eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders

Hypokalemia: Treatment & Medication

Author: Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Coauthor(s): Rosemary Ouseph, MD, Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine; Leslie Ford, MD, Assistant Professor of Medicine, Kidney Disease Program, University of Louisville School of Medicine
Contributor Information and Disclosures

Updated: Aug 5, 2009

Treatment

Medical Care

Orient medical care toward 4 different aims: (1) decreasing potassium losses, (2) replenishing potassium stores, (3) evaluating for potential toxicities, and (4) determining the cause to prevent future episodes.

  • In treating hypokalemia, the first step is to identify and stop ongoing losses of potassium.
    • Discontinue diuretics/laxatives.
    • Use potassium-sparing diuretics if diuretic therapy is required (eg, severe heart failure).
    • Treat diarrhea or vomiting.
    • Use H2 blockers to decrease nasogastric suction losses.
    • Control hyperglycemia if glycosuria is present.
  • Repletion of potassium losses is the second step.
    • As a first approximation, for every decrease in serum potassium of 1 mEq/L, the potassium deficit is approximately 200-400 mEq. However, bear in mind that many factors in addition to the total body potassium stores contribute to the serum potassium concentration. Therefore, this calculation could either overestimate or underestimate the true potassium deficit.
    • Oral potassium is absorbed readily. Relatively large doses can be given safely. Oral administration is limited by patient tolerance because some individuals develop nausea or even gastrointestinal ulceration with enteral potassium formulations.
    • Intravenous potassium is less well tolerated because it can be highly irritating to veins and can be given only in relatively small doses, generally 10 mEq/h. Under close cardiac supervision in emergent circumstances, as much as 40 mEq/h can be administered through a central line.
    • Oral and parenteral potassium can be used safely simultaneously.
    • Take ongoing potassium losses into consideration by measuring the volume and potassium concentration of body fluid losses.
    • If the patient is severely hypokalemic, avoid glucose-containing parenteral fluids to prevent an insulin-induced shift of potassium into the cells.
    • If the patient is acidotic, correct the potassium first to prevent an alkali-induced shift of potassium into the cells.
    • Replete magnesium if low.
    • Tailor treatment to the individual patient. For example, if diuretics cannot be discontinued due to an underlying disorder such as congestive heart failure, institute potassium-sparing therapies such as a low-sodium diet, potassium-sparing diuretics, ACE inhibitors, and angiotensin receptor blockers. The low-sodium diet and potassium-sparing diuretics limit the amount of sodium reabsorbed at the cortical collecting tubule, thus limiting the amount of potassium secreted. ACE inhibitors and angiotensin receptor blockers inhibit the release of aldosterone, thus blocking the kaliuretic effects of that hormone.
  • Monitor for toxicity of hypokalemia. Generally, the toxicity of hypokalemia is cardiac in nature. Monitor the patient if evidence of cardiac arrhythmias is observed, and institute very aggressive replacement parenterally under monitored conditions.
  • Determine the underlying cause to treat and prevent further episodes.
    • Again, history and physical examination findings clarify the cause in the vast majority of cases.
    • Look for clues to the etiology.
      • Urine potassium concentration
      • Presence of hypertension or hypotension
      • Acid-base disturbances
      • Family history
      • Tooth erosion; melanosis coli; obsession with body image; high-risk behaviors such as cheerleading, wrestling, or modeling; or evidence of alcohol abuse
    • Tailor the workup to the individual patient if the cause is not completely apparent.

Surgical Care

Generally, hypokalemia is a medical, not a surgical, condition. Surgical intervention is required only after determining that the etiology requires it. Etiologies that may require surgery include the following:
  • Renal artery stenosis
  • Adrenal adenoma
  • Intestinal obstruction producing massive vomiting
  • Villous adenoma

Consultations

The following consultations may be appropriate, depending on the clinical findings:

  • Renal specialist for evaluation of unexplained urinary potassium losses suggested to be secondary to a tubular disorder
  • Endocrinologist if Cushing syndrome, primary hyperaldosteronism, glucocorticoid-remediable hypertension, or congenital adrenal hyperplasia is suggested
  • Psychiatrist for alcoholism or eating disorders
  • Surgeon (see Surgical Care)

Diet

In general, a low-sodium and high-potassium diet is appropriate.

Activity

Unless the patient has severe underlying cardiac disease, no restrictions are necessary. Instruct patients to discontinue exercise if muscle pain or cramps develop because this may herald hypokalemia significant enough to produce rhabdomyolysis.

Medication

The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to correct the deficiency.

Electrolytes

Oral or parenteral therapy for potassium replacement.


Potassium chloride (K-Dur, K-Lyte Cl, Kay Ciel)

Essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal excretion, through GI loss, or because of low intake. Most respond well to small supplements. Unflavored liquid replacement has an unpleasant taste, and pills may be conducive to better compliance. Long-acting supplements often are not as well absorbed, but microencapsulated forms often are better tolerated. Tailor dose to patient's needs.

Adult

<10 mEq/h IV
Emergent conditions: 40 mEq/h IV can be given through central venous line

Pediatric

Not established

Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; in patients taking digoxin, hypokalemia may result in digoxin toxicity; caution if discontinuing potassium administration in patients maintained on digoxin

Documented hypersensitivity; hyperkalemia, renal failure, and conditions in which potassium retention is present; oliguria or azotemia, crush syndrome, severe hemolytic reactions, anuria, and adrenocortical insufficiency

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Do not infuse rapidly; high plasma concentrations of potassium may cause death due to cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; monitor potassium replacement therapy whenever possible by continuous or serial ECG; when a concentration of >40 mEq/L is infused, local pain and phlebitis may follow; GI irritation may occur with oral preparations


Potassium citrate (Urocit K, Polycitra, Bicitra)

Oral preparation with a base instead of an acid anion. Generally used for patients who form calcium stones or for severe metabolic acidosis. Not as effective as potassium chloride for replacement in the general population. Tailor dose to patients' needs.

Adult

Urocit: 3 tab PO tid
Polycitra or Bicitra: 1 mL/kg/d PO

Pediatric

Urocit: Not established
Polycitra or Bicitra: Administer as in adults

Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; in patients taking digoxin, hypokalemia may result in digoxin toxicity; caution if discontinuing potassium administration in patients maintained on digoxin

Documented hypersensitivity; hyperkalemia

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Caution in patients taking potassium-sparing diuretics, ACE inhibitors, or angiotensin II receptor blockers

Angiotensin-converting enzyme inhibitors

Inhibit production of aldosterone and decrease renal potassium losses. All the drugs in this category work in the same way. Differences are in the duration of action and the ability to inhibit locally produced and circulating ACE.


Captopril (Capoten)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. Shortest acting and requires bid or tid dosing. Others in class can be taken qd.

Adult

6.25 mg PO bid; not to exceed 100 mg PO tid

Pediatric

Not established

NSAIDs may reduce hypotensive effects; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics

Documented hypersensitivity, renal impairment, hyperkalemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimesters; can result in fetal abnormalities if taken during pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure; can cause hypotension, hyperkalemia, or angioedema


Enalapril (Vasotec)

Competitive inhibitor of ACE. Reduces angiotensin II levels, decreasing aldosterone secretion.

Adult

2.5 mg PO qd; not to exceed 40 mg PO qd

Pediatric

1 month to 16 years: 0.08 mg/kg (up to 5 mg) qd

NSAIDs may reduce hypotensive effects; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimesters; can result in fetal abnormalities if taken during pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure; can cause hypotension, hyperkalemia, or angioedema


Fosinopril (Monopril)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Adult

10-40 mg PO qd

Pediatric

<50 kg: Not established
>50 kg: 5-10 mg qd

NSAIDs may reduce hypotensive effects; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimesters; can result in fetal abnormalities if taken during pregnancy; caution in severe congestive heart failure; can cause hypotension, hyperkalemia, or angioedema


Ramipril (Altace)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Adult

2.5-5 mg PO qd; not to exceed 20 mg/d

Pediatric

Not established

NSAIDs may reduce hypotensive effects of ramipril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases ramipril levels; probenecid may increase ramipril levels; the hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics

Documented hypersensitivity; history of angioedema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimesters; caution in renal impairment, valvular stenosis, or severe congestive heart failure; may cause fetal abnormalities if taken during pregnancy

Potassium-sparing diuretics

Excellent adjunct therapy when ongoing renal losses are anticipated. May be used in conjunction with thiazide or loop diuretics.


Triamterene (Dyrenium)

Potassium-sparing diuretic with relatively weak natriuretic properties. Exerts diuretic effect on distal renal tubule to inhibit reabsorption of sodium in exchange for potassium and hydrogen. Not a competitive antagonist of mineralocorticoids, and potassium-conserving effect is observed in patients with Addison disease (ie, without aldosterone).

Adult

100-300 mg/d PO in divided doses

Pediatric

Not established

Coadministration with other potassium-conserving agents (eg, spironolactone, amiloride HCl) or other formulations containing triamterene may significantly increase serum potassium levels; lithium generally should not be given with diuretics; reduced renal clearance of lithium and high risk of lithium toxicity with concomitant diuretics; acute renal failure reported in patients receiving indomethacin and formulations containing triamterene; administer NSAIDs with caution (monitor serum potassium frequently); may interfere with measurement of quinidine

Documented hypersensitivity, elevated serum potassium levels (>5.5 mEq/L); impaired renal function (anuria, acute and chronic renal insufficiency, or significant renal impairment); diabetes

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Severe hepatic encephalopathy, diabetes, renal dysfunction, history of renal stones


Amiloride (Midamor)

Pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. Potassium-sparing (antikaliuretic) drug that, compared to thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.

Adult

5-20 mg PO qd

Pediatric

<6 kg: Not established
>6 kg: 0.625 mg/kg/d PO

Concomitant therapy with potassium supplementation may increase serum potassium levels; if concomitant use of these agents indicated because of demonstrated hypokalemia, caution and monitor serum potassium frequently; lithium generally should not be given with diuretics; reduced renal clearance of lithium and high risk of lithium toxicity with concomitant diuretics; administration of NSAIDs can reduce diuretic, natriuretic, and antihypertensive effects of loop, potassium-sparing, and thiazide diuretics when used concomitantly; observe patient closely to determine if desired effect of diuretic obtained; indomethacin and potassium-sparing diuretics, including amiloride, may be associated with increased serum potassium levels, consider potential effects on potassium kinetics and renal function

Documented hypersensitivity, elevated serum potassium levels (>5.5 mEq/L), impaired renal function, acute or chronic renal insufficiency, and evidence of diabetic nephropathy; monitor electrolytes closely if evidence of renal functional impairment, BUN >30 mg/100 mL, or serum creatinine levels >1.5 mg/100 mL

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Potassium retention associated with use of antikaliuretic agent accentuated in presence of renal impairment and may result in rapid development of hyperkalemia; monitor serum potassium level, mild hyperkalemia usually not associated with abnormal ECG


Spironolactone (Aldactone)

For management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.

Adult

25-200 mg/d PO bid

Pediatric

60 mg/m2/d PO q6-24h

May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity

Documented hypersensitivity, anuria, renal failure, or hyperkalemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal and hepatic impairment

Angiotensin II receptor blockers

These agents competitively inhibit the ability of angiotensin II to interact with and stimulate angiotensin II receptors. This action results in decreased aldosterone secretion and, consequently, decreased renal potassium excretion.


Valsartan (Diovan)

Prodrug that produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Can be used as alternative therapy, especially in patients unable to tolerate ACE inhibitors.

Adult

80-160 mg/d PO

Pediatric

Not established

Hyperkalemic effects can be potentiated by concomitant use of NSAIDs, ACE inhibitors, potassium supplements, potassium-sparing diuretics, or other drugs that impair renal potassium secretion; hypotensive effects can be potentiated by diuretics or other antihypertensive agents

Documented hypersensitivity; bilateral renal artery stenosis; hypotension; hyperkalemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimester; initiate therapy gradually and monitor closely in patients on drugs that can increase serum potassium level, patients on diuretics, and patients with congestive heart failure, renal insufficiency, or known renal artery stenosis


Candesartan (Atacand)

Produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Can be used as alternative therapy, especially in patients unable to tolerate ACE inhibitors.

Adult

4-32 mg PO qd

Pediatric

Not established

Hyperkalemic effects can be potentiated by concomitant use of NSAIDs, ACE inhibitors, potassium supplements, potassium-sparing diuretics, or other drugs that impair renal potassium secretion; hypotensive effects can be potentiated by diuretics or other antihypertensive agents

Documented hypersensitivity, bilateral renal artery stenosis; hypotension; hyperkalemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimester; initiate therapy gradually and monitor closely in patients on drugs that can increase serum potassium level, patients on diuretics, and patients with congestive heart failure, renal insufficiency, or known renal artery stenosis


Losartan (Cozaar)

Angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. Angiotensin II receptor antagonists can be used as alternative therapy, especially in patients who cannot tolerate ACE inhibitors.

Adult

25-100 mg PO bid

Pediatric

<6 years: Not established
6-16 years: 0.7 mg/kg qd (max 50 mg/d)
>16 years: Administer as in adults

Hyperkalemic effects can be potentiated by concomitant use of NSAIDs, ACE inhibitors, potassium supplements, potassium-sparing diuretics, or other drugs that impair renal potassium secretion; hypotensive effects can be potentiated by diuretics or other antihypertensive agents

Documented hypersensitivity; bilateral renal artery stenosis; hypotension; hyperkalemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimester; initiate therapy gradually and monitor closely in patients on drugs that can increase serum potassium level, patients on diuretics, and patients with congestive heart failure, renal insufficiency, or known renal artery stenosis

Selective aldosterone blockers

These agents selectively block aldosterone binding at mineralocorticoid receptors.


Eplerenone (Inspra)

Selectively blocks aldosterone at the mineralocorticoid receptors in epithelial (eg, kidney) and nonepithelial (eg, heart, blood vessels, and brain) tissues; thus, decreases blood pressure and sodium reabsorption. More selective for mineralocorticoid receptors than spironolactone, thus has lesser incidence of side effects associated with androgen antagonism, such as gynecomastia.

Adult

50 mg PO qd; may increase dose after 4 wk, not to exceed 100 mg/d

Pediatric

Not established

CYP450 3A4 substrate; potent CYP3A4 inhibitors (eg, ketoconazole) increase serum levels about 5-fold; less potent CYP3A4 inhibitors (eg, erythromycin, saquinavir, verapamil, fluconazole) increase serum levels about 2-fold; grapefruit juice increases serum levels about 25%; coadministration with potassium supplements, salt substitutes, or drugs known to increase serum potassium (eg, amiloride, spironolactone, triamterene, ACE inhibitors, angiotensin II inhibitors) increases risk of hyperkalemia

Documented hypersensitivity; hyperkalemia or coadministration with drugs causing increased potassium; type 2 diabetes with microalbuminuria; moderate-to-severe renal insufficiency (eg, CrCl <50 mL/min or serum creatinine > 2 mg/dL in males or >1.8 mg/dL in females)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause hyperkalemia, headache, and dizziness; caution with hepatic insufficiency

More on Hypokalemia

Overview: Hypokalemia
Differential Diagnoses & Workup: Hypokalemia
Treatment & Medication: Hypokalemia
Follow-up: Hypokalemia
References
Further Reading
[ CLOSE WINDOW ]

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Further Reading

Related eMedicine topics:
Bartter Syndrome [Nephrology]
Bartter Syndrome [Pediatrics: General Medicine]
Conn Syndrome
Hyperaldosteronism [Pediatrics: General Medicine]
Hyperaldosteronism [Radiology]
Hyperaldosteronism, Primary
Hyperkalemia [Emergency Medicine]
Hyperkalemia [Nephrology]
Hyperkalemia [Pediatrics: Cardiac Disease and Critical Care Medicine]
Hypokalemia [Emergency Medicine]
Hypokalemia [Pediatrics: Cardiac Disease and Critical Care Medicine]
VIPoma
VIPomas

Clinical guidelines:
Case detection, diagnosis, and treatment of patients with primary aldosteronism: an Endocrine Society clinical practice guideline. The Endocrine Society - Disease Specific Society.  2008 Sep.  26 pages.  NGC:006766

Hyperglycemic crises in diabetes. American Diabetes Association - Professional Association.  2000 Oct (revised 2001; republished 2004 Jan).  9 pages.  NGC:003428

Clinical trials:
Safety of Continuous Potassium Chloride Infusion in Critical Care (ASPIC)

Spironolactone to Decrease Potassium Wasting in Hypercalciurics on Thiazides Diuretics

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Keywords

hypokalemia, low potassium, symptoms of low potassium, lack of potassium, causes of low potassium, low potassium symptoms, Bartter's syndrome, Gitelman's syndrome, Bartter syndrome, Gitelman syndrome, symptoms of hypokalemia, potassium homeostasis, potassium excretion, potassium intake

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Contributor Information and Disclosures

Author

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Rosemary Ouseph, MD, Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine
Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, and American Society of Transplant Surgeons
Disclosure: Nothing to disclose.

Leslie Ford, MD, Assistant Professor of Medicine, Kidney Disease Program, University of Louisville School of Medicine
Leslie Ford, MD is a member of the following medical societies: American Medical Association, American Society of Nephrology, and Kentucky Medical Association
Disclosure: Nothing to disclose.

Medical Editor

James W Lohr, MD, Fellowship Program Director, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Buffalo
James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Christie P Thomas, MBBS, FRCP, FASN, FAHA, Professor, Department of Internal Medicine, Division of Nephrology, University of Iowa Hospitals and Clinics; Director of Transplantation Services, Veterans Affairs Medical Center
Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Nephrology, American Society of Transplantation, American Thoracic Society, International Society of Nephrology, and Royal College of Physicians
Disclosure: Genzyme Grant/research funds Other

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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