Primary Care - Nephrology Interface: Providing Coordinated CKD Care

PRIMARY CARE NEPHROLOGY
INTERFACE
PROVIDING COORDINATED CKD CARE
MARIA CAMILA BERMUDEZ
MD

Objectives
CKD history, background, prevalence,

epidemiology, definition and risk factors.
Discuss occurrence of complications and

co-morbid conditions of CKD.
Overview of NKF (KDOQI) treatment

guidelines.

HISTORY
THE THREE ERAS OF MEDICINE IN

CHRONIC DISEASE:
Predict natural history
Manage complications
Change the natural history

PAST

ONE OF THE LUCKY 13

PRESENT

HISTORY
The 1920-1930s: Predict natural history
The 1940s: Inspiration, war and progress
First dialysis machine
The 1950s: Solutions, accesses and hope
First catheter
The 1960s: Committees, controversy and future.
Where to go from here?
1970: peritoneal dialysis establishes as continued
therapy.
1990-2000s Change the natural history

Change the natural history, how?
EARLY DETECTION
OF AKI AND CKD.
ACTIVE SEARCH
FOR THE RENAL
TROPONIN
RECOGNITION OF
RENAL ANGINA
PREEMPTIVE
TRANSPLANTATION
NEW CRITERIA FOR

AKI (RIFLE-AKIN
STAGES) AND CKD
(STAGES 1-5).
TREATING
COMORBILITIES IN
A COOPERATIVE
EFFORT,
MULTIDICIPLICARY
CARE.

CKD OVERVIEW
Serious public health problem that is

rapidly approaching epidemic proportions.
One in nine americans age > 20 has CKD,

but most dont know it.

Silent killer lack of symptoms and

delay of diagnosis.

CKD OVERVIEW
26 million American adults
have CKD and millions of
others are at increased risk.
Early detection can help
prevent the progression of
kidney disease to kidney
failure.
Heart disease is the major
cause of death for all people
with CKD.
Glomerular filtration rate

(GFR)-MDRD is the best
estimate of kidney
function.
Hypertension causes
CKD and CKD causes
hypertension.
Coordinated care
between PCP -
nephrology improves
outcomes.

9th leading cause of death in the
U.S.
Number of deaths for leading causes of death: 2007
Heart disease: 616,067
Cancer: 562,875
Stroke (cerebrovascular diseases): 135,952
Chronic lower respiratory diseases: 127,924
Accidents (unintentional injuries): 123,706
Alzheimer's disease: 74,632
Diabetes: 71,382
Influenza and Pneumonia: 52,717
Nephritis, nephrotic syndrome, and nephrosis: 46,448
Septicemia: 34,828

Kidney Failure vs Cancer Deaths (in Thousands Kidney Failure vs Cancer Deaths (in Thousands) )
Lung
Cancer
Kidney
Failure
Colon
Cancer
Breast
Cancer
Prostate
Cancer
57
99
42
32
157
Minio AM, et al. Natl Vital Stat Rep. 2002;50:1-119.

Chronic Kidney Disease (CKD)
Includes all types and levels of kidney

dysfunction
Avoid usage of CRI and CRF, which do not

indicate severity of dysfunction
CKD is not etiology-specific and causation must

always be pursued
Kidney/Dialysis Outcomes Quality Initiative. Am J Kidney Dis. 2002;40:S1S246.

The CKD Epidemic
McCullough . McCullough . Rev Cardiovasc Med Rev Cardiovasc Med. 2002;3:71-76. . 2002;3:71-76.
Epidemic Drivers
Epidemic Drivers
Accelerated atherosclerosis
Increased AMI mortality
Procedural complications
Incident diastolic CHF
Increased heart failure mortality
Increased risk of arrhythmias
Accelerated atherosclerosis
Increased AMI mortality
Procedural complications
Incident diastolic CHF
Increased heart failure mortality
Increased risk of arrhythmias
Diabetes Diabetes
Hypertension Hypertension
CKD CKD
Obesity Obesity
26%
44%

CKD OVERVIEW
Incidence of CKD is
doubling every 10
years in the United
States
More patients
diagnosed since new
staging in 2007.

< 15
Stage 5
1529
Stage 4
3059
Stage 3
6089
Stage 2
> 90
Stage 1
The Prevalence of CKD in the General Population
3.6M
6.5M
G
F
R
0.4M
0.7M
15.5
M
Coresh et al: JAMA Nov 7, 07; 298(17):2038-2047. Coresh et al: JAMA Nov 7, 07; 298(17):2038-2047.
m
L
/
m
i
n
/
1
.
7
3
2
26 Million CKD Patients (US)

CKD: Care is Costly
CKD
Care
$19.3
Billion/Yr
Total NIH
Budget
$17.8
Billion/Yr
CKD Accounts for 6%
of Medicare Payments
Lost Income for pts is
$24 Billion/Yr
TH Hostetter, National Kidney Education Program, 2003.

ESRD: Disease of the Elderly
0
5
10
15
20
25
30
35
40
45
Percent (%)
0-19 20-39 40-59 60-79 >80
Age Group (Yr)
Cases of ESRD
n=361,031
5961
55,105
125,280
148,508
26,177
United States Renal Data System (USRDS) 1997 Annual Data Report.

United States Renal Data System (USRDS) 2000 Annual Data Report
WWW.USRDS.ORG.
ESRD: ^ Risk by Ethnicity
Racial Differences in ESRD in U.S.
reference
*
*
*
*P <0.0001
1.00
4.45
3.57
1.59
0
1
2
3
4
5
White Black Native Asian
O
d
d
s

R
a
t
i
o

ESRD: Racial Distribution for
Comorbidities in Dialysis (1999)
Diabetes mellitus as a primary diagnosis or contributing diagnosis.
Diabetes mellitus that requires insulin treatment, which is a subset of the diabetes category.
United States Renal Data System (USRDS) 2000
Annual Data Report WWW.USRDS.ORG
0
20
40
60
80
100
History of
Hypertension
Diabetes Congestive
Heart Failure
Diabetes
Insulin
Treated
P
e
r
c
e
n
t

o
f

P
a
t
i
e
n
t
s
Black Asian Native White
0
20
40
60
80
100
History of
Hypertension
Diabetes Congestive
Heart Failure
Diabetes
Insulin
Treated
P
e
r
c
e
n
t

o
f

P
a
t
i
e
n
t
s
Black Asian Native White

Am J Kidney Dis. 2003
Nov;42(5):972-81
Inpatient Days among
Elderly Medicare Pts
with CKD in the United
States.
Overall Rates of
Hospitalization

GFR and Hospitalization
Age-Standardized Rates of Hospitalization
13.54
17.22
45.26
86.75
144.61
0
20
40
60
80
100
120
140
160
>=60 45-49 30-44 15-29 <15
Estimated GFR (mL/min/1.73 m2)
A
g
e
-
S
t
a
n
d
a
r
d
i
z
e
d

R
a
t
e

o
f

H
o
s
p
i
t
a
l
i
z
a
t
i
o
n

(
p
e
r

1
0
0

p
e
r
s
o
n
-
y
r
)
Go et al. New Engl J Med. 2004;351:1296-1305.

NKF Nephrology initiative
a) Early CKD identification mechanism.

b) Algorithmic approach that collaboratively
involves PCPs and Nephrologists.

Timely Referral Keeps pts Out of
the Blue Zone
Kidney/Dialysis Outcomes Initiative. Am J Kidney Dis. 2002;39:S1S266.
GFR (mL / min / 1.73 m
2
) GFR (mL / min / 1.73 m
2
)
2
90
1
120
3
60
4
30
E
S
R
D
5
15
NORMAL AGE DECLINE
REFER
TO
KIDNEY
DOCTOR
REFER
TO
KIDNEY
DOCTOR
NKF CKD Stage by MDRD GFR Equation NKF CKD Stage by MDRD GFR Equation
Refer in Stage 1 or 2:
Uncontrolled HTN
Hematuria
Proteinuria
Structural lesion

CKD: Early CKD Treatment
Preserves Kidney Function
TH Hostetter, National Kidney Disease Education Program, 2003.
GFR
Time (yr.)
100
75
50
25
10
4 7 9 11

CKD : Three-Fold Initiative
1. Screen and prevent CKD in pts who are
at-risk.
2. Develop an early CKD identification
process.
3. Establish a collaborative disease
management model for internists, family
practitioners, and nephrologists

RISK FACTORS OF CKD
DM, HTN

Risk Factors for CKD
Consider evaluation
Consider evaluation
Diabetes Diabetes
Hypertension Hypertension
Older age Older age
Male gender Male gender
Family history of kidney disease or diabetes Family history of kidney disease or diabetes
1
st
degree relatives of ESRD pts
MYH9 and
APOL1 gene polymorphisms.
Periodontal Dz, inflammatory state Periodontal Dz, inflammatory state
Small number of nephrons: nephrect, low Small number of nephrons: nephrect, low
birth weight, kidney recipients. birth weight, kidney recipients.
Autoimmune disease Autoimmune disease
Viral hepatitis: HBV-MN/MPGN Viral hepatitis: HBV-MN/MPGN
HCV- MPGN/cryoglob. HCV- MPGN/cryoglob.
HIV HIV HIV-associated HIV-associated
nephropathy, nephrotoxins nephropathy, nephrotoxins
Racial/Ethnic Background: Racial/Ethnic Background:
African American African American
Native American Native American
Asian-American Asian-American
Pacific Islander Pacific Islander
Latin American Latin American
Substance abuse: Substance abuse:
Tobacco , cocaine, heroine (HAN) Tobacco , cocaine, heroine (HAN)
Recurrent kidney stones Recurrent kidney stones
CHF- cardiorenal syndrome CHF- cardiorenal syndrome
Liver disease: Hepatorenal Liver disease: Hepatorenal

syndrome/ATN syndrome/ATN
Sepsis nephrotoxic AB Sepsis nephrotoxic AB
Vol depletion Vol depletion
Recurrent AKI Recurrent AKI
Chronic use of NSAIDS Chronic use of NSAIDS
Concomitant use of NSAIDs and Concomitant use of NSAIDs and

ACEI/ARBs. ACEI/ARBs.


Tobacco Use:
Tobacco Use:
Independent CV
Independent CV
risk factor among
risk factor among
patients with CKD
patients with CKD

Detection of pts at Risk
Detection of pts at Risk
BUN = blood urea nitrogen; GFR = glomerular filtration rate.
Pereira. Personal communication.
Measures of Kidney
Function
Serum creatinine
BUN
Creatinine clearance
GFR
Markers of
Kidney Damage
Microalbuminuria
Overt proteinuria
Other Physiologic
Markers
Hemoglobin/hematocrit
Total cholesterol
Triglycerides
Calcium/phosphorus
Intact parathyroid hormone
Serum bicarbonate
Serum electrolytes
Albumin

CKD: High-Risk Groups
Diabetics with urine Alb:Cr ratios

>30 mg Alb/1 g Cr
Non-diabetics with urine Alb:Cr ratios

>300 mg Alb/1 g Cr
Non-diabetics with MDRD GFR

<60 mL/min/1.73 m
2

CKD: Screening and Prevention
Screening at-risk pts
Biochemical profile
Urinalysis with microscopic exam
Urine protein (albumin) determinations
MDRD GFR estimation

CKD: Three-Fold Initiative
2. Development of an early CKD
identification process

CKD: Evolution of GFR Estimating
Methods
BUN
S
Cr
BUN
S
Cr
Highly
Insensitive
For CKD
Detection
Highly
Insensitive
For CKD
Detection
24-h CrCl 24-h CrCl
Overestimates GFR
Unnecessary test
Overestimates GFR
Unnecessary test
Cockroft
Gault Eqn
Cockroft
Gault Eqn
Estimates raw
CrCl, not GFR
Estimates raw
CrCl, not GFR
MDRD
GFR Eqn
MDRD
GFR Eqn
Validated
Best choice
Validated
Best choice
A Akbari, et al. Arch Intern Med. 2003;163:356360.
S Klahr, et al. MDRD Study Group. N Engl J Med. 1994;330:877884.

CKD: MDRD GFR
Multi-variable equation
Demographics: Age, Gender, Ethnicity

Biochemical: Albumin, S
Cr
, BUN
Validated in 577 pts
By iothalamate clearance
For GFRs 3090 mL/min/1.73 m

2
MDRD GFR Eqn. 7 (mL/min/1.73 m

2
)
= 170 S
Cr
0.999
Age
0.176
BUN
0.17
Alb
0.318
0.762 (female) ; 1.18 (African-American)
G Manjunath, et al. Postgrad Med. 2001;110(6):5562.

CKD: Classification by MDRD GFR
Rationale for use
GFR direct measurement of kidney

function
GFR best index of kidney function in

health and disease
GFR correlates with pathologic severity

of disease
GFR correlates functional level with risks

of CKD progression and development of
CV disease
G Manjunath, et al. Postgrad Med. 2001;110(6):5562.

SPECIAL POPULATIONS:
GFR
Not good estimation

of renal function in:
Elderly
Obese
Advanced CKD
Creatinine
Not good estimation of renal

function in
Extremes of life
Malnourished
Paraplejic
Liver Dz
Obese patients
Vegeterians??

CKD: NKF Definition
Disorder must be >3 mo duration
MDRD GFR <90 mL/min/1.73 m
2
or
GFR >90 mL/min/1.73 m
2
with either
Parenchymal abnormality (cyst, scar) or
Hematuria (>4 RBCs/hpf) confirmed by microscopical
examination on 2 occasions or
Proteinuria (2 occasions, 1 mo apart)
Dipstick 2+ or 100 mg/dL
Pro:Cr ratio 1.0 (Pro and Cr in mg/dL)
Alb:Cr ratio 500 mg/g
24-h collection 1.0 g/24-h/1.73 m
2
S Klahr, et al. N Engl J Med. 1994;330:877.

CKD: Normal Kidney Function
MDRD GFR >90 mL/min/1.73 m

2
and all of
the following
No hematuria
No proteinuria
No parenchymal or structural abnormality

(cyst, scar, hydronephrosis)

CKD: Age-Related Decline in GFR
Age-related declines in GFR occur
Should not be considered disease
GFR 6089 mL/min/1.73 m

2
Do not refer pt to nephrologist if GFR is

stable and all of the following
No proteinuria
No hematuria
No structural lesion(s)

RENAL AGING?

RENAL AGING?
Between the ages of 50 and 80 years the
renal mass diminishes by a mean of 20
percent, to the expense of the renal
cortex.
Glomerular sclerosis results in a gradual
fall in the number of functioning
glomeruli.
7 % decrease of GFR/ decade after the
age of 40 years. (~0.5-1 ml.year).

10% decrease in renal plasma flow /
decade.
Increased filtration fraction.
Delay in renal adjustment to sodium
overload
Decrease in concentrating and, to a
lesser extent, diluting capacity.
Intensity of glomerular sclerosis varies
considerably from one subject to another,
and the decrease in GFR is far from being
constant.
These changes are perhaps not ineluctably
associated with aging; they might result
from pathological processes that have gone
unnoticed.

<15 or dialysis Kidney failure 5
1529 Severe GFR 4
3059 Moderate GFR 3
6089* Mild GFR 2
> 90 Chronic kidney damage
with normal or GFR
1
GFR Description Stage
GFR: mL/min/1.73 m
2
*May be normal for age PrepublishedStaging Classification
<15 or dialysis Kidney failure 5
1529 Severe GFR 4
3059 Moderate GFR 3
6089* Mild GFR 2
> 90 Chronic kidney damage
with normal or GFR
1
GFR Description Stage
GFR: mL/min/1.73 m
2
*May be normal for age PrepublishedStaging Classification
NKF CKD Stages 15

CKD: Screening and Prevention
Summary
Spot urine Alb:Cr
ratio is adequate!!!

CKD: Three-Fold Initiative
3. Establishment of a collaborative disease
management model between internists
and family practitioners and
nephrologists

CKD: Under-recognized Problem
Patients unaware
Only 13% of pts with CrCl <60 mL/min or

+1 dipstick proteinuria aware of their CKD
Only 8% of pts with known CKD aware

of their CKD, despite recent physician
visit
Am J Kidney Dis. 2002;40:11731178.

CKD: Under-recognized Problem
Only 10% of Medicare beneficiaries with

diabetes receive annual urine albumin
tests
Less than 1/3 of hospitalized CKD pts with

proteinuria are prescribed an ACEI at
discharge
Medicare data on file: WM McClellan, et al. Am J Kidney Dis. 1997;29:368.

CKD: Survey of PCPs
A Stack. Am J Kidney Dis. 2003;41:310318.
CKD: Delayed Referral to
Nephrologist

CKD: Reasons for Delayed
Referral to Nephrologist
CKD is under-recognized, GFR not meassured.
Failure to screen pts at-risk
Fear of loss of control over pt
PCPs unaware of incremental benefits of

earlier referral
Fewer ER visits (pulmonary edema)
Significant healthcare cost savings
Lack of education regarding CKD management

R Sesso, AG Belasco. Nephron Dial Transplant. 1998;11:2417. DW Eadington. Nephron Dial
Transplant. 1996;11:2124-2126. RJ Schmidt, et al. Am J Kidney Dis. 1996;32:278283. P Jungers,
et al. Kidney Int. 1993;41:S170S173.

CKD: Consequences of Delayed
Referral
A Stack. Am J Kidney Dis. 2003;41:310318.
Late referral means <4 mo between time of initial Nephrology consultation and dialysis.
AVF, arteriovenous fistula; AVG, arteriovenous graft.
15.8 21.1 Malnutrition (%)
30.7 29.8 Hct at Referral (%)
3.53 3.41 Albumin (g/dl)
40.8 22.6 Received Vascular Access (%)
68; 23 Death Risk ^at 1- and 2-Yr (%)
Time to Referral
>4 mo <4 mo Parameter
32 10.5 Tx with EPO (%)
14.5; 26.3 5.7; 16.9 Access Type (AVF; AVG) (%)
15.8 21.1 Malnutrition (%)
30.7 29.8 Hct at Referral (%)
3.53 3.41 Albumin (g/dl)
40.8 22.6 Received Vascular Access (%)
68; 23 Death Risk ^at 1- and 2-Yr (%)
Time to Referral
>4 mo <4 mo Parameter
32 10.5 Tx with EPO (%)
14.5; 26.3 5.7; 16.9 Access Type (AVF; AVG) (%)

CKD: Delayed Referral Results in
Higher Medical Costs in Early
ESRD
Source: BA Boissonault for the Niagara Health Quality Coalition, 2003.

Ultimate Goal
Delay CKD Progression
Diagnose / treat comorbid conditions
Evaluate / treat CVD
Iatrogenic risks @ CKD Stage 3
protect against further insults (e.g., AKI)

PREVENT & STABILIZE
CKD STAGE 4
A Clinical Event

CKD: AKI Prevention
Rationale for Intervention
AKI often preventable
AKI produces residual kidney

damage, i.e., CKD
CKD pts at higher risk for AKI

PA McCullough, et al. Am J Med. 1997;103:368375
L Gruberg, et al. J Am Coll Cardiol 2000;36:15421548

INTRODUCTION
AKI INCREASED MORTALITY AND ESRD

CKD: Increased Risk for AKI
ECF volume depletion fosters AKI
High-risk groups
DM, types 1 and 2
Non-DM CKD Stage 35 (i.e., GFR <60)*
Liver failure
Heart failure
CV operations
Radiocontrast procedures
E Nikolsky, et al. Rev Cardiovasc Med 2003;4(Suppl 1):S7S14.
*Data extrapolated from multiple studies

Avoid Iatrogenic Injury
AVOID NEPHROTOXINS
NSAIDs, AGs, Amphotericin B
Radiocontrast
1. Stop diuretics 34 d before
procedure
2. ECF volume expansion
(preferably with HCO
3
?)
3. N-Acetylcysteine (S
Cr

dependent)
Preferred contrast media
Non-ionic, low osmolar
contrast
Iso-osmolar agents, if
available
AVOID NEPHROTOXINS
NSAIDs, AGs, Amphotericin B
Radiocontrast
1. Stop diuretics 34 d before
procedure
2. ECF volume expansion
(preferably with HCO
3
?)
3. N-Acetylcysteine (S
Cr

dependent)
Preferred contrast media
Non-ionic, low osmolar
contrast
Iso-osmolar agents, if
available
Contrast induced
nephropathy
Significant morbidity and / or
mortality
Event-free survival is + by
contrast nephropathy
In-hospital mortality + by
contrast nephropathy
M Tepel, et al. NEJM, 343:180184, 2000
C Caputo, et al. AJKD Dis 39:A14, 2002 (abstract)

Biphosphonates in CKD stage IV-V
Milk of Mag (risk of Mg toxicity)
Fleet enemas (Sodium phosphate toxicity)
Antiacids with aluminum (aluminum tox-

neuropathy-adynamic bone disease).
Regular-over-the-counter MVI in advanced

CKD risk of retinal toxicity due to vit A. (give
renal caps, nephro-vite instead).
Dose all meds for e GFR. (less than 10 if patient

in acute kidney injury).
Low molecular weight heparins, caution in

advanced CKD, no RCC proven safety.

NEPHROGENIC SYSTEMIC FIBROSIS
Avoid gadollinium if GFR <30:
Painful, debilitating or fatal.
characterized by pain and thickening of the skin

and fibrosis of almost all organs in the body.
It can involve the joints and cause significant

limitation of motion within weeks to months.
Irreversible. Role HD unclear.
Liability

P
eff
P
eff
P
eff
P
eff
Acute Kidney Injury: NSAID-Induced
Afferent Arteriolar Constriction
VA Valentini, et al. Arch Intern Med. 1991;151:23672372.
R
AA
, afferent arteriolar resistance.
P
aff
P
aff
NSAID
P
aff
P
aff
P
GC
P
GC
^ R
AA
NORMAL
P
GC
NORMAL
P
GC

NSAIDS
NSAIDs (COX-1/-2 inhibitors) lower GFR,

retain sodium and may cause
hyperkalemia.
May cause secondary glomerula disease

with chronic use including membranous
nephropathy, minimal change disease,
AIN.

People at risk for NSAID-induced
AKI
Activated Renin-
Angiotensin-
Aldosterone system:
_ Advanced age
Diabetes
Hypertension
Dehydration
Concomitant diuretic
use
Nephrotoxin co-
administration:
NSAID (not aspirin)
Diuretics
ACEI, ARB
Aminoglycosides
Cyclosporine,
tacrolimus
cis-platinol

NSAID+ACEI/ARB if renal
autoregulation is already impaired

NSAIDS
ACEI/ARBS

CKD Guidelines for Treatment
National Kidney Foundations Kidney

Disease Outcomes Quality Initiative
(NKF KDOQI)
Based heavily on Evidenced Based

Medicine
Offers opinions that guide treatment

NKF Guidelines address
domains of CKD care

NKF Guidelines address
domains of CKD care
Periodic
eGFR
Cancer
Screening

Decrease CV Disease Risk
Factors

CV risk factor modification

Shulman et al. Hypertension. 1998;13(supple 1):I-80I-93.
Major Cause of Death in CKD
Cardiovascular Disease

CKD: CVD Risks
CVD risk + 1.42.05 X if S
Cr
>1.41.5 mg/dL.
CVD risk + 1.53.5 X with microalbuminuria.
First-year CVD mortality of CKD (3.5%) increases

5-fold (17%) with addition of diabetes.
Annual CVD +10100 X in ESRD.

Multiple Sources: J Flack, et al., 1993. AS Levey, et al., 1998. Jensen, et al., 2000.
Ruilope, et al., 2001. JFE Mann, et al. 2001. AS Collins, et al., 2002.

CKD should be considered

an equivalent to CAD

Hypertension & CKD

Guideline: Hypertension
1.1 Antihypertensive therapy should be used in CKD to:
1.1.a. Lower blood pressure (A);
1.1.b. Reduce the risk of CVD, in pts with or without hypertension (B)
1.1.c. Slow progression of kidney disease, in pts with or without
hypertension (A)
1.2 Modifications to antihypertensive therapy should be considered
based on the level of proteinuria during treatment (C)
1.3 Antihypertensive therapy should be coordinated with other
therapies for CKD as part of a multi-intervention strategy (A).
1.4 If there is a discrepancy between the treatment recommended to
slow progression of CKD and to reduce the risk of CVD,
individual decision-making should be based on risk stratification
(C).

JNC 7 Reclassification of BP
Based on Risk
Source for JNC VI: Arch Intern Med. 1997;157:2413-2446.
Adapted from Chobanian AV, et al. Hypertension. 2003;42:1206-1252.
Optimal
Normal
<120/80
<120/80
Stage 1
Hypertension
Stage 1 140-159/90-99 140-159/90-99
Normal
Borderline
Prehypertension
120-129/80-84
130-139/85-89
120-139/80-89
Stage 2
Stage 3
Stage 2
160-179/100-109
180/110
160/100
JNC VI
BP (mm Hg)
JNC VI
BP (mm Hg)
JNC 7
BP (mm Hg)
JNC 7
BP (mm Hg)

HTN Treatment by JNC 7
HTN w/ No
Compelling Indications
HTN w/ No
Compelling Indications
Stage 1 HTN
(SBP 140-159 or
DBP 9099 mmHg)
Thiazide
diuretic for most
Consider
ACEI, ARB,
-blocker, CCB
or combination
Stage 1 HTN
(SBP 140-159 or
DBP 9099 mmHg)
Thiazide
diuretic for most
Consider
ACEI, ARB,
-blocker, CCB
or combination
Stage 2 HTN (SBP
160 or DBP 100
mmHg)
2-drug combo
for most
Usually thiazide +
ACEI, ARB,
-blocker, or CCB
Stage 2 HTN (SBP
160 or DBP 100
mmHg)
2-drug combo
for most
Usually thiazide +
ACEI, ARB,
-blocker, or CCB
Drug(s) for
compelling
indications
Other BP drugs
(thiazide + ACEI,
ARB, -blocker,
CCB)
as needed
Drug(s) for
compelling
indications
Other BP drugs
(thiazide + ACEI,
ARB, -blocker,
CCB)
as needed
C(KD)ompelling
Indications
C(KD)ompelling
Indications
Chobanian AV, et al. The JNC 7 Report. JAMA. 2003;289:2560-2572.
Compelling indications: CHF, post-MI, high risk of CAD, DM, CKD, stroke, migraine

BP Targets in Diabetic and
Nondiabetics
with Kidney Disease
Type of Kidney
Disease
BP Target
(mm Hg)
Preferred Agents
for CKD, with or
without HTN
Other Agents to
Reduce
CVD Risk and Reach
BP Target
Diabetic CKD
SBP
<125130
DBP
<7580
ACE inhibitor
or ARB
Diuretic preferred,
then BB or CCB
Nondiabetic CKD
UPC 200 mg/g
Nondiabetic CKD
UPC <200 mg/g
None preferred Diuretic preferred,
then ACEI/ARB,
BB or CCB
CKD in TX Recipient CCB, diuretic, BB,
ACE inhibitor, ARB
Am J Kidney Dis, May (Suppl.), 2004

HTN Treatment in CKD
Diabetic or Nondiabetic

Hypertension in CKD
Elevated BP worsens CKD
GFR declines faster with HTN
Rapid decline rate is >4 ml/min/1.73 m
2
/yr
Target BP
<130/80 mmHg if proteinuria <1 g/d
<125/75 mmHg if proteinuria >1 g/d

BP Control Prevents CKD
Progression
GFR
Decline
(mL/min/y)
0
-2
-4
-6
-8
-10
-12
-14
MAP (mm Hg)
95 98 101 107 104 110 113 116 119
r=0.69; P<.05
Untreated
HTN
130/85 140/90
GFR, glomerular filtration rate; HTN, hypertension; MAP, mean arterial pressure.
Adapted from Bakris GL et al. Am J Kidney Dis. 2000;36:646-661.

Hypertension & CKD
Optimal BP Control
No edema
Limit daily sodium intake
6 gm NaCl (102 mEq)
2400 mg sodium (104 mEq)
Diuretics
GFR >40 ml/min/1.73 m
2
, HCTZ
GFR <40 ml/min/1.73 m
2
, loop agent
RAAS blockade
ACEI
ARB
ACEI+ARB ? INCREASED
INCIDENCE OF ESRD AND MORTALITY
ON TARGET TRIAL

Glycemic Control

84
Diabetes (DM) affects more than
170 million people worldwide
Number will rise to 370 million by 2030

About 1/3 of affected will eventually

develop progressive renal deterioration
Microalbuminuria (MA) develops in

25% of pts per year
25% of pts per year



25% of pts per year
25% of pts per year
Type 2 Diabetic Nephropathy
Global Perspective

Epidemiology of Diabetes
19 million persons
0.5 million type 1 DM
Remainder, type 2
Over-representation in ESRD population

worldwide
Over-representation in U.S. ESRD population
Incidence increasing with rate of obesity

Predictions Regarding T2DM
A. Year 2000 and beyond
One of three newborns will develop type II

diabetes as an adult
One of two newborns, Hispanic or African

American, will develop type II diabetes as an
adult
A. Year 2050
A. U.S.: 4550 million will develop T2DM
C. Implications for CKD and RRT uncertain
Dr. KM Venkat Narayan

DM
50%
HTN
27%
GN 13%
Other
10%
ESRD: Etiology by 1 Diagnosis
United States Renal Data System (USRDS) 2000 Annual Data Report
WWW.USRDS.ORG.

Natural History of Diabetic Nephropathy
Proteinuria
End-stage
renal disease
Functional changes*
Structural changes
Rising blood pressure

Rising serum
creatinine levels
Cardiovascular death
Microalbuminuria
Insulin resistance syndrome
Clinical type 2 diabetes
Years
20 30 10 5 2 -1
Proteinuria
End-stage
renal disease
Functional changes*
Structural changes
Rising blood pressure

Rising serum
creatinine levels
Cardiovascular death
Microalbuminuria
Insulin resistance syndrome
Clinical type 2 diabetes
Years
20 30 10 5 2 -1

Glomerulus: Site of Hyperfiltration
in Diabetes and Obesity

Glycemic Control Retards
Progression of CKD
Adapted with permission from Skyler JS. Endocrinol Metab Clin North Am. 1996;25:243
Retinopathy
Nephropathy
Neuropathy
Microalbuminuria
R
e
l
a
t
i
v
e

R
i
s
k
A
1
C (%)
15
13
11
9
7
5
3
1
6 7 8 9 10 11 12
*
Based on Diabetic Control and Complications Trial data
50%
Reduction

HbA1c: Delay DN
EUGLYCEMIA
Partially reverses glomerular hypertrophy and

hyperfiltration
Type 1 DM delays onset of

microalbuminuria
Kidney-Pancreas transplant pancreatic

transplant prevents recurrent nephropathy in
allograft kidney
EUGLYCEMIA
Partially reverses glomerular hypertrophy and

hyperfiltration
Type 1 DM delays onset of

microalbuminuria
Kidney-Pancreas transplant pancreatic

transplant prevents recurrent nephropathy in
allograft kidney
Fioretto, et al. New Engl J Med 339:6975, 1998

AGENTS
Glipizide oral hypoglycemic drug of choice in patients
with CKD
Glyburide can be given at reduced dose if the GFR is
above 50 mL/min, but should be avoided with more
severe renal Dz.
Glimepiride (amaryl) use with cautionif GFR <22.
Thiazolidinediones associated with HF, rosiglitazone
has associated with increased all-cause and
cardiovascular mortality in dialysis patients.
AVOID IN CKD MOSTLY IF CHF.

AGENTS
Acarbose largely renally excreted, no in

CKD.
Nateglinide or repaglinide renally

excreted, avoid in advanced CKD.
Metformin Stop when Cr = 1.5, risk of

life-threatening lactic acidosis emergent
dialysis.

Proteinuria Reduction

Proteinuria
Dual Significance
Proteinuria results from injury to

glomerular circulation
Increased proteinuria is associated with

progressive CKD
In diabetes and hypertension, proteinuria

signifies injury to the systemic circulation
Proteinuria is associated with increased

CV risk

CKD: Anti-Proteinuric Therapy
Microalbuminuria independent CVD risk

factor
In-hospital mortality + 3-fold by proteinuria

(100 mg pro/g Cr)
Proteinuria correlates with CKD progression
Proteinuria may worsen CKD

Adapted from multiple studies. HOPE subanalysis: JFE Mann, et al. J Am Soc Nephrol.
2003; 14:641647. MARVAL: Circulation. 2002;106:672-678. RENAAL: N Engl J Med.
2001;345:861869. IDNT: N Engl J Med. 2001;345:851860.

Albuminuria Decreases Survival
Graded Effect
1.0
0.9
0.8
0.7
0.6
0.5
0 1 2 3 4 5 6
Years
S
u
r
v
i
v
a
l

(
a
l
l
-
c
a
u
s
e

m
o
r
t
a
l
i
t
y
)
Normoalbuminuria
(n=191)
Microalbuminuria
(n=86)
Macroalbuminuria
(n=51)
P<0.01 normoalbuminuria vs microalbuminuria
P<0.001 normoalbuminuria vs macroalbuminuria
P<0.05 microalbuminuria vs macroalbuminuria
Gall MA, et al. Diabetes. 1995;44:1303-1309.
Copyright 1995, American Diabetes Association. Reprinted with permission.
www.hypertensiononline.org
Gall MA, et al. Diabetes 1995;44:1303-1309

Renin-Angiotensin System
Blockade
Moderate to high doses of ACEIs / ARBs

have been associated with beneficial effects
on kidney disease progression in controlled
trials
Where tested, ACEIs / ARBs have generally

similar effects on BP, urine protein excretion,
and slowing CKD progression
Greatest efficacy in proteinuric disorders

ACEIs / ARBs
Clinicians often avoid / withdraw ACEIs /

ARBs in CKD
fearing hyperkalemia or S
Cr
Tolerate
up to 30% increases of S
Cr

[K] of 5.55.8 mEq/L
Kidney dietitian, not Kayexelate

FF Hou, et al. NEJM, 2006.

Alternative to RAAS Blockers
Non-dihydropyridine CCBs for those who cannot tolerate
anti-RAAS agents, especially with proteinuria
Diltiazem
Verapamil
Direct renin-inhibitors (Tekturna) ?

CKD: Anti-Proteinuric Therapy
RAAS blockade
ARBs preferred in type 2 diabetic nephropathy
ACEIs preferred in type 1 diabetic

nephropathy
Quantitate proteinuria q1-2 mo
Proteinuria reduction maximized by

Week 8 of tx
Perform spot urine tests to assess efficacy

From HOPE: JFE Mann, et al. J Am Soc Nephrol 2003; 14:641647.
MARVAL. Author. Circulation 2002;106:672-678. RENAAL. BM Brenner, et al. N Engl J Med
2001;345:861869. IDNT. EJ Lewis, et al. N Engl J Med;345:851860.

RENAAL: Combined CCB and ARB
Reduce Progression to Diabetic
Nephropathy
Adapted from RENAAL Study. BM Brenner, et al. N Engl J Med. 2001;345:861869.
R
AA
, afferent arteriolar resistance. R
EA
, efferent arteriolar resistance.
P
eff
P
eff
P
aff
P
aff
CCB
P
eff
P
eff
P
aff
P
aff
NORMAL
P
GC
NORMAL
P
GC
+R
AA
ACEI (type 1 DM)
ARB (type 2 DM)
+R
EA
NORMAL
P
GC
NORMAL
P
GC

Lipid Control

Guideline: Lipids in CKD 14
1.1. All adults and adolescents with CKD should be
evaluated for dyslipidemias. (B)
1.2. For adults and adolescents with CKD, the
assessment of dyslipidemias should include a
complete fasting lipid profile with total
cholesterol, LDL, HDL, and triglycerides. (B)
1.3. For adults and adolescents with Stage 5 CKD,
dyslipidemias should be evaluated upon
presentation (when the pt is stable), at 23 MO
after a change in treatment or other conditions
known to cause dyslipidemias; and at least
annually thereafter. (B)

Treatment of Dyslipidemia
Therapeutic Targets
CKD pts are considered the highest CV

risk population
Primary Target: LDL-C reduction to <70-

100 mg/dL
Secondary Target: TG reduction to <150

mg/dL
Constant reinforcement of therapeutic
lifestyle changes

CKD Dyslipidemia Treatment
Smoking cessation
Aspirin use
Wt loss
Aerobic Exercise
Statins
Fibric Acid Derivatives
LDL Goal < 100mg/dL, HDL > 40mg/dL, TG

< 150mg/dL, Non-HDL-C < 130mg/dL
K/DOQI Clinical Practice Guidelines for Managing Dyslipidemias in Chronic Kidney
Disease. Am J Kidney Dis 2003:41(Suppl 3):S1S91.

CKD: Dyslipidemia Therapy
HMG-CoA synthetase inhibitors
Fibric acid derivatives
Use with caution
Gemfibrozil preferred
Cholesterol absorption inhibitor
Ezitimibe (Zetia) statin-sparing
No controlled trials in CKD

Kidney/Dialysis Outcomes Quality Initiative Clinical Practice Guidelines for Managing
Dyslipidemias in Chronic Kidney Disease. Am J Kidney Dis. 2003:41(Suppl 3):S1S91.

Anemia of CKD

Adapted from Radtke, et al. Blood. 1979;54:877884 (original study used Hct).
CKD: Anemia O as GFR O
GFR (mL/min/1.73 m
2
)

M
e
a
n

H
b
*

(
g
/
d
L
)
91 91 9040 9040 3930 3930 2920 2920 1910 1910 < < 10 10
n=18 n=59 n=18 n=34 n=18 n=29
5
6
7
8
9
10
11
12
13
14
15

CKD: Anemia Induces LVH
Excerpt: H Hampl, L Henning and E Riedel. Dialysis Times 2003;9(5):16
A Mohanran and AS Kliger presentations at NKF Meeting 2003

NKF KDOQI Guideline & CPR 2.1:
Hb range
Moderately strong recommendation

2.1.1 Lower limit of Hb
In pts with CKD, the Hb should be 10- 11
g/dL, GOALS TO CHANGE. Increased
mortality with higher Hb. (>11-12?).
2.1.2 Upper limit of Hb

In the opinion of the Work Group, there is
insufficient evidence to recommend routinely
maintaining Hb levels > 12 g/dL in ESA treated
pts, increased mortality, DM high risk population.

CKD: Anemia Therapy
Anemia worsens with CKD progression
Tx regresses LVH/LVMI
Tx prevents CHF and hospitalization
Tx slows CKD progression?
QOL improved by O Hb
Cognition
Sexual function
Exercise tolerance
Excerpt: H Hampl, et al. Dialysis Times 2003;9(5):16. Presentations: A Mohanran
and AS Kliger. National Kidney Foundation Annual Meeting, 2003.

IV Iron May Have an Independent
Erythropoietic Effect in HD
*P <0.01 vs baseline.
Fudin et al. Nephron. 1998;79:299305.
39 new HD pts (no EPO therapy) with baseline iron deficiency by
bone marrow aspiration.
39 new HD pts (no EPO therapy) with baseline iron deficiency by
bone marrow aspiration.
H
g
b
,

g
/
d
L
*
*
5
6
7
8
9
10
11
IV Iron Oral Iron No Iron
Baseline
12 mo
26 mo

CKD: Anemia Therapy
Begin tx at Hb <11 g/dL (Hct 33%)- <10?
Steps (by Nephrology CKD Clinic)
1. Replete iron stores
Oral iron salts
Iron dextran (INFeD) or
Iron gluconate (Ferrlecit) or
Iron sucrose (Venofer)
1. Use erythropoietic agent
Epoetin- (Procrit) or
Darbepoetin (Aranesp)
J Yee, A Besarab. Am J Kidney Dis 2002;40:11111121

CKD: Anemia Therapy
Targets
Hb >11 g/dL (Hct 33%)
TSAT >20%; Ferritin >100 ng/mL
EPO level
Does not predict marrow response
Two-thirds of levels in normal range
Do not obtain EPO levels
R/O blood loss and/or iron deficiency

A Besarab, J Yee. J Am Soc Nephrol 1999;10:20292043
AR Nissenson. Am J Kidney Dis 2001;38:13901397

Chronic Kidney DiseaseMineral
and Bone Disorder

Position Statement from KDIGO
(Kidney Disease Improving Global Outcomes)
Definition of CKD-MBD
A systemic disorder of mineral and bone
metabolism due to CKD manifested by either one
or a combination of the following:
Abnormalities of calcium, phosphorus, PTH, or

vitamin D metabolism
Abnormalities in bone turnover, mineralization,

volume, linear growth, or strength
Vascular or other soft tissue calcification

Definition, evaluation, and classification of renal osteodystrophy. KI, April 2006

Definition of Renal Osteodystrophy
Renal osteodystrophy is an alteration of bone
morphology in pts with CKD.
It is one measure of the skeletal component
of the systemic disorder of CKD-MBD that is
quantifiable by histomorphometry of bone
biopsy.
Definition, evaluation, and classification of renal osteodystrophy. KI, April 2006
Position Statement from KDIGO
(Kidney Disease Improving Global Outcomes)

CKD: Metabolic Bone Disease
Consequence of + renal mass

+ Vitamin D
3

^ P
+ Ca
2+
Metabolic acidosis
Increased protein catabolism
Increased bone lysis / loss

Draft: Kidney/Dialysis Outcomes Initiative Clinical Practice Guidelines for Bone
Metabolism and Disease. National Kidney Foundation Task Force, 2003

Definition any / all metabolic bone

disorders associated with CKD
2 hyperparathyroidism
Osteoporosis
Osteomalacia
Adynamic bone disease
Mixtures of above
KA Hruska, SL Teitelbaum. New Engl J Med. 1995;333(3):166-174.
DJ Sherrard, et al. Kidney Int. 1993;43(2):436442.

Multiple aberrations of Ca/P/PTH and bone

metabolism accompany GFR decline.
Hyperphosphatemia is an independent CV
risk factor in ESRD (presumed in non-ESRD
CKD).
ESRD pts develop CV calcification (by

EBCT) from ^ Ca P product.
WG Goodman, et al. New Engl J Med. 2000;342(20):14781483.

+ Vit D
3
^
P
+
Ca
2+
^
PTH
^
PTH
CKD
Systemic Toxicity
Bone Disease
CKD: Pathophysiology of 2 HPT

CKD: Renal Osteodystrophy
Targets
Ca 8.49.5 mg/dL
P 2.75.5 mg/dL
Ca P <55 mg
2
/dL
2
HCO
3
2226 mEq/dL
PTH depending on stage of CKD


CKD: Renal Osteodystrophy
^ P ^ Relative Risk of Mortality
GA Block, et al. Am J Kidney Dis 1998;31:607617.
1.39**
1.18*
1.02
1
1
0.5
1.0
1.5
2.0
1.1-4.5 4.6-5.5 5.6-6.5 6.6-7.8 7.9-16.9
Serum Phosphorus Quintile (mg/dL)
R
e
l
a
t
i
v
e

M
o
r
t
a
l
i
t
y

R
i
s
k
1.39**
1.18*
1.02
1
1
0.5
1.0
1.5
2.0
1.1-4.5 4.6-5.5 5.6-6.5 6.6-7.8 7.9-16.9
Serum Phosphorus Quintile (mg/dL)
R
e
l
a
t
i
v
e

M
o
r
t
a
l
i
t
y

R
i
s
k

Vitamin D in CKD 3-4
Stages 3 and 4: Stages 3 and 4: Measure serum 25(OH) D in pts with Measure serum 25(OH) D in pts with PTH. PTH.
If normal, repeat q12 mo. If normal, repeat q12 mo.
NKF. Am J Kidney Dis. 2003;42(4 suppl 3):S1-S201.
Level Treatment with Vitamin D
2

(Ergocalciferol, 50,000 IU capsules)
<5 ng/mL 50,000 IU/wk x 12, then q MO x 6
515 ng/mL 50,000 IU/wk x 4, then q MO x 6
1629 ng/mL 50,000 IU/MO x 6
Normal 25(OH)D Normal 25(OH)D 30 ng/mL 30 ng/mL
Insufficiency <20-30 Insufficiency <20-30
Deficiency <20 ng/mL Deficiency <20 ng/mL
DO NOT MEASSURE VIT 1,25 OH DO NOT MEASSURE VIT 1,25 OH

Tx
Vascular calcification at any site
Avoid Ca-containing P-binders
Use sevelamer (not confined to ESRD)
Ca >10.2 mg/dL, stop calcitriol
Switch to non-Ca-containing P-binders (sevelamer)
Limit elemental Ca in Ca-based binders to 1500 mg/d or
sum of total dietary Ca plus elemental Ca to 2000 mg/d
P >5.5 mg/dL
Switch to non-Ca-containing P-binders (sevelamer)
Restrict P to 0.81.0 g/d if P >5.5 mg/dL
Restrict P to 0.81.0 g/d if PTH >50 pg/mL

High-Turnover Bone Disease Can
Result in Soft-Tissue Calcification
PTH
Calcium
Magnesium
Phosphorus
Calcification
Deposition
Into Tissues

Low-Turnover Bone Disease Can Result
in Soft-Tissue Calcification
Calcium
Magnesium
Phosphorus
Deposition
Into Tissues
Calcification
PTH

CKD: Metabolic Acidosis
The serum bicarbonate reflects the degree or

severity of systemic acidosis. This parameter
should be at 22 meq/L or greater, to offset
acidosis-driven bone lysis.
Bicarbonate therapy
NaHCO
3
dose: 0.51.0 mEq/kg bw/d
3.87 mEq per 325 mg tablet
7.73 mEq per 650 mg tablet
Usual CKD dose 1300 mg TID

FC Husted, et al. J Clin Invest. 1975;56(2):414419.

Acidosis Aggravates Renal
Osteodystrophy

Acidosis Treatment
May occur earlier in diabetic CKD,

compared to non-diabetic CKD
Type IV RTA
Treatment same in diabetic and non-

diabetic CKD
HCO
3
> 22 mEq/L
NaHCO
3
tablets (0.51.0 mEq/kg/day)
Verify acidemia with ABG

Nutritional Assessment

Nutrition Assessment
Dietician (RD) integral part of CKD

management.
Consultation at any CKD stage.
Utilize within 2 wk of initial consultation for

dietary assessment and recommendations.
RD will educate pts on food preparation

techniques increasing compliance with
dietary restrictions.

Rationale for RD consult
Malnutrition evolves during the

progression of CKD
Hypoalbuminemia and vitamin

deficiencies are common INCREASED
MORTALITY.
Diet high in biological value must be

maintained, while restricting Na, P, K

Intervention
Caloric restriction:
25 cal/kg of SBW to lose wt
30 cal/kg of SBW to maintain wt
3540 cal/kg of SBW to gain wt
Fluid restriction:
implement only if Na<132 mEq/L and pt is

compliant with low Na diet.
may be temporary

CKD: Nutrition Therapy
Consult Renal Dietitian at CKD Stage 3
Protein restrict @ GFR <25 mL/min/1.73 m

2
High biologic protein: 0.60.75 g/kg bw
Initiate dialysis if
GFR <1520 with energy malnutrition from low protein

intake
6% wt loss or <90% of IBW in <6 mo

Kidney/Dialysis Quality Outcomes Initiative Clinical Practice Guidelines for Managing
Dyslipidemias in Chronic Kidney Disease. Am J Kidney Dis 2003:41(Suppl 3):S1S91.

Vaccinations

Vaccinations
CKD pts immunocompromised
Despite immunodeficiency, CKD pt

immunized less frequently against flu and
S pneumoniae than general medical pts

Vaccinations: Recommendations
Annual influenza A/B
23-valent polysaccharide pneumoccocal

(Pneumovax, PPV23) Q6 years
HBV vax give at any CKD stage.

Immunization series should be
completed by stage 4 since late stage 5
vax induces lower Ab titers

Influenza Vax rates Below National
Target (Healthy People 2000)
Gilbertson et al, Kidney Int 2003; 63:738-743; MMWR 2001, 50:532-37
_______________ __________________________
Dialysis pts General Population
60%
30%
60%
39%
49%
0%
10%
20%
30%
40%
50%
60%
70%
80%
HD PD Whites Non Whites 2000

Odds of Hospitalization & Death are
Reduced In Vaccinated HD pts
0.6
0.7
0.8
0.9
1
1.1
1.2
1.3
Any Cause Influenza Any Cause Cardiac Infection
_________________ __________________________
Hospitalization Death
Gilbertson et al, Kidney Int 2003; 63:738-743

Evaluate Progression of CKD

Strategies to Improve Vascular
Access Education
NKF-K/DOQI Guidelines
Education when eGFR <30
Preserve arm veins suitable for placement of
vascular access, regardless of arm
dominance.
Arm veins, especially cephalic veins of the
non-dominant arm, should not be used for
venipuncture or iv catheters.

Vascular Access
Dorsum of the hand should be used for iv

lines. When venipuncture of the arm veins
is necessary, sites should be rotated.
Avoid subclavian vein cannulation

increases risk of central vein stenosis

DIALYSIS Arteriovenous Fistula
Surgically connect endogenous artery to
endogenous vein (no Gortex, AVG)
Safest and longest half-life of all accesses
Least expen$ive

Strategies to Improve Vascular Access Timing
of Access Placement
NKF-K/DOQI Guidelines
Refer to surgery for primary AVF

construction if
GFR <25 30 mL/min
within 1 yr of anticipated dialysis
AVF maturation time
Okay: >1 month
Ideal: 34 mo, prior to cannulation

Fistula: Disadvantages
Bulge unattractive
Never matures
Conversion to AVG, possible
Temporary HD catheter may be reqd

Vascular Access: AVG
Construction timing 3 to 6 weeks

before anticipated need
When AVG reserved for pts who are

not candidates for an AVF or where AVF
failed
Clot more frequently than AVFs
Overall half-life 2.5 yr

Catheters
Cannulation of large central vein
Temporary in most cases
Lower Qb, i.e., less efficient HD
Requires meticulous care
Much higher infection/mortality rates
~50% infection rate at 6 mo

Majority of Pts Start RRT Without
A Permanent Vascular Access
No
48.2%
Yes
43.9%
Unsure
7.9%
Held et al, AJKD 1996, 28 (Suppl. 2):58-78, USRDS DMMS I (1,997 pts incident in 1993)
Permanent Access Placed or Attempted Before Start of RRT ?

Vascular Access Used for the
First Chronic Hemodialysis
Pisoni et al, Kidney Int 61:305-16, 2002. Random sample of 2,179 US and 875
European pts who began HD between 7/1996-10/2000 (US) and 7/1998-10/2000
(Europe) DOPPS.
24%
60%
15%
66%
31%
2%
0%
10%
20%
30%
40%
50%
60%
70%
AV Fistula AV Graft Catheter
US Europe

Risk of Infectious Mortality is
Increased with Temporary
Access
1.00 1.00
2.47
1.27
2.30
1.83
0.0
0.5
1.0
1.5
2.0
2.5
3.0
R
R

o
f

I
D

M
o
r
t
a
l
i
t
y
Dhingra et al, Kidney Int 60:1443-51, 2001. Adjusted for age, gender, race, BMI, smoking,
education level, ability to ambulate, and history of PVD, CHD, CAD and cancer.
P <0.02 P <0.06 Ref. Ref. P <0.33 P <0.04
AVF AVG CVC
Diabetics Non-Diabetics
AVF AVG CVC

Pts With Temporary Access Have
Higher Rate of Hospital Utilization
Arora et al , JAmSocNephrol , 11:740-7476
17.6
14.6
13.7
22.7
12.1
41.9
0
10
20
30
40
50
Overall First 3 months After 3 months
N
u
m
b
e
r

o
f

h
o
s
p
i
t
a
l

d
a
y
s

p
e
r

p
a
t
i
e
n
t
-
y
r

a
t

r
i
s
k
Temporary Permanent

Fistula First Initiative
A national initiative to expand the number

of pts with AVFs, as opposed to
catheters or AVGs.
Year 2010: goal is 50% of all new pts on

HD. 66% of continued pts will use
fistulas.

Download information
Updated editions of
Chronic Kidney Disease (CKD): Clinical
Practice Recommendations For Primary Care
Physicians and Healthcare Providers
A Collaborative Approach (Ed 5.0)
can be downloaded from:
Ghsrenal.Com/CKD/Hfhs_CKD_Guidelines_v5.0.pdf

Renal Transplantation
Disease donor kidney transplant: 5-7 year

waiting list.
Living donation!!
Preemptive (before dialysis is needed)
Referal once eGFR <25
Prompt medical optimization.

Primary Care - Nephrology Interface: Providing Coordinated CKD Care

Transféré par

Informations du document

Description originale:

Titre original

Copyright

Formats disponibles

Partager ce document

Partager ou intégrer le document

Options de partage

Avez-vous trouvé ce document utile ?

Ce contenu est-il inapproprié ?

Droits d'auteur :

Formats disponibles

Primary Care - Nephrology Interface: Providing Coordinated CKD Care

Transféré par

Droits d'auteur :

Formats disponibles

PRIMARY CARE NEPHROLOGY

CKD history, background, prevalence,

Discuss occurrence of complications and

Overview of NKF (KDOQI) treatment

THE THREE ERAS OF MEDICINE IN

Predict natural history

Change the natural history

NEW CRITERIA FOR

Serious public health problem that is

One in nine americans age > 20 has CKD,

Silent killer lack of symptoms and

Glomerular filtration rate

Number of deaths for leading causes of death: 2007

Heart disease: 616,067

Stroke (cerebrovascular diseases): 135,952

Chronic lower respiratory diseases: 127,924

Accidents (unintentional injuries): 123,706

Alzheimer's disease: 74,632

Influenza and Pneumonia: 52,717

Nephritis, nephrotic syndrome, and nephrosis: 46,448

Includes all types and levels of kidney

Avoid usage of CRI and CRF, which do not

CKD is not etiology-specific and causation must

Racial/Ethnic Background: Racial/Ethnic Background:

African American African American

Native American Native American

Pacific Islander Pacific Islander

Latin American Latin American

Substance abuse: Substance abuse:

Tobacco , cocaine, heroine (HAN) Tobacco , cocaine, heroine (HAN)

Recurrent kidney stones Recurrent kidney stones

CHF- cardiorenal syndrome CHF- cardiorenal syndrome

Liver disease: Hepatorenal Liver disease: Hepatorenal

Sepsis nephrotoxic AB Sepsis nephrotoxic AB

Vol depletion Vol depletion

Recurrent AKI Recurrent AKI

Chronic use of NSAIDS Chronic use of NSAIDS

Concomitant use of NSAIDs and Concomitant use of NSAIDs and

Diabetics with urine Alb:Cr ratios

Non-diabetics with urine Alb:Cr ratios

Non-diabetics with MDRD GFR

Screening at-risk pts

Urinalysis with microscopic exam

Urine protein (albumin) determinations

MDRD GFR estimation

Demographics: Age, Gender, Ethnicity

Validated in 577 pts

For GFRs 3090 mL/min/1.73 m

MDRD GFR Eqn. 7 (mL/min/1.73 m

Rationale for use

GFR direct measurement of kidney

GFR best index of kidney function in

GFR correlates with pathologic severity

GFR correlates functional level with risks

Not good estimation

Not good estimation of renal

MDRD GFR >90 mL/min/1.73 m

No parenchymal or structural abnormality

Age-related declines in GFR occur

Should not be considered disease

GFR 6089 mL/min/1.73 m

Do not refer pt to nephrologist if GFR is