re-Evaluation of Risks Associated with Hyperphosphatemia and Hyperparathyroidism:
Recommendations for a Change in Management. Am J Kidney Dis 35(6):1226-1237, 2000
8-11

PROTOCOLS FOR THE ADMINISTRATION OF VITAMIN D AND VITAMIN D ANALOGS


There is considerable variation in the definition and treatment of osteodystrophy in CKD which, in part, stimulated the
convening of the NKF K/DOQI Work Group for Bone Metabolism and Disease. The clinical practice guidelines for
bone metabolism and disease are being developed and will provide evidence-based recommendations. As with the other
K/DOQI guidelines, clinicians are encouraged to review and implement the recommendations as appropriate to
individual clinical practice and the needs of their patients. Assessment, monitoring and treatment of abnormal bone
metabolism in CKD lends itself to care maps or protocols. Protocols should:

1. Promote patient safety and incorporate strategies with the fewest side effects.
2 Be consistent with current, valid research, and be regularly updated to reflect changes in research.
3. Reflect the care team consensus for management of bone disease in CKD (or other problems).
4. Provide a schedule for changes (dose, medication, and method of administration) that allows time for the effect of
therapy to be observed.
5. Be logical and easy to follow, minimize paperwork, and allow for timely, appropriate interventions.
6. Include a mechanism to inform the patient of his/her role and progress.
7. Define limits that allow the physician to delegate tasks to other members of the care team.
8. Return responsibility for monitoring and administering patient care to the physician when requested/needed
therapies exceed the protocol limits.
9. Identify outcome measures and provide tracking mechanisms. Tracking outcomes provide guidance for appropriate
changes in protocols to ensure continuous improvement of outcomes.
10. Provide regular assessment and revision of protocols in light of facility needs or limitations and patient outcomes.

8-12
MANUFACTURERS’ SUGGESTED DOSING FOR VITAMIN D OR ANALOGS
PTH Level Calcijex® Zemplar® Rocaltrol® Hectorol® IV Hectorol® Caps
Initial dose 0.2 mcg/kg 0.04 - 0.1 mcg/kg 0.25 mcg/day 4 mcg 3x week if 10 mcg 3x week
3 x wk 3 x wk (2.8-7 mcg) Most dialysis pts need PTH >400 pg/mL if PTH
(1-2 up to 4 mcg) 0.5-1 mcg/d >400 pg/mL

Other miscellaneous Initial from Shown safe up to Capsule (0.25/0.5 mcg ) Administer 3 x wk at Soft gelatin
information 0.5 – 4 mcg 0.24 mcg/kg or Oral solution: 1mcg/mL the end of dialysis capsules, 2.5 mcg
3x wk 16.8 mcg
Frequency of 2-4 week 2-4 week intervals 4-8 week intervals 8 week intervals 8 week intervals
dose changes intervals

Usual dose change 0.5 – 1 mcg 2 – 4 mcg 0.25 mcg 1 – 2 mcg 2.5 mcg
PTH same Increase dose Increase dose Not noted Increase dose Increase dose
high or ↑
Decreasing by <30% Increase dose Increase dose Not noted PTH: <50% decrease, PTH: <50%
↑ dose by 1-2 mcg decr., ↑ dose by
2.5 mcg
Decreasing ≥30 <60% Maintain dose Maintain dose Not noted PTH: PTH:
150-300 pg/ mL: 50-300 pg /mL,
maintain dose maintain dose

Decreasing by ≥60% Decrease dose Decrease dose Not noted PTH: <100 hold PTH: <100
1 week, restart at mg pg/mL, hold for
lower dose 1 week, restart at
lower dose
PTH in desired range Maintain dose Maintain dose Maintain dose Maintain dose Maintain dose

8-13

FACTORS AFFECTING THERAPEUTIC RESPONSE TO VIT D/ANALOGS IN


HYPERPARATHYROIDISM

Factor Response To Vitamin D/Analogs Effects/Limitations


Hyperphosphatemia Decreased Inhibits Vitamin D production/effect
Type of binder utilized:
Aluminum gels Enhanced by better control of serum P Risk for aluminum toxicity/bone disease
Calcium salts May require large doses for P control Risk for hypercalcemia
Sevelamer HCL May allow more aggressive Vitamin D Cost/reimbursement
therapy with acceptable Ca x P product
Dialysate Calcium:
3.0 to 3.5 mEq/L May limit dose of Vitamin D/analog Increased risk for hypercalcemia
2.5 mEq/L Allows more therapeutic Vitamin D/analog Better PTH suppression, phosphorus control,
and/or binder dose less hypercalcemia
2.0 mEq/L May allow even higher Vitamin D doses Monitor for low serum levels

Parathyroid gland
changes: Diffuse, ↑ cells, but uniform Increased hormone production
Increased size Nodular glands, less response ↓ vitamin D receptors, ↓ suppression
Hyperplasia
Dosing Route: Oral Both good with adequate doses, depending Reimbursement issues for some products.
IV on level of disease Hypercalcemia/high Ca x P product.

Editor’s Note: Calcium-free, aluminum-free binders can help minimize hypercalcemia/soft tissue calcification.

Reference: Coburn J, Frazao J: Calcitriol in the Management of Renal Osteodystrophy. Sems in Dial 9:316-326, 1996

8-14
MANAGEMENT OF ADYNAMIC (LOW TURNOVER) BONE DISEASE
1. Aluminum Bone Disease - generally symptomatic (bone pain, myopathy, pathologic fractures).
2. Non-aluminum Aplastic Bone Disease - because of hypercalcemia, may have increased risk for extra-skeletal calcifications, but
generally are not very symptomatic. Risk factors include peritoneal dialysis with high calcium solutions, use of calcium based
binders, presence of diabetes mellitus, advanced age, and vitamin D treatment.
3. Diagnosis: iPTH of <100-150 pg/mL is associated with a higher incidence of low turnover bone disorder. “Normal” PTH levels
are not “normal” for renal patients.

Management
Serial monitoring of iPTH
Do NOT routinely order Vitamin D for all patients. Initiation should be based on iPTH levels specific to unit or physician
parameters or when iPTH is >300 pg/mL (original article suggests 200-400pg/mL). If iPTH levels drop to <100-150 pg/mL,
DC/hold Vitamin D and/or titrate the dose to maintain iPTH between 150-300 pg/mL.
Avoid or limit the use of aluminum binders and other sources of aluminum.
Maintain serum calcium in the lower range, which stimulate PTH secretion and help normalize bone metabolism. Usually requires
decreased dialysate Ca++ levels and decreased reliance on Ca based binders.
Individualize patient treatment with dialysate calcium concentration, binders, and supplements to maintain serum phosphorus,
serum calcium, and iPTH levels within acceptable ranges.

Editor’s Note: iPTH goals vary depending on the reference (1.5-3x upper normal, 150-300 pg/mL for PTH2 (1-84 + 7-84
fragment). PTH3 (1-84) values are approximately 50% lower than PTH2 in most patients. Target ranges and interpretation of PTH3
are still being investigated with bone biopsies to correlate bone histology with specific PTH3 values. For those who are already
using PTH3, Vitamin D protocol goals could be adapted using target PTH2 values divided by two. When transitioning from PTH2 to
PTH3 clinicians should pay special attention to those patients who fall out of the observed 2:1 ratio and those whose PTH values are
inconsistent with bone-related clinical symptoms.

Reference: Pei Y, Hercz G: Low Turnover Bone Disease in Dialysis Patients. Sems in Dial 9(4): 327-331, 1996
8-15

FORMULAS FOR ADJUSTED CALCIUM


1. Adjusted serum calcium = measured total calcium + 0.0176 (34 - serum albumin (g/dL))

Reference: Fernandez E, Montoliu J. Successful treatment of massive uremic tumoral calcinosis with daily hemodialysis and very
low calcium dialysate. Nephrol Dial Transplant 9:1207-1209, 1994.

2. Adjusted serum calcium = Total calcium mg/dL + 0.8 x (4.0 - serum albumin (g/dL))

Reference: Portale AA. Blood calcium, phosphorus, and magnesium in Primer on Metabolic Bone Diseases and Disorders of
Mineral Metabolism, Ed. Favus MJ. Lippincott, Williams, and Wilkins, Philadelphia, 1999, pp 115-118.

There are a number of different formulas that correct serum calcium for low albumin or low total protein. Formula 1 above was
derived in a study employing good statistical methods and strict control of blood processing. This formula had an interclass
correlation value of 0.84 and most closely approximates total calcium in patients with CKD. Formula 2 is a commonly used,
simplified formula for adjustment total calcium for changes in plasma albumin. It is accepted that total calcium needs to be adjusted
for the level of albumin to better reflect free calcium. Symptoms of hypercalcemia have been observed in hypoalbuminemic CKD
patients with high normal serum calcium levels. If adjustment results are questioned, one should perform an ionized calcium
measurement.

IONIZED CALCIUM CALCULATION


Ionized calcium in mg/dL = (Total serum Ca++ mg/dL X 6) - (Total Protein/3) (1)
Total protein + 6

Ionized calcium in mg/dL = 1- (8 X albumin) + (2 X globulin) + (3 X unadjusted serum calcium) (2)


(where globulin = total protein - albumin)

References: 1 Raphael SS: Lynch’s Medical Laboratory Technology, 4th Ed, W.B. Saunders, 1983
2
Kaminsky M: (Ed) Hyperalimentation: A Guide for Clinicians, Dekker, Inc., NY, 1985

8-16
SYMPTOMS OF HYPERCALCEMIA AND HYPOCALCEMIA

Hypercalcemia: Mild- May be asymptomatic. Weakness, headache, nausea, somnolence or irritability,


Early Stage vomiting, dry mouth, constipation, muscle pain, metallic taste, shortened Q-T interval
on EKG, abnormal U waves
Severe - Late Stage
Elevated BUN & SGOT/SGPT, pruritus, hypertension, anorexia, weight loss, calcific
conjunctivitis, pancreatitis, mental confusion, overt psychosis, cardiac arrhythmias,
sensitivity to light, rhinorrhea, polydipsia, hyperthermia
Hypocalcemia:
Mild - Early Stage May be asymptomatic. Prolonged Q-T interval, EKG T wave may be lower/inverted
Severe - Late Stage Tetany, numbness/tingling progressing to muscle spasm and seizure

ETIOLOGY OF HYPERCALCEMIA

Absorptive Resorptive
Pharmacological doses of active Vitamin D Primary hyperparathyroidism
Large doses of calcium Malignant neoplasms
(supplements, binders, foods, dialysate) Vitamin D intoxication, excessive Vitamin A
Prolonged immobilization
Adrenal insufficiency/Hyperthyroidism

References: The Merck Manual of Diagnosis and Therapy, 13th Edition, Rahway, NJ, 1977
Tisher C, Wilcox C: Nephrology for the House Officer, Williams & Wilkins, 1993

8-17

POTENTIAL INDICATIONS FOR PARATHYROIDECTOMY


While treatment with Vitamin D/analogs has substantially improved the course of secondary hyperparathyroidism, the need for
parathyroidectomy still exists in certain clinical situations. The list below outlines some of the conditions which may indicate the
need for consideration of parathyroidectomy.

1. Hypercalcemia, resistant to medical therapy and/or in the presence of bone erosions, marked elevations of parathyroid hormone,
and bone biopsy results demonstrating osteitis fibrosa.
2. Ischemic skin ulcerations associated with vascular calcifications or calciphylaxis. Extensive vessel calcifications without
symptoms may NOT absolutely indicate the need for a parathyroidectomy since some research has shown that the calcification
progresses even after parathyroidectomy is performed.
3. Extremely severe, unresolving pruritus in the presence of significantly elevated iPTH.
4. Persistent hyperphosphatemia unresponsive to medical therapy.
5. PTH is considered to be a uremic toxin which may cause adverse effects such as bone marrow dysfunction (anemia), myocardial
dysfunction (congestive heart failure), and neuromuscular problems (peripheral neuropathy). Such toxic effects may be
considered indications for parathyroidectomy, but without proof of a clear, direct relationship, these problems should not be the
sole reason for recommending parathyroidectomy.
6. Severe hyperparathyroidism resistant to medical therapy. (i.e. iPTH > 800 pg/mL).

Reference: Llach F, Nikakhtar B: Parathyroidectomy in Dialysis Patients: Indications, Surgical Approach, Complications, and
Clinical Management. Sems in Dial 9(4):332-338, 1996

8-18
COMMON CLINICAL COURSE AFTER PARATHYROIDECTOMY

Time Clinical Course Intervention


Immediate post-op and up to Hypophosphatemia (more profound in Serum P should be maintained at 3.5 to 5.0
one year patients with higher PTH and plasma mg/dL. Oral calcitriol is generally most
alkaline phosphatase) secondary to effective in correcting hypocalcemia and
decreased mobilization of P from bone hypophosphatemia.
and/or increased movement into bone.
~Day 2 post-op to months Significant, precipitous decline (as much as Large doses of oral or IV calcium are always
after surgery 60%) in serum calcium which may be needed to correct hypocalcemia. Increase
accompanied by numbness, paresthesia, daily doses from 0.5 to 1 gm at an interval
and tetany. The decline is correlated with of 3 to 7 days until serum calcium begins to
the severity of hyperparathyroidism. An rise. Give IV calcium with corrected serum
insignificant drop in calcium suggests that level <7.5 mg/dL or tetany. Prompt post-op
too much of the gland was left or bone use of calcitriol enhances calcium
pathology was not severe (osteitis fibrosa). absorption/bone formation.
~Day 4 post-op A marked increase in alkaline phosphatase All laboratory parameters of bone health
(peak 7-14 days) with an increase in should be carefully and regularly monitored.
osteoblastic activity, then decline typically
begins by week 3 and may reach normal
after 6 months.

Reference: Llach F, Nikakhtar B: Parathyroidectomy in Dialysis Patients: Indications, Surgical Approach, Complications, and
Clinical Management. Sems in Dialysis 9(4):332-338, 1996

8-19

UROLITHIASIS (NEPHROLITHIASIS/KIDNEY STONES)


Urolithiasis is the presence of calculi in the urinary tract. The male-to-female incidence ratio is 4:1, with 240,000 to 720,000
Americans affected yearly. Eighty percent of calculi are composed of calcium (either oxalate or phosphate), with others composed of
struvite, uric acid, or cystine.

Type of stone indicates cause:


1. Calcium type I—increased small bowel absorption of calcium unrelated to intake
2. Calcium type II—increased dietary calcium intake
3. Calcium type III—increased vitamin D synthesis
4. Calcium oxalate-idiopathic/primary intestinal disorders, chronic diarrhea with inflammatory bowel or steatorrhea
5. Struvite (magnesium ammonium phosphate)-mainly women, due to infection with urease-producing organisms
6. Uric acid—metabolic defects or dietary excess of uric acid; bowel disease or chemotherapy
7. Cystine-due to chronic diarrhea, type I renal tubular acidosis, chronic hydrochlorothiazide treatment

Risk Factors
Excess intake of calcium, oxalate, or purines in predisposed individuals
Inadequate fluid intake
Sedentary occupation
Area of high humidity, elevated temperatures (summer)
Hyperparathyroidism
Renal tubule defects (renal tubule acidosis)
Bowel disease or ileal bypass for obesity
Genetics-cystinuria, an autosomal recessive disorder (markedly increased cystine excretion)
Excessive intake of certain vitamins and minerals
Gout
Use of certain diuretics

8-20
TREATMENT OF CALCIUM STONES
Nutrient Recommendation
Calcium Children: RDA for age/gender
Adult men/women: 800 mg/day
Pregnant/lactating women: 1200 mg/day
Post-menopausal women: 1200-1500 mg/day
Sodium 100-150 mEq sodium/day
Protein Children: RDA for age/gender/treatment modality
Adults: 1 gm/kg
Phosphorus Unrestricted
Fluid Children: Unrestricted, high intake encouraged
Adults: > 2 L/day
Vitamins C & D Avoid levels above RDA
Oxalate Limit dietary sources, especially nuts/chocolate

Diet is used as first line treatment and in conjunction with drug therapy.

References: See next page.

8-21

HYPEROXALURIA
The most common cause of hyperoxaluria is intestinal disease with increased oxalate absorption. It is rarely caused by a metabolic
abnormality that results in the body producing too much oxalate.

Type Cause Dietary Treatment


Hyperoxaluria Increased excretion in urine due to Dietary oxalate: <40-50 mg/day
excessive absorption of dietary oxalate Protein: Adults: 1 gm/kg
Children: RDA for age/gender
Fat: <30% of total calories/day
Calcium: <1 gm/day, if MD ordered
Vitamin C or D Limit to RDA
Fluid:
Adults: >2 L/day
Children: Unrestricted, high intake encouraged

References: Brzezinski E et al: Oxalate Content of Selected Foods. UC, San Diego, 1996
Laumann E et al: Management of primary hyperoxaluria: efficiency of oral citrate administration. Ped Nephrol 7:207,
1993
Massey L et al: Effect of dietary oxalate and calcium on urinary oxalate and risk of formation of calcium oxalate
kidney stones. J Am Dietetic Assoc 903(8):901, 1993
Ono K: Secondary hyperoxalemia caused by vitamin C supplementation in regular hemodialysis patients. Clin Nephrol
26(5):239-243, 1986
Polinsky M et al: Renal Stones: Hypercalcuria. Advances in Pediatrics, Vol 49, 1993
Smith CL et al: Dietary Factors in Calcium Nephrolithiasis. JRN 2:146-153, 1992
Wendland B: Nutrition management of the patient with urolithiasis. In: Stover, J., Ed.
A Clinical Guide to Nutrition Care in End Stage Renal Disease. ADA, 1994

8-22
OXALATE CONTENT OF COMMON FOODS

Low <2 mg/serving Medium 2-10 mg/serving High >10 mg/serving


MEATS/SUB: Eggs, cheese, lean MEATS/SUB: Sardines, bacon MEATS/SUB: Baked beans in tomato sauce,
meats, seafood VEGETABLES: Asparagus, peanut butter, soybean curd (tofu)
VEGETABLES: Avocado, broccoli, carrots-canned, cauliflower, corn, VEGETABLES: Beans - boiled or raw,
cabbage, potato, radish, turnips, cucumber, onions, peas, lettuce, beets, celery, Swiss chard, chives, collards,
water-chestnuts, mustard greens dandelion greens, eggplant, escarole, leeks, mustard greens, okra, peppers, sweet
FRUITS: Banana, cherries, kale, parsnips, lima beans, tomato, potato, rutabaga, spinach, summer squash,
cranberries-canned, green seedless mushrooms watercress
grapes, lemon/lime juice, mangos, FRUITS: Apple, apricots, black FRUITS: Berries, concord grapes, red
melons, nectarines, peaches-Hiley currants, cranberries-dried, currants, fruit cocktail, gooseberries,
canned, pineapple, plums- grapefruit, orange, peaches-Alberta, lemon/orange peel, raspberries, rhubarb,
green/Golden age, pears-Bartlett pears - raw, plums-stewed, prunes- strawberries-canned, tangerine, plums-
canned, orange juice, papaya, Italian, pineapple-Dole, coconut, Damson
strawberries-fresh. kiwi STARCHES: Fruitcake, grits,
STARCHES: Barley, cornflakes, STARCHES: Cornbread, sponge soybean/graham crackers, wheat germ, fig
macaroni, rice/wild rice, noodles, cake, spaghetti in tomato sauce, cookies, popcorn, whole wheat flour
oatmeal, white bread cornmeal, Cheerios®, bagel, brown FATS: Nuts - peanuts/pecans, sunflower
FATS: Mayonnaise, salad dressing, rice, garbanzo beans-canned, lentils, seeds, mayonnaise-Heinz
vegetable oils, butter, margarine split peas, macaroni, spaghetti, corn MISCELLANEOUS: Chocolate, dry cocoa,
MISCELLANEOUS: Jams, jellies tortilla, English muffin, whole wheat pepper in excess of 1 tsp/day, cinnamon,
from fruit listed above, sugar, honey, bread marmalade, jellies from fruits listed above.
corn syrup, unflavored gelatin, maple MISCELLANEOUS: Vegetable/
syrup, vanilla extract, vinegar, tomato soup, tofu-firm, malt,
cornstarch, salt, pepper <1 tsp/day mustard-Dijon, ginger-raw

Reference: Brzezinski E at al: Oxalate Content of Selected Foods. Clinical Research Center, UCSD Med Center, 1996

8-23

SOFT TISSUE CALCIFICATION AND CALCIFIC UREMIC ARTERIOPATHY


(CALCIPHYLAXIS)
Factors that may predispose CKD patients to soft tissue calcification:

High calcium x phosphorus product An increase in local tissue pH


Secondary hyperparathyroidism Local tissue injury
Dialysis removal of calcification inhibitors

A high calcium x phosphorus product in the extracellular fluid is probably the most pathogenic factor but the exact calcium x
phosphorus level at which soft tissue calcification begins is not absolutely known. The current literature supports maintaining the
calcium x phosphorus product in the range of 55 or below because of other contributing factors and the differences in the chemical
nature of soft tissue calcification.

Dietitians can help monitor for vascular calcification during monthly visits and/or during physical exams (especially in
diabetics):

Long term hyperphosphatemia? Significant calcium load?


Calcium can be normal or elevated
Lesions may be preceded or accompanied by severe pain
Before a lesion appears, there may be tender, subcutaneous nodules or blotchy, bluish discoloration
Raynaud’s disease (gangrene phenomenon) may also precede lesions on the fingers or toes
Ulcers usually develop slowly over several months; skin or muscle necrosis may appear and progress rapidly

Calcific uremic arteriopathy (calciphylaxis) can be life-threatening and must be treated early and aggressively.

References: Goodman WG, Goldin J, Kuizon BD, et al. Coronary artery calcification in young adults with ESRD undergoing
dialysis. N Eng J Med 342(20):1478-1483, 2000
Kimura K, Saika Y, Otani H, et al. Factors associated with calcification of the abdominal aorta in HD patients.
Kidney Int (Suppl) July 71:S238-S241, 1998 8-24
Chapter 9:

MALNUTRITION
IN CHRONIC KIDNEY DISEASE

ADULT MALNUTRITION
Type Kwashiorkor Marasmus Mixed
CAUSE/ Acute protein deficiency, rapid Chronic protein/energy Advanced protein/energy
DESCRIPTION onset/catabolic stress in a previously deficit, gradual wasting, deficit superimposed with
well-nourished pt. adaptive decrease in energy increased protein needs or
expenditure losses

ANTHRO- Less wasting of muscle stores, less Diminished fat and muscle Rapid depression of fat and
POMETRY weight loss than marasmus due to stores, growth retardation in muscle stores
rapid onset children
LAB Serum proteins are generally low, Serum proteins are preserved Serum visceral proteins are
diagnosis with albumin <3 g/dL, initially by recycling of aa very depressed
altered electrolyte state and ↓ urea synthesis

OTHER Characterized by pitting, painless Nutrition-related edema is Notable edema, wasting


SIGNS edema to extremities, not present, levels of insulin and multiple organ system
notable skin lesions/peeling and thyroid hormone are ↓ deterioration

INTERVENTION Supplement with fluids, electrolytes, Calories and protein orally; Prompt feeding (enteral or
vitamins, minerals, protein as aggressive support if weight parenteral or both)
indicated is ↓ by 20-30% to avoid mortality

Reference: Simko MD: Nutritional Assessment: A Comprehensive Guide for Planning Intervention, ASPEN, 1995

9-2
FACTORS THAT CAN CAUSE OR EXACERBATE MALNUTRITION IN CHRONIC
KIDNEY DISEASE
1. Increased needs and additional losses
2. Abnormal metabolism, absorption, or utilization of nutrients
3. Inadequate dialysis treatment
4. Anorexia, inappropriate or poor intake
5. Excessive dietary restriction
6. Psychosocial problems
7. Superimposed illness
8. Catabolism of dialysis (including bioincompatible membranes)
9. Endocrine disorders
10. Acidosis

Reference: Kopple JD, Massry S, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997

9-3

EVALUATION OF WEIGHT LOSS OVER TIME

Time Significant Loss Severe Loss


1 Week 1% >1%
1 Month 5% >5%
3 Months 7% >7%
6 Months 10% >10%
Other Indications for Risk of Malnutrition
Oral intake compromised for >2 weeks
Extensive nutrient loss for >1 week
Weight < 95 % of usual/standard weight (See page 1-18)
BUN < 40 mg/dL (in dialysis patients)
Cholesterol <150-180 mg/dL
Body Mass Index < 20 (See page 1-20 & 21) (Dialysis M:23.6 F:24)
Recent hospitalization
Chronic acidosis/serum bicarbonate < 22 mEq/L

Note: SGA rates any weight change (within 6 months) of +/− 5% as normal, loss of > 5% to 10% as significant for mild to
moderate malnutrition, and a weight change of >10% as significant for severe malnutrition.

Values in italics signify K/DOQI recommendations.

References: Page CP: Nutritional Assessment and Support: A Primer, Williams & Wilkins, 1994
Blackburn G: Nutrition & metabolic assessment of the hospitalized patient. JPEN 1:11-22, 1977
Mitch WE: Mechanisms Causing Muscle Wasting in Uremia. J Ren Nutr 6(2):75-78, 1996
NKF K/DOQI Clinical Practice Guidelines for Nutrition in CRF. Am J Kidney Dis 35 (Suppl 2), June, 2000
9-4
CRITICAL PROTEINS FOR ASSESSING MALNUTRITION

Protein Half Life Depleted Level Body Pool Limitations


Albumin* 3 weeks <3.5 g/dL (depends 3-5 gm/kg Slow response to depletion or
on type of repletion, altered by factors
measurement/lab other than malnutrition
normals)
Transferrin 8 days <200 mg/dL <0.1 gm/kg Affected by Fe++ stores
Not considered a good marker
in CKD patients.
TBPA1 2 days <22 mg/dL 0.01 gm/kg Not routinely performed in all
(CKD < 29-30 facilities. TBPA is excreted by
mg/kg) the kidneys, thus reference
RBP 2 12 hours <4.5 mg/dL 0.002 gm/kg range is higher in CKD.

1
Thyroxine Binding Prealbumin (Transthyretin)
2
Retinol Binding Protein

*Potential Effects of Hypoalbuminemia Alteration in GI function; promotion of gastric stasis; prolongation of bowel transit time,
decreased colon resorption of salt/water, decreased absorption of food and drugs, diarrhea, cholestasis, altered intravascular oncotic
pressure, and fluid balance. Potential for decreased immunity/delayed wound healing/infection and predictor of increased
morbidity/mortality. Hypoalbuminemia may be a nonspecific marker of illness as well as a marker of malnutrition. Inflammation
and infection can cause low serum albumin in the absence of malnutrition.

References: Abstract: Gastroenterology 88:1336, 1984; and 90:1401, 1986


Page CP: Nutritional Assessment and Support: A Primer. Williams & Wilkins, 1994
Gibson RS: Principles of Nutritional Assessment, Oxford Press, 1990

9-5

GUIDELINES FOR ENTERAL FEEDING

Indications for Use* Complications Possible Solutions


Failure of intense nutrition GI disturbance Dilute formula, limit volume per
counseling feeding, change formula, use lactose-
Functional GI tract free, review/change meds, decrease
Patient willingness osmolality, stop for 8-12 hrs; restart
Tolerance of fluid load with smaller, more frequent doses
Inability to meet needs w/traditional Over/underhydration Change formula concentration and/or
foods volume
Insufficient/excess kcals or protein Change formula or concentration, add
modular fat, CHO or protein source
to tailor kcal or protein levels
*If a patient is unable to eat, sleep, Electrolyte imbalance Modify intake of other foods, change
has poor appetite, or unexplained formula, change volume
N & V, assess dialysis adequacy
Advantages: Enteral feeding maintains gut integrity and host defenses. It is safe and less costly than IDPN,
TPN. It stimulates a favorable insulin response

Reference: Page CP: Nutrition Assessment and Support: A Primer. Williams & Wilkins, 1994

9-6
ENTERAL NUTRITION SUPPLEMENTS
This list of products is limited to those that could be used in CKD patients. Most basic or non-specific supplements were eliminated in the
interest of space. CHO/protein/fat are in grams; sodium/potassium/phosphorus/calcium are in milligrams.
PRODUCT Amt Kcal CHO PRO Fat Na+ K+ P Ca++ Uses
(gm) (gm) (gm) (mg) (mg) (mg) (mg)

Boost Plus 8 oz 360 45 14 14 200 350 200 200 C,V, O, S, T, HC, HP


Choice DM 8 oz 250 25 10.6 10.3 200 430 310 330 C, S, DM, F , T
Choice 8 oz 250 25 10.6 12 200 430 250 250 C, S, F
Enlive 8 oz 300 65 10 0 65 40 20 60 HC, clear liquid
Ensure Hi Pro 8 oz 225 31 12 6 290 500 250 300 C, O, S, HP, V
Glucerna Shake 8 oz 220 22 10 11 210 370 250 250 C, DM, O
Magnacal Renal 8 oz 470 47 17.7 24.1 190 300 189 240 C, O, T, Renal
Nepro 8 oz 475 52.8 16.6 22.7 200 250 165 325 C, O, T, S, Renal
Novasource Renal 8 oz 475 47.3 17.4 24.1 250 192 154 308 C, HC, V, O, T, S
NuBasics Coffee 2 scp 125 18.8 6.25 2.8 210 270 480 110 C, S
NuBasic Juice 5.5 oz 163 34 6.5 0.1 50 50 166 83 S, O
Nubasic Soup 1 pkt 250 33.1 8.75 9.2 390 310 165 165 S, O,
Nubasic VHP 8 oz 250 28.2 15.6 8.3 219 312 145 145 C, S, O, HP, LR, T
NutriRenal (250 ml) 8 oz 500 51.2 17.5 20 185 314 176 350 C, S, O, HP, HC, V, T
ReNeph 4 oz 250 31 8 11 NA 15 60 NA S
ReNeph No Sugar 4 oz 230 23 9 11 NA 15 60 NA S, DM
Resource Diabetic 8 oz 250 23.4 15 11.1 230 270 220 220 DM, F, O
Resource Frt Drink 8 oz 180 36 9.0 0 <70 <22 160 135
Suplena 8 oz 475 61 7.1 22.7 185 265 175 330 C, S, O, T, V, HC
V=volume restricted, C=complete, S=supplement to food, O=appropriate for oral, T=appropriate for tube, DM=appropriate for persons
with diabetes, A=additive to other foods, HP=high protein, HC=high calorie, LR=low residue, F=added fiber, NA=information not
available. Due to frequent changes, clinicians are encouraged to update the information regularly.
2-7:
Reference: Internet/Manufacturers’ Product Information
9-7

SPECIALTY NUTRITION BARS/COOKIES

Product Amt Kcal CHO PRO Fat Na+ K+ P Ca++ Uses


(gm) (gm) (gm) (mg) (mg) (mg) (mg)
Boost Bar 1.6 oz 190 29 4 6 90 105 150 150 S,V, O
Choice DM Bar 1.23 oz 140 19 6 4.5 65 105 110 133 DM, S, V, O
Ensure Bar 1 bar 130 21 6 3 115 200 150 80 C, S, V, O
Glucerna Bar 1.34 oz 140 24 6 4 75 80 150 250 C, DM, F, V, O
NuBasic Bar 1 bar 125 16.6 4.4 4.6 135 220 100 100 C, S, V, O
ProFortified Cookie 1 260 28 7 14 180 138 57.3 NA S, O, V
ReNeph Cookies 2 oz 210 29 9 7 NA 125 64 NA S, O, V

SPECIALTY NUTRITION PUDDINGS

Product Amt Kcal CHO PRO Fat Na+ K+ P Ca++ Uses


(gm) (gm) (gm) (mg) (mg) (mg) (mg)
Boost Pudding 5 oz 240 32 7 9 120 320 200 200 O, V, S
Ensure Pudding 5 oz 250 27 4 5 240 330 200 200 C, S,O, V

V=volume restricted, C=complete, S=supplement to food, O=appropriate for oral, T=appropriate for tube, DM=appropriate
for persons with diabetes, A=additive to other foods, HP=high protein, HC=high calorie, LR=low residue, F=added fiber,
NA=information not available. Due to frequent changes, clinicians are encouraged to update the information regularly.

Reference: Manufacturers’ Information

9-8
MODULAR PRODUCTS (Added to other sources of nutrition)

Product Amount Kcal CHO Pro Fat Na+ K+ P Ca++ Adds


(gm) (gm) (gm) (mg) (mg) (mg) (mg)
Additions® 1 scoop 100 9 6 5 100 3 34 3 Protein
Boost High Pro® 54 gm 200 36 13 1 190 560 250 290 Protein
Casec Dry® 1 1 Tbsp 17 0 4 0.09 4.4 Neg. 35 62 Protein
ProCel® 3 1 scoop 28 <0.4 5.3 <0.5 <10 <30 <23 <30 Protein
Pro Mod®5 6.6 gm 28 0.67 5 0.6 25 45 33 <30 Protein
Resource® Inst. Pro 2 1 scoop 25 0 6 0 35 7 3.5 7 Protein
Vyo Whey Pro® 4 1 scoop 82 3 20 1 60 185 NA NA Protein
Moducal® Dry1 1 Tbsp. 30 8 -- -- -- -- -- -- CHO
Polycose® Dry 5 Per gm 3.8 0.94 -- -- <1.1 Neg. Neg. <0.3 CHO
Polycose® Liquid5 Per ml 2.0 0.2 -- -- Neg. Neg. Neg. Neg CHO
MCT Oil®1 Per ml 7.7 -- -- -- -- -- -- -- Fat
Microlipid® 1 Per ml 4.5 -- -- -- -- -- -- -- Fat
1
Mead Johnson 2Novartis 3Tyler Medical Supplies 4
Nutrition 5
Ross Products Division, Abbott Labs
Reference: Internet, Manufacturers’ Information

9-9

ORAL AMINO ACID THERAPY

Oral essential amino acid supplements are safe and effective in treating people with kidney disease. They have been
successfully used to enhance the efficacy of a low protein diet in CKD (not on dialysis) and to treat hypoalbuminemia
in CKD patients. They are not recommended as the sole source of nutrition.

Product Amino Acid Content Form Manufacturer/Distributor


Aminess® Each table contains 720 mg of amino acid Tablets Recip AB, Stockholm
and 88 mg of nitrogen (= to 0.55 gm
protein)
Nutramine T™ 3.5 gm UPS grade amino acid Powder/granules to Calwood Nutritionals, Inc.
in 1 packet be used with
foods/liquid to make
chewable “candy,”
custard, beverage,
other foods

9-10
TUBE FEEDINGS – Special Considerations for CKD

1. Moderate protein and electrolyte levels plus added fiber may be best. Too much protein can add risk for dehydration,
hypernatremia, hyperchloremia, and azotemia especially in elderly and those with compromised kidney function.
2. Concentrate formulas to minimize fluid load. May need to dilute concentrated formulas at initiation.
3. Start slowly. Continuous or cyclic delivery may be tolerated best.
4 May not tolerate the free water or flush volumes suggested by manufacturers. Monitor fluid status carefully.
5. Cyclic delivery may decrease daytime fullness and allow the patient to eat at mealtimes, if physically possible.
6. Portable pumps allow easy transport to dialysis treatment.
7. Monitor chemistries (urea, electrolytes/minerals). Phosphate binders may need to be held if refeeding syndrome occurs.
8. Review formulas considering that some products may have inappropriate levels of vitamins, minerals, electrolytes, protein,
calories. If renal formulations are used as the sole source of nutrition, monitor for low levels of minerals and electrolytes.
9. Monitor for diarrhea (too rapid infusion, bacterial contamination, fecal impaction, antibiotic-induced, hypoalbuminemia,
malabsorption)

Feeding Type Description Advantages Disadvantages


Continuous Pump is used to deliver Reach goals more quickly Requires pump
feeding at a regulated rate Patient tolerance enhanced Difficult in disoriented patients
Nutrient absorption is More costly
maximized Decreased mobility
Intermittent Given in specific volumes Mobility Fullness, Discomfort
every 3 to 4 hours over a Less costly Reflux, Staff time
specified period of time
Cyclic Feeding the patient Frees patient during the Need higher hourly rate of
continuously via pump day infusion or more concentrated
over only part of the day May be more well tolerated formula to meet needs (requires
(usually 12-16 hours) than intermittent more water volume)
Decreased fullness
Can help transition to full
oral intake

Reference: SpringNet, CE Connection, Internet

9-11

COMMON TUBE FEEDING SITES

Site Characteristics
Intragastric Tube through nose or mouth into stomach; used for short term <6 weeks;
easily inserted; risk for aspiration pneumonia; potential discomfort; remains
in place between meals; can be administered intermittent or continuous.
Nasoduodenal or Nasojejunal Short term enteral feeding; may allow feeding after gastric surgery; difficult
to place and maintain.
PEG: (Percutaneous Endoscopic Used for long term tube feedings into stomach of patients; often used for
Gastrostomy) alterations in swallowing; less discomfort than nasogastric, can be inserted at
bedside with local anesthesia; risk of skin breakdown around tube;
contraindicated in peritonitis, ascites, morbid obesity, obstruction, esophageal
obstruction or reflux. Formula can be given at night as intermittent,
continuous, or cyclic.
Jejunostomy Direct access to jejunum when stomach must be bypassed; potential for
dumping syndrome/diarrhea; lower risk of aspiration; pumped with slow
infusion working up to strength/volume needed to meet nutritional needs of
the patient.
Always increase rate first, then strength.

Reference: Rombeau J, Caldwell M: Clinical Nutrition: Enteral and Tube Feeding, W.B. Saunders, 1990
SpringNet, CE Connection, Internet

9-12
TUBE FEEDING FORMULAS

Type Examples (partial list) Characteristics Indications


Isotonic balanced Osmolite, Isocal Osmolality between 280-350 Tube feeding is sole source of
mOsm/kg water; 1 kcal/ml nutrition; calorie needs 2-3000/d
Complete Ensure, Nutren 1.0, Osmolality more than 350 Can be used to supplement normal
balanced Resource, Sustacal, Boost mOsm/kg water; 1 kcal/ml diet or tube for 2-3000 kcal/d
HC complete Ensure Plus, Comply, Osmolality more than 350 Oral supplement or tube for reduced
Isosource, Nutren 1.5, Boost mOsm/kg water; 1.5 kcal/ml volume and high calories
Plus
High nitrogen Ensure HN, Magnacal, Can be isotonic or hypertonic; Oral supplement or tube for higher
TwoCal HN, Nutren 2, 1-2 kcal/ml, more pro protein w/ or w/ out higher kcals
Impact, Respalor
Fiber containing Ensure Fiber,Ultracal, Can be iso- or hypertonic; Primarily long term tube feeding to
Jevity, Sustacal Fiber, 1 kcal/mL; varied fiber maintain normal bowel patterns
Compleat Mod.
Partially hydro- Vital HN, CriticareHN, High pro level, hydrolyzed to Used with malabsorption/radiation
lyzed elemental TraumaCal, Peptamen peptides/aa, 1 kcal/ml Osmolality treatment, usually administered by
Propeptite, Vivonex + >350 mOsm/kg water tube, but can be taken orally
Glucose intolerance Glucerna, Choice DM Low CHO/minimize affect on Type I or Type II diabetes or stress-
blood sugar 1 kcal/mL induced hyperglycemia
Specialized for CKD CKD: Suplena, Amin-Aid Protein/electrolyte content Oral or tube for patients unable to
On Dialysis: Nepro, modified for renal disease; meet nutrition needs with traditional
MagnaCal Renal, NutriRenal 2 kcal/ml foods

Reference: SpringNet CE Connection, Internet

9-13

COMMON TUBE FEEDING PRODUCTS/1000 ml (Incomplete List)

Product Kcal CHO PRO Fat Na+ K+ P Ca++


Comply 1500 180 60 61 1200 1850 1200 1200
Criticare HN 1060 220 38 5.3 630 1310 530 530
Isocal 1060 135 34 44 530 1320 530 630
Isocal HN 1060 124 44 45 930 1610 850 850
Jevity 1060 154.7 44.3 34.7 930 1570 760 910
Nutren 1.0 1000 127 40 38 876 1248 668 668
Osmolite 1060 151.1 37.1 34.7 640 1020 535 535
Osmolite HN 1060 143.9 44.3 34.7 930 1570 760 760
Two-cal HN 2000 216 83.5 89.1 1460 2450 1055 1055
UltraCal HN+ 1200 156 54 40 1350 1850 1000 1000

References: Internet, Manufacturers’ Information

9-14
INTRADIALYTIC PARENTERAL NUTRITION (IDPN)

Indications for Use Potential Complications Possible Solutions


All less intense therapies fail Loss of infused nutrients to dialysate Most retained with aa/glucose combination, add
Permanent, significant GI impairment vitamins last 10 minutes
MD prescription Damage to vascular access Diluted 50-60 x before reaching endothelial wall
Severe protein/calorie depletion
Significant weight loss Hypoglycemia Provide snack 30 min prior to end of infusion
ADVANTAGES:
Enhanced use of dialysis time Hyperglycemia Can add insulin (BS >275 mg/dL)
Increased patient morale Decrease dextrose, slow infusion, adjust
Convenient access to circulation carbohydrate to patient body size
Reduced catabolic stress Electrolyte imbalance Change dialysate/IDPN, oral supplements
Can replace dialysis aa losses Azotemia Decrease aa, provide adequate dialysis
Extra fluid is removed as solution is Fluid overload Encourage fluid compliance, decr volume,
infused ensure adequate treatment time
Less costly than TPN/hospitalization Hypotension/Cramping/Hyponatremia Increase Na+ intake, add Na+ to IDPN if MD
for complications of malnutrition order, increase total concentration, encourage
May be tolerated best if infused over fluid compliance, keep Hct at adequate level
at least a 3 hour treatment Elevated liver enzymes May be imbalance of aa/decrease lipid if due to
fat/glycogen in liver
Acidosis Decrease aa if oral protein intake is high
Hyperlipidemia Infuse/increase lipids slowly, decrease
concentration, d/c lipids if allergic reaction
occurs

K/DOQI: “Additional research is needed to document the absolute benefit of IDPN.”


Reference: Satellite Healthcare Policy/Procedure Manual/Information from FMC Nutrition Support Service

9-15

GASTROINTESTINAL MOTILITY STUDIES

Test Description Identifies Significant Findings


Scintigraphic Study Solid phase emptying study Gastroparesis < 3 hr transit time from stomach
determines stomach to jejunum* Small Bowel to jejunum or right colon does not
transit time. Injection or ingestion Dysmotility qualify for parenteral nutrition.
of radioisotope, usually mixed
w/food followed by sequential
gamma imaging of the abdomen.
Radiographic Ingestion of radiopaque pellets (or Gastroparesis 3-6 hour transit time requires tube
Pellet Study barium) followed by sequential Small Bowel feeding trial, as does diagnosis of
abdominal radiographs to Dysmotility gastroparesis.
determine pellet transit time from
stomach to jejunum.*
Manometric Study Pressure measuring device passed Gastroparesis
into GI tract to take sequential
pressure measurements to
determine gastric emptying time.

*If transit time to jejunum is >6 hours, use transit time to right colon.
Reference: Medicare Parenteral Nutrition Policy, 1996

Other significant medical diagnoses to look for in the patient’s medical history: Amyloidosis, AIDS/ARC with related
symptoms, chronic recurring pancreatitis, collagen vascular disease or myopathies, familial autonomic dystrophies, intestinal
neuropathies, ischemic bowel disease, mesenteric infarction, myotonic or muscular dystrophy, motility disorders such as blind
loop/dumping syndrome, delayed gastric emptying, gastric stasis, pyloric stenosis or obstruction, gastric outlet obstruction,
gastroparesis.

9-16
IDPN SOLUTIONS

Characteristic Prescription Total Formula Composition Kcals


Volume
Lipid free 250 cc D50 500 cc 125 gm dextrose 525
250 cc 10% aa 25 gm protein
Increased kcal, higher protein with 250 ml D50 1050 cc 125 gm dextrose 1145
lipids 550 ml 10% aa 55 gm protein
250 ml 20% lipid 50 gm fat
High protein, lipid free 500 ml D50 1050 cc 250 gm dextrose 1070
550 ml 10% aa 55gm protein
High protein, lipid free, limited vol 250 ml D50 800 cc 125 gm dextrose 645
550 ml 10% aa 55 gm protein
High protein, high calorie (Use D70 250 ml D70 1000 cc 175 gm dextrose 1395
to limit volume) 500 cc 15% aa 75 gm protein
250 ml 20% lipid 50 gm fat

Reference: Goldstein, J. Intradialytic parenteral nutrition: Evolution and current concepts. J Ren Nutr, 1:9, 1991.

Editorial Note: Many renal patients tolerate IDPN formulas that contain dextrose levels well above (2-3x) the published glucose
oxidation rate of 5-8 mg/kg/minute. Rather than rely upon standard formulas, it may be prudent to formulate IDPN solutions based
on individual patient needs and safe, effective utilization rates for specific substrates by starting slowly and working up to a level
that provides maximum nutrients without adverse side effects (D70 is commonly used for decreased volume), base aa content on
recommended protein levels (15% solutions are commonly used), and infuse 20% lipids at 1cc/min (FDA limits). Recent research
(Satellite Dialysis Centers, Inc., Redwood City, CA) indicates that administration of IDPN with a high level of aa may increase urea
generation. More research is needed to ascertain optimum therapy, appropriate solutions, nutrient levels, and document
effectiveness.

9-17

RECOMMENDED TPN SOLUTION FOR ACUTE OR CKD


Nutrient Amount Comment
Mixed Amino Acids 1-1.5 gm/kg BW Base on treatment/GFR/stress/metabolic state, maint N2 bal
kcals: Hypertonic 35-40 kcal/kg BW Include dialysate kcals in CRRT, prevent CHO overfeeding
Dextrose 20- 30% total kcal
Lipids (20%) 35-40 mmol/L Final concentration of electrolytes should include those in aa
Electrolytes: Acetate 25-35 mmol/L solutions, adjust electrolyte content based on serum levels
Chloride 5 mmol/day
Calcium 2 mg /day
Iron 4 mmol/day Monitor closely for refeeding syndrome in severely
Magnesium 8 mmol/day malnourished patients; refeeding syndrome is characterized
Phosphorus ≤35 mmol/day by acute changes in phosphorus, potassium, magnesium,
Potassium 40-50 mmol/L vitamins, and/or glucose tolerance
Sodium 60-100 mg
Vitamin: Ascorbic Acid 200 µg\day
Biotin 3 µg/day (IV/oral)
B12 1 mg/day (IV/oral)
Folic Acid 20 mg
Niacin 10 mg
Pantothenic Acid 10 mg
Pyridoxine 2 mg of each May need increased Vit K with lipid administration
Riboflavin, Thiamine 7.5 mg /wk (IV/oral)
Vitamin K 10 IU/day
Vitamin E Individualize
Vitamin D Add if > 3 wk TPN
Vitamin A/Trace Mins
References: Monson P, et al: Nutrition in acute renal failure: A reappraisal for the 1990s. J Ren Nutr 4(2):58-77, 1994
Grant JP: Handbook of Total Parenteral Nutrition, W.B. Saunders, Philadelphia, 1992
Kopple JD, Massry S, Eds: Nutritional Management of Renal Disease, Williams & Wilkins, 1997
9-18
NUTRIENT CALCULATIONS FOR PARENTERAL NUTRITION

1. Determine total daily calorie needs


2. Determine protein needs
3. Determine fluid allowance
4. Determine the kcals to be provided by fat (usually 30-40% of total calories)
Estimated kcals x desired percentage of fat = kcal as fat
Example: 1700 kcals x 30% fat = 510 kcals from fat
Convert to volume of lipid emulsion: 510 kcals /1.1 kcals/mL (10% emulsion) = 463 mL
or 510 kcals/2.0 kcals/mL (20% emulsion) = 255 ml
5. Determine kcals to be provided by protein:
Estimated protein needs x kcals/gm protein
Example: 70 gm protein x 4 kcals = 280 kcals as protein
6. To calculate kcal:nitrogen ratio = Total kcals/grams of nitrogen.
7. Calculate total kcals, determine grams of protein and divide by 6.25 to calculate grams of nitrogen.
In this example, Kcal:N ratio = 1700/(70/6.25) or 152 kcal:1 gm nitrogen
8. Determine the kcals to be provided by carbohydrate:
Estimated kcal needs - (fat kcals + protein kcals) = kcals as carbohydrate
Example: 1700 kcals - (510+280) = 910 kcals
9. Common solutions are 70% dextrose, 10 or 15% aa, and 20% lipids.
Determine volume of D70, 10% aa, and 20% lipid needed to reach target concentrations.
Carbohydrate: 268 gm /70/100 mL = 383 mL 70% dextrose solution
Protein: 70 gm/10/100mL = 700 mL 10% aa solution
Fat: see step 2 above

Reference: Fish J: Worksheet for Calculation TPN. ADA Support Line XVII(6):10, 1995
Specialty Cards-Nutrition, 1998

9-19

NUTRITION SUPPORT MONITORING GUIDELINES IN THE STABLE DIALYSIS


PATIENT
Metabolic TPN IDPN IPN Tube Feeding
Albumin, Total protein 2-3 x/wk Monthly Monthly Monthly
Blood gases, pH Weekly w/ problems w/ problems w/ problems
BUN/Electrolytes Daily Stable, Monthly Monthly Monthly
Ca++/P/ Mg++ 2-3x/wk Stable, Monthly Monthly Monthly
Fluids Daily Daily Daily Daily
Glucose Daily Pre/post tx Diab: Per exch As situation dictates
Lipids 2-3 x/wk after test Monthly after test Monthly Monthly
Liver enzymes Weekly Monthly Monthly Monthly
UNA 2-3 x/wk NA NA NA
ANTHROPOMETRICS
Weight Daily Per treatment Daily Daily
Arm anthropometrics/BMI Monthly Monthly Monthly Monthly
NUTRITION
Appetite NA Weekly Weekly Weekly
nPNA w/UNA Monthly Quarterly Monthly
Diet record NA Monthly Monthly Monthly
DIALYSIS ADEQUACY
Kt/V Monthly Monthly Quarterly Monthly/Quarterly
Creatinine Clearance NA NA Quarterly Monthly/Quarterly
Note: An individual monitoring schedule should be established for the medically unstable dialysis patient. The changing clinical
situation will dictate the timing, aggressiveness, and extent of monitoring that should be undertaken. Patients who are receiving a
combination of nutritional support should be monitored closely for refeeding syndrome.

References: Goldstein DJ: IDPN: Evolution and current concepts, J Ren Nutr 1(1):9-22, 1991
Mitch WE, Klahr S, Eds: Nutrition and the Kidney. Lippencott-Raven, 1998
Nutrition Support Dietetics Core Curriculum, ASPEN, Second Edition, 1993 9-20
INTRAPERITONEAL AMINO ACIDS AS NUTRITION SUPPORT IN PD

The cost of compounded aa/dextrose dialysate is not covered by Medicare. Some private insurance companies will pay for therapy on a
case by case basis. The patient must meet criteria similar to those for IDPN. Solutions using amino acids as the osmotic agent are
currently under consideration for FDA approval in the US. These bulk-produced, shelf-stable solutions (Nutrineal® Baxter Healthcare)
are available in Canada, Europe, and Asia.
Solutions Special Considerations Potential Benefits Side Effects
Compounded Solutions Follow provider’s directions, but -Replace dialysate losses of Uremic symptoms
(Generally 0.5-2% aa, with must be refrigerated and not over- aa/protein. (Incr dialysis dose or decr aa)
or without dextrose) heated. Usually suggest using at
long dwell time for maximum -Promote anabolism
absorption.

Nutrineal® 1.1% aa Dose: 1– 2 liter exchange/day w/in 1 -Improve nitrogen balance/ Metabolic acidosis
solution, no glucose; 15 hr before or after highest kcal meal. plasma aa patterns/serum (decr aa/ incr alkalizing agent)
different aa incl 64% In extreme malnutrition can consider proteins
essential aa; 1 exch=22 gm 2 exchanges/day with strict -Reverse/halt malnutrition N & V, other GI symptoms
aa; UF equivalent to a monitoring for acidosis, uremic progression; replace losses (decrease aa or identify and
1.5% dextrose, may require symptoms, and fluid balance; in peritonitis treat other causes)
other hypertonic for fluid alternate with glucose -Improve immune function
balance; 2 year shelf-life; should be stored in -Boost energy
4-6 hour dwell allows original shipping carton until use- -Improve patient’s sense of
65-90% aa absorption protected from sunlight; not well-being
depends on membrane microwaved -Improve appetite
transport characteristics Reduced glucose load may require an
adjustment in insulin therapy.

Reference: Satellite Dialysis Centers, Redwood City, CA and Baxter Healthcare Asia, Nutrineal® Prescriber’s Guide
9-21

Clinical Associations with Negative Nitrogen Balance

Loss of body weight/Diminished muscle mass


Hypoproteinemic edema
Impaired immunocompetence (humoral/cellular)
Increased susceptibility to infection
Poor wound healing
Increased morbidity and mortality

Reference: Dickerson WT: Nutrition in Clinical Management of Disease, Edward Arnold, 1988

Estimation of Nitrogen Balance

Nitrogen balance = Nitrogen in - Nitrogen out

Nitrogen in = Enteral + parenteral protein in grams


6.25
(converts protein to nitrogen)
1
Nitrogen out=Urinary urea nitrogen (UUN g/d) + insensible loss (0.5 gm N/day) + dialysate losses

1
HD est=1-1.5 g N/dialysis
PD est=0.05-0.08 g aa/exch and 0.1+/-0.08 g Pro/hour of treatment (can double with peritonitis).
CRRT est=1.5-2.0 g N/day

Reference: Monson P: Nutrition in acute renal failure: A reappraisal for the 1990s. J Ren Nutr 4(2):58-77, 1994
9-22