Contents

Contributors .................................................................... ix Chapter 8

Preface ............................................................................ xi Metabolic Alkalosis .......................................109
Acknowledgments..........................................................xiii Adam M. Franks, MD and Joseph I. Shapiro, MD

Chapter 1 Chapter 9
Introduction ......................................................1 Respiratory and Mixed AcidBase
Mark A. Perazella, MD Disturbances ................................................123
Adam M. Franks, MD and Joseph I. Shapiro, MD
SECTION I Fluids, Electrolytes and Acid-base ...... 11
Chapter 2 SECTION II Mineral Metabolism ....................... 131
Disorders of Sodium Balance ...........................13 Chapter 10
Robert F. Reilly Jr., MD Disorders of Calcium HomeostasisHypo
and Hypercalcemia ........................................133
Chapter 3 Nishank Jain, MD, MPH and Robert F. Reilly Jr., MD
Disorders of Water BalanceHypo
and Hypernatremia ..........................................27 Chapter 11
Robert F. Reilly Jr., MD Disorders of Phosphate HomeostasisHypo
and Hyperphosphatemia ................................149
Chapter 4 Nishank Jain, MD, MPH and Robert F. Reilly Jr., MD
Diuretics.........................................................47
Mark A. Perazella, MD and Mandana Rastegar, MD Chapter 12
Disorders of Magnesium HomeostasisHypo
Chapter 5 and Hypermagnesemia ..................................165
Intelligent Use of IV Fluids................................61 Robert F. Reilly Jr., MD
Robert F. Reilly Jr., MD
Chapter 13
Chapter 6 Nephrolithiasis..............................................179
Disorders of Potassium Homeostasis ...............71 Robert F. Reilly Jr., MD
Mark A. Perazella, MD and Mandana Rastegar, MD
SECTION III Intrinsic Renal Diseases ................ 195
Chapter 7
Metabolic Acidosis ..........................................89 Chapter 14
Urinalysis and Urine Microscopy .....................197
Adam M. Franks, MD and Joseph I. Shapiro, MD
Mark A. Perazella, MD
 vii

Contents
Chapter 15
Acute Kidney Injury ........................................217
Mark A. Perazella, MD and Mandana Rastegar, MD

Chapter 16
Chronic Kidney Disease .................................245
Mark A. Perazella, MD and Edgar V. Lerma, MD

Chapter 17
Glomerular Diseases .....................................277
Robert F. Reilly Jr., MD and Mark A. Perazella, MD

Chapter 18
Tubulointerstitial Diseases .............................307
Mark A. Perazella, MD and Edgar V. Lerma, MD

Chapter 19
Obstruction of the Genitourinary Tract .............323
Richard N. Formica, MD
Contents
Contents

TABLE 1-1. Determinants of Glomerular Filtration

(Primates)
GLOMERULAR PRESSURES
(mmHg)
A FFERENT E FFERENT
A RTERIOLE A RTERIOLE
Hydraulic Pressure
Capillary 46 45
Interstitium 10 10
Mean gradient 36 35
Oncotic Pressure
Capillary 23 35
Interstitium 0 0
Mean gradient 23 35
Mean gradient +13 0
favoring filtration
(mean = +6 mmHg)

TABLE 2-1. Sensors and Effectors of Sodium Balance

SODIUM AND VOLUME
SENSORS
Low-pressure receptors
(atria and veins)
High-pressure receptors
(aortic arch and carotid
sinus)
Hepatic volume receptor
system
Cerebrospinal fluid
sodium receptor
Renal afferent arteriole
receptors
EFFECTORS
Glomerular filtration rate
Peritubular physical factors
(ionic, osmotic, and
hydraulic gradients)
Sympathetic nervous
Renin-angiotensin-
ldosterone system
Atrial natriuretic factor
Other natriuretic hormone
Contents
TABLE 2-2. Pathophysiology of Edema Formation
INCREASED DECREASED ILL-DEFINED
FORMATION REMOVAL MECHANISMS
Increased capillary Decreased Idiopathic cyclic
hydrostatic plasma colloid edema
pressure osmotic pressure
Venous/lymphatic Nephrotic Pregnancy
obstruction syndrome
Congestive heart Malabsorption Hypothyroidism
failure
Cirrhosis of Cirrhosis of
the liver the liver
Primary salt Impaired
excess (nephritic lymphatic outflow
syndrome)
Increased capillary
permeability
Traumaburns
Allergic reactions
TABLE 2-3. Pathophysiology of Extracellular Fluid Volume (Total-Body Sodium) Expansion
Hypertension PresentEdema Present
Kidney disease
HypertensionPresent, EdemaAbsent
Mineralocorticoid excess
Primary aldosteronism
Renal artery stenosis
Renin-producing tumors
Glucocorticoids bindingto the mineralocorticoid receptor
Cushing disease
Licorice
Apparent mineralocorticoid excess
Increased distal sodium reabsorption
Liddle syndrome
Familial hyperkalemic hypertension
HypertensionAbsent, EdemaPresent
Decreased cardiac output
Congestive heart failure
Constrictive pericarditis
Pulmonary hypertension
Decreased oncotic pressure
Nephrotic syndrome
Peripheral vasodilation
Cirrhosis
High-output heart failure

Contents
Pregnancy
Increased capillary permeability
Burns
Sepsis
Pancreatitis

TABLE 2-4. Manifestations of Extracellular Fluid Volume (Total-Body Sodium) Depletion

SYMPTOMS SIGNS
Increased thirst Orthostatic fall in blood
pressure
Weakness and apathy Orthostatic rise in pulse
Headache Decreased pulse volume
Muscle cramps Decreased jugular venous
pressure
Anorexia Dry skin and decreased sweat
Nausea Dry mucous membranes
Vomiting Decreased skin turgor

TABLE 3-1. Disease Processes Causing Syndrome of Inappropriate Antidiuretic Hormone

PULMONARY
CARCINOMAS DISEASES CNS DISORDERS
Lung Viral pneumonia Encephalitis
(small cell)
Duodenum Bacterial Meningitis
pneumonia
Pancreas Pulmonary Acute psychosis
abscess
Tuberculosis Stroke
Aspergillosis Porphyria (AIP)
Mechanical Tumors
ventilation
Abscesses
Subdural injury
Guillain-Barr syndrome
Head trauma
Abbreviations: AIP, acute intermittent porphyria; CNS, central nervous system.
Contents
TABLE 3-2. Drug-Induced Euvolemic Hyponatremia
STIMULATE AVP RELEASE OTHER MECHANISMS
Nicotine Chlorpropamide: enhance
renal effect of AVP
Clofibrate Tolbutamide
Vincristine Cyclophosphamide
Isoproterenol Morphine
Chlorpropamide Barbiturates
Antidepressants (SSRIs) Carbamazepine
Antipsychotic agents Acetaminophen
Ecstacy NSAIDs: inhibit PG that
antagonize AVP
Abbreviations: AVP, arginine vasopressin; PG, prostaglandins; NSAIDs: nonsteroidal antiinflammatory drugs; SSRI, selective serotonin reuptake inhibitors.

TABLE 3-3. Treatment of Central Diabetes Insipidus

CONDITION DRUG DOSE
Complete
dD-AVP 5 to 20 g intranasally q12-24h
0.1 to 0.4 mg orally q12-24h
Incomplete
Chlorpropamide 125 to 500 mg/day
Carbamazepine 100 to 300 mg bid

Clofibrate 500 mg qid

Abbreviations: bid, Twice a day; qid, 4 times a day.
Contents
TABLE 4-1. Adverse Effects of Diuretic Drugs
Proximal Tubule Diuretics
Carbonic anhydrase inhibitors (acetazolamide)
Hypokalemia, metabolic acidosis
Drowsiness, fatigue, lethargy, paresthesias Bone marrow suppression
Calcium phosphate stones
Osmotic diuretics (mannitol)
Hypokalemia, hyperkalemia (cell shift)
Expansion of the ECF, CHF
Nausea and vomiting, headache
Osmotic nephropathy
Loop Diuretics (Furosemide, Bumetanide, Torsemide, Ethacrynic Acid)
Hypokalemia, hypomagnesemia, hyponatremia Metabolic alkalosis, hypovolemia
Ototoxicity, diarrhea
Blood dyscrasia (thrombocytopenia, agranulocytosis)
Distal Convoluted Tubule Diuretics (Thiazides, Chlorthalidone, Indapamide, Metolazone)
Hypokalemia, hypomagnesemia, hyponatremia Hypercalcemia, hyperuricemia
Metabolic alkalosis, hypovolemia
Mild hyperglycemia, hyperlipidemia
Hypersensitivity, interstitial nephritis
Leukopenia, thrombocytopenia, aplastic and hemolytic anemia
Cortical Collecting Duct Diuretics
Mineralocorticoid receptor antagonists
(spironolactone*, eplerenone)
Hyperkalemia
Gynecomastia*, hirsutism*, menstrual
irregularities*, testicular atrophy*
Sodium channel inhibitors (amiloride, triamterene)
Hyperkalemia
Glucose intolerance, megaloblastic anemia, urinary crystals
Contents
TABLE 4-2. Ceiling Doses of Intravenous and Oral Loop Diuretics in Various Clinical Conditions
FUROSEMIDE (mg) BUMETANIDE (mg) TORSEMIDE (mg)
CLINICAL
CONDITION IV PO IV PO IV PO
Kidney disease
GFR 20 to 50 mL/min 80 60 to 80 2 to 3 2 to 3 20 to 50 20 to 50
GFR <20 mL/min 200 240 8 to 10 8 to 10 50 to 100 50 to 100
CHF 40 to 80 160 to 240 2 to 3 2 to 3 20 to 50 20 to 50
Nephrotic syndrome 120 3 50
Cirrhosis 40 to 80 80 to 160 1 1 to 2 10 to 20 20 to 50
Abbreviation: PO, oral (per os).

TABLE 4-3. Approach to Patients with Diuretic Resistance

Step 1: Define diuretic resistance as failure to resolve edema or hypertension with standard diuretic doses.
Step 2: Identify cause of edema as renal-related edema versus edema from other causes (obstruction of veins or lymphatics, cyclic
edema, calcium channel blocker therapy).
Step 3: Examine for incomplete therapy of the primary disorder requiring diuretic therapy.
Step 4: Assess patient compliance with salt-restricted diet and diuretic regimen.
Step 5: Consider pharmacokinetic alterations of the diuretic including incomplete or delayed medication absorption and/or
impaired kidney function (acute or chronic renal failure).
Step 6: Consider pharmacodynamic alterations of the diuretic regimen, including severity of the edema state,
activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, and compensatory hypertrophy of the
distal nephron sites (particularly the DCT).
Step 7: Explore for adverse drug interactions including concurrent traditional NSAID or selective cyclooxygenase (COX)-2
inhibitor therapy.

TABLE 4-4. Dosing Guidelines for Continuous Infusions of Loop Diuretics

BOLUS
DIURETIC DOSE (mg) INFUSION RATE (mg/kg/h)
Furosemide 20 to 80 2 to 100 (up to 1.0 mg/kg/h)
Torsemide 25 1 to 50 (up to 0.5 mg/kg/h)
Bumetanide 1.0 0.2 to 2 (up to 0.02 mg/kg/h)
Contents
TABLE 4-5. Dosing Guidelines for Diuretics Added to Loop Diuretics for Combination Therapy
Class of Diuretic Dose Range (mg/day)
Proximal Tubule Diuretics
Acetazolamide 250 to 375; up to 500 (IV)
Distal Convoluted Tubule
Diuretics
Chlorothiazide 500 to 1000 (IV)
Metolazone 2.5 to 10 (oral)
Chlorthalidone 25 to 50 (oral)
Indapamide 1.25 to 2.5 (oral)
Hydrochlorothiazide 25 to 100 (oral)
Collecting Tubule Diuretics
Amiloride 5 to 10 (oral)
Spironolactone 100 to 200 (oral)
Eplerenone 25 to 100 (oral)

TABLE 5-1. Mechanism of Edema Formation

INCREASED HYDROSTATIC
PRESSURE
Venous/lymphatic
obstruction
Congestive heart failure
Cirrhosis of the liver
DECREASED CAPILLARY
ONCOTIC PRESSURE
Nephrotic syndrome
Malabsorption
Cirrhosis of the liver

TABLE 5-2. Commonly Used Crystalloid Solutions

OSMOLALITY GLUCOSE SODIUM CHLORIDE LACTATE
PREPARATION (mOsm/L) (g/L) (mEq/L) (mEq/L) (mEq/L)
D5W 252 50 - - -
0.9% NS 308 - 154 154 -
0.45% NS 154 - 77 77 -
Ringers lactate 272 - 130 109 28
Abbreviations: D 5 W, 5% dextrose in water; NS, normal saline.
Contents
TABLE 5-3. Albumin Versus Hetastarch
ALBUMIN HETASTARCH
Molecular weight 69,000 480,000
Made from Human sera Starch
Compound Protein Amylopectin
Preparations 5% and 25% 6%

TABLE 5-4. Electrolyte Content of Body Fluids

SODIUM (mEq/L) POTASSIUM (mEq/L) CHLORIDE (mEq/L) BICARBONATE (mEq/L)
Sweat 30 to 50 5 50 -
Gastric 40 to 60 10 100 0
Pancreatic 150 5 to 10 80 70 to 80
Duodenum 90 10 to 20 90 10 to 20
Ileum 40 10 60 70
Colon 40 90 20 30

TABLE 6-1. Factors That Influence Renal Potassium Excretion

Aldosterone
Plasma potassium concentration
Tubular flow rate
Tubular sodium concentration
Antidiuretic hormone
Glucocorticoids
Metabolic alkalosis
Metabolic acidosis
Impermeant anions in the urine (sulfate, bicarbonate, carbenicillin)
Contents
TABLE 6-2. Causes of Hypokalemia

Dietary Potassium
Inadequate oral intake (in combination with other factors)
Cellular Uptake of Potassium
Insulin
Catecholamines ( 2-adrenergic)
Endogenous catecholamines
Epinephrine
Dopamine
Aminophylline
Isoproterenol
Chloroquine intoxication
Metabolic alkalosis
Hypokalemic periodic paralysis
Hypothermia
Cell growth from vitamin B 12 therapy
Renal Excretion of Potassium
Hyperaldosteronism (primary or secondary) Corticosteroid excess
High urine flow rate from diuretics
High distal delivery of urine sodium
Renal tubular acidosis
Drugs
Amphotericin B
Diuretics
Aminoglycosides
Lithium
Cisplatinum, ifosfamide, pemetrexed
Some penicillins
Tenofovir, cidofovir, adefovir
Genetic renal diseases
Bartter syndrome
Gitelman syndrome
Liddle syndrome
Apparent mineralocorticoid excess syndrome
Gastrointestinal Potassium Loss
Vomiting
Diarrhea
Ostomy losses
Contents
Skin Loss of Potassium
Strenuous exercise
Severe heat stress

TABLE 6-3. Causes of Hyperkalemia

Dietary Potassium
Excessive oral or intravenous intake (in combination with other factors)
Cellular Release of Potassium
Lack of insulin (fasting, diabetes mellitus) 2-Adrenergic blockade
Propranolol
Labetalol
Carvedilol
Metabolic acidosis
Hyperkalemic periodic paralysis
Succinylcholine
Hyperosmolality
Hyperglycemia
Mannitol
Aminocaproic acid, lysine
-Adrenergic agonist
Phenylephrine
Midodrine
Digoxin toxicity
Cell lysis (hemolysis, rhabdomyolysis, tumor lysis) Severe exercise
Renal Retention of Potassium
Hypoaldosteronism
Hypoadrenalism
Hyporeninemic hypoaldosteronism
Heparin
ACE inhibitors, angiotensin receptor blockers NSAIDs
Low urine flow rate
Low distal delivery of urine sodium
Renal tubular resistance to aldosterone
Obstructive uropathy
Systemic lupus erythematosis
Sickle cell disease
Contents
Drugs
Amiloride
Triamterene
Spironolactone, eplerenone, drospirenone Trimethoprim
Pentamidine
Calcineurin inhibitors

Genetic renal diseases

Pseudohypoaldosteronism type 1
Pseudohypoaldosteronism type 2 (Gordon syndrome)
Advanced Renal Failure
Abbreviations: ACE, angiotensin-converting enzyme; NSAIDs, nonsteroidal antiinflammatory drugs.

TABLE 6-4. Treatment of Hyperkalemia

TREATMENT DOSE ONSET DURATION MECHANISM

Calcium gluconate (10%) 10 to 20 mL IV 1 to 5 minutes 30 to 60 Stabilize excitable
minutes membranes
Insulin and glucose 10 U of IV insulin and 25 g 30 minutes 4 to 6 hours Cell uptake
of glucose
Albuterol ( 2 agonist) 20 mg in 4 mL of normal 30 minutes 1 to 2 hours Cell uptake
saline for nebulization
Terbutaline ( 2 agonist) 7 g/kg by subcutaneous 10 to 15 minutes 1 to 2 hours Cell uptake
injection
Sodium bicarbonate 50 to 75 mEq IV 30 to 60 minutes 1 to 6 hours Cell uptake
Sodium polystyrene 30 to 45 g oral 2 to 4 hours 4 to 12 hours GI excretion
sulfonate
Hemodialysis 1 to 2 mEq/L potassium Immediate 2 to 8 hours Removal
bath from the blood
Abbreviations: IV, intravenous; U, units.
Contents
TABLE 7-1. Causes of Increased Anion Gap (Organic) Metabolic Acidosis
Increased Acid Production
Lactic acidosis
Ketoacidosis
Diabetic ketoacidosis
Starvation
Alcoholic ketoacidosis
Inborn errors of metabolism
Toxic alcohol ingestions
Pyroglutamic acidosis
Salicylate overdose
Other intoxications (eg, toluene, isoniazid)
Failure of Acid Excretion
Acute kidney injury
Chronic kidney disease

TABLE 7-2. Causes of Hyperchloremic Metabolic Acidosis

Gastrointestinal Loss of HCO3
Diarrhea
Gastrointestinal drainage and fistulas
Urinary diversion to bowel
Chloride containing anion-exchange resins
CaCl 2 or MgCl 2 ingestion
Renal Loss of HCO3
Renal tubular acidosis
Carbonic anhydrase inhibitors
Hypoaldosteronism
Potassium-sparing diuretics
Miscellaneous Causes of Hyperchloremic Acidosis
Recovery from ketoacidosis
Dilutional acidosis
Addition of HCl
Parenteral alimentation
Sulfur ingestion
Contents
TABLE 8-1. Causes of Chloride-Responsive Metabolic Alkalosis
Gastrointestinal Causes
Vomiting or gastric drainage
Villous adenoma of the colon
Chloride diarrhea
Renal Causes
Diuretic therapy
Posthypercapnia
Poorly reabsorbable anions
Exogenous Alkali Administration or Ingestion
Bicarbonate administration
Milk-alkali syndrome
Transfusion of blood products (sodium citrate)

TABLE 8-2. Causes of Chloride-Resistant Metabolic Alkalosis

With Hypertension
Primary aldosteronism
Renal artery stenosis
Renin-producing tumor
Cushing syndrome
Licorice or chewing tobacco
Apparent mineralocorticoid excess
Congenital adrenal hyperplasia
Liddle syndrome
Without Hypertension
Bartter syndrome and Gitelman syndrome
Current diuretic use
Profound potassium depletion
Hypercalcemia (nonhyperparathyroid etiology) Poststarvation (refeeding alkalosis)
Transfusion of blood products (sodium citrate)
Contents
TABLE 8-3. Renin and Aldosterone Concentrations in Patients
with Chloride-Resistant Metabolic Alkalosis and Hypertension
RENIN ALDOSTERONE
CONCENTRATION CONCENTRATION
Primary Decreased Increased
aldosteronism
GRA Decreased Increased
Renal artery Increased Increased
stenosis
Renin-producing Increased Increased
tumor
Cushing syndrome Decreased Decreased
Licorice ingestion Decreased Decreased
AME Decreased Decreased
Liddle syndrome Decreased Decreased

Abbreviations: GRA, glucocorticoid-remediable aldosteronism; AME, apparent mineralocorticoid excess.

TABLE 9-1. Causes of Respiratory Acidosis

Acute Airway obstructionaspiration of foreign body or vomitus, laryngospasm, generalized bronchospasm,
obstructive sleep apnea
Respiratory center depressiongeneral anesthesia, sedative overdosage, cerebral trauma or infarction,
central sleep apnea
Circulatory catastrophescardiac arrest, severe pulmonary edema
Neuromuscular defectshigh cervical cordotomy, botulism, tetanus, Guillain-Barr syndrome, crisis in
myasthenia gravis, familial hypokalemic periodic paralysis, hypokalemic myopathy, toxic drug agents (eg,
curare, succinylcholine, aminoglycosides, organophosphates)
Restrictive defectspneumothorax, hemothorax, flail chest, severe pneumonitis, hyaline membrane
disease, adult respiratory distress syndrome
Pulmonary disorderspneumonia, massive pulmonary embolism, pulmonary edema, mechanical
underventilation
Chronic Airway obstructionchronic obstructive lung disease (bronchitis, emphysema)
Respiratory center depressionchronic sedative depression, primary alveolar hypoventilation, obesity
hypoventilation syndrome, brain tumor, bulbar poliomyelitis
Neuromuscular defectspoliomyelitis, multiple sclerosis, muscular dystrophy, amyotrophic lateral sclerosis,
diaphragmatic paralysis, myxedema, myopathic disease (eg, polymyositis, acid maltase deficiency) Restrictive
defectskyphoscoliosis, spinal arthritis, fibrothorax, hydrothorax, interstitial fibrosis, decreased diaphragmatic
movement (eg, ascites), prolonged pneumonitis, obesity
Contents
TABLE 9-2. Causes of Respiratory Alkalosis
Hypoxia
Decreased inspired oxygen tension
Ventilation-perfusion inequality
Hypotension
Severe anemia
CNS Mediated
Voluntary hyperventilation
Neurologic disease: cerebrovascular accident
(infarction, hemorrhage); infection (encephalitis,
meningitis); trauma; tumor
Pharmacologic and hormonal stimulation: salicylates;
ditrophenol; nicotine; xanthines; pressor hormones;
pregnancy
Hepatic failure
Gram-negative septicemia
Anxiety-hyperventilation syndrome
Heat exposure
Pulmonary disease
Interstitial lung disease
Pneumonia
Pulmonary embolism
Pulmonary edema
Mechanical overventilation

TABLE 9-3. Syndromes Commonly Associated with Mixed Acid-Base Disorders

Hemodynamic Compromise
Cardiopulmonary arrest
Pulmonary edema
Sepsis
Liver failure
Poisonings
Ethylene glycol intoxication
Methanol intoxication
Aspirin intoxication
Ethanol intoxication
Metabolic Disturbances
Severe hypokalemia
Severe hypophosphatemia
Diabetic ketoacidosis
Bowel ischemia
 Chronic obstructive pulmonary disease
Chronic kidney disease
TABLE 10-1. Etiologies of Hypercalcemia
Increased Bone Resorption

Contents
Hyperparathyroidism (primary and secondary) Malignancy
Thyrotoxicosis
Immobilization
Paget disease
Addison disease
Lithium
Vitamin A intoxication
Familial hypocalciuric hypercalcemia
Increased GI Absorption
Increased calcium intake
Calcium-alkali syndrome
Chronic kidney disease (calcium and vitamin D supplements)
Increased vitamin D concentration
Vitamin D intoxication
Granulomatous disease
Decreased Renal Excretion
Thiazide diuretic TABLE 10-2. Etiologies of Hypocalcemia
Decreased PTH Concentration or Effect
Hypomagnesemia
Decreased PTH secretion
Postsurgical
Polyglandular autoimmune syndrome, type I Familial hypocalcemia
Infiltrative disorders
End-organ resistance to PTH
Pseudohypoparathyroidism (types I and II)
Defects in Vitamin D Metabolism
Nutritional
Malabsorption
Drugs
Liver disease
Kidney disease
Vitamin D-dependent rickets
Shift of Calcium Out of the ECF
Acute pancreatitis
Hungry bone syndrome
Tumor lysis syndrome
Miscellaneous
Osteoblastic metastases
Toxic shock syndrome
Sepsis
Pseudohypocalcemia
 Contents TABLE 10-3. Oral Calcium Preparations
ELEMENTAL
TABLET CALCIUM/TABLET
PREPARATION (mg) (mg)
Calcium carbonate 500 200
Calcium citrate 950 200
Calcium lactate 650 85
Calcium gluconate 1000 90
Contents
TABLE 11-1. Sodium Phosphate Cotransporter Isoforms
LOCATION IN CELLULAR OTHER TRANSPORT
ISOFORMS HUMAN LOCALIZATION TRANSPORT MODE FUNCTIONS HUMAN DISEASE
Npt1 Ubiquitous Apical Electrogenic Cl channel, organic

Unknown
anions (urate)
Npt2 Apical
a Kidney (70%) Electrogenic
b Intestine Electrogenic Pulmonary alveolar
microlithiasis
c Kidney (30%) Electroneutral Hypophosphatemic rickets
with hypercalciuria in
Bedouin tribe
Npt3 Basolateral Electrogenic
PiT-1 Osteoblast Increased expression at
Chondrocytes vascular calcification sites
in Werner syndrome
Salivary glands
PiT-2 Kidney (minimal Salivary glands No human disease has
Pi transport) been identified
 TABLE 11-2. Etiologies of Hyperphosphatemia
Decreased renal excretion
Decreased glomerular filtration rate

Contents
Acute kidney injury
Chronic kidney disease
Increased renal phosphorus reabsorption
Hypoparathyroidism
Acromegaly
Thyrotoxicosis
Drugsbisphosphonates
Tumoral calcinosis
Acute phosphorus addition to extracellular fluid
Endogenous
Tumor lysis syndrome
Rhabdomyolysis
Severe hemolysis
Exogenous
Vitamin D intoxication
Sodium phosphate-containing bowel preparation
solutions
High-dose liposomal amphotericin B
Improperly purified fresh-frozen plasma
Pseudohyperphosphatemia
Hyperbilirubinemia, hyperlipidemia, hemolysis, paraproteinemia

TABLE 11-3. Phosphate Binders

CALCIUM LANTHANUM
BINDER CALCIUM ACETATE (1 g) CARBONATE (1 g) SEVELAMER (800 mg) (750mg)
Amount of 253 mg 400 mg None None
elemental calcium
Amount of 40 mg 44 mg 64 mg 130 mg
phosphorus bound
Cost per pill $0.21 (667 mg) $0.02 (1 gram) $0.98 (800 mg) $1.32 (750 mg)
Contents TABLE 11-4. Etiologies of Hypophosphatemia
Decreased net GI absorption
Decreased dietary intake
Phosphate-binding agents
Alcoholism
Shift into ICF
Respiratory alkalosis
Refeeding
Diabetic ketoacidosis
Hungry bone syndrome
Sepsis
Increased renal excretion
Primary hyperparathyroidism
Secondary hyperparathyroidism from vitamin D deficiency
X-linked hypophosphatemic rickets
Autosomal dominant hypophosphatemic rickets Oncogenic osteomalacia
Fanconi syndrome
Osmotic diuresis
Partial hepatectomy
Pseudohypophosphatemia
Contents
TABLE 11-5. Phosphate Preparations
PREPARATION CONTENTS PHOSPHORUS SODIUM POTASSIUM

K-phos-neutral Dibasic Na phosphate 250 mg/tab 13 mEq/tab 1.1 mEq/tab

Monobasic Na phosphate
Monobasic K phosphate
K-phos original Monobasic K phosphate 114 mg/tab - 3.7 mEq/tab
Fleets phosphosoda Monobasic Na phosphate 129 mg/mL 4.8 mEq/mL -
Dibasic Na phosphate
Neutra-phos-K Monobasic K phosphate 250 mg/cap - 13.6 mEq/capsule
Dibasic K phosphate
Neutra-phos Monobasic and dibasic Na and 250 mg/cap 7.1 mEq/capsule 6.8 mEq/capsule
K phosphates
IV Na phosphate Monobasic Na phosphate 93 mg/mL 4.0 mEq/mL -
IV K phosphate Monobasic K phosphate 93 mg/mL - 4.4 mEq/mL

TABLE 12-1. Etiologies of Hypomagnesemia

Gastrointestinal Causes
Decreased oral intake
Malabsorption
Diarrhea
Primary intestinal hypomagnesemia
Proton pump inhibitor use
Increased Renal Losses
Primary
Drugs
Toxins
Leptospirosis
Miscellaneous tubular injury
Genetic disorders
Secondary
Osmotic diuresis, saline infusion
Diuretics
Hypercalcemia
Shifts from the Extracellular to the Intracellular Space
Hungry bone syndrome
Refeeding syndrome
Hyperthyroidism
Contents
TABLE 12-2. Oral Magnesium Preparations
PREPARATION MOLECULAR WEIGHT FORMULA mg Mg/g mEq Mg/g
Mg carbonate 84 MgCO 3 289 24
Mg chloride 203.3 MgCl 2 6H 2 O 119 10
Mg gluconate 414.6 (CH 2 OH(CHOH) 4 COO) 2 Mg 58 5
Mg lactate 202.4 Mg(C 3 H 5 O 3) 2 120 10
Mg oxide 40.32 MgO 602 50
Mg sulfate 246.5 MgSO 4 7H 2 O 98 8

TABLE 12-3. Etiologies of Hypermagnesemia

Intravenous Magnesium Load in the Absence of CKD
Treatment of preterm labor
Treatment of eclampsia
Oral Magnesium Load in the Presence of CKD
Laxatives
Antacids
Epsom slats
Miscellaneous
Saltwater drowning

TABLE 13-1. Likelihood of Spontaneous Kidney Stone Passage

Size
>6 mm: 0% to 25%
>4 to 6 mm: 20% to 60%
<4 mm: 50% to 90%
Location
Upper ureter
>6 mm: <1%
<4 mm: 40% to 80%
Lower ureter
<4 mm: 70% to 95%
Contents
TABLE 13-2. Abnormal Values for Calcium Oxalate Stone
Risk Factors
mg/24 h
SUBSTANCE MALE FEMALE
Calcium >200 >200
Uric acid >800 >750
Oxalate >45 >45
Citrate <320 <320

TABLE 13-3. Randomized Placebo-Controlled Trials

TREATMENT DOSE PATIENT GROUP
Water Urine volume Unselected
>2 L
HCTZ 25 mg BID Unselected
(hydrochlorothiazide)
Chlorthalidone 25 mg daily Unselected
Indapamide 2.5 mg daily Hypercalciuria
Allopurinol 300 mg daily Hyperuricosuria
K citrate 60 mEq daily Hypocitraturia
K-Mg citrate 40 mEq daily Unselected

TABLE 13-4. Risk of Uric Acid Stones in Patients with

Primary Gout as a Function of Serum Urate Concentration
SERUM URATE (mg/dL) WITH STONES (%)
5.1 to 7.0 11
7.1 to 9.0 18
9.1 to 11.0 25
11.1 to 13.0 28
>13.1 53
Adapted from Riese RJ, Sakhaee K. Uric acid nephrolithiasis: pathogenesis and treatment. J Urol. 1992;148:765-771.
Contents
TABLE 13-5. Risk of Uric Acid Stones in Patients with Primary Gout as a Function of Urate Excretion
URINARY URATE EXCRETION
(mg/24 h) WITH STONES (%)
<300 11
300 to 499 21
500 to 699 21
700 to 899 34
900 to 1,099 38
>1100 50

Adapted from Riese RJ, Sakhaee K. Uric acid nephrolithiasis: pathogenesis and treatment. J Urol.
1992;148:765-771.