eMedicine Specialties > Nephrology > Glomerular Diseases

Proteinuria: Treatment & Medication

Author: Edgar V Lerma, MD, Clinical Associate Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Consulting Staff, Associates in Nephrology, SC
Coauthor(s): Kevin McLaughlin, MB, ChB, MSc, PhD, Associate Professor, Department of Medicine, University of Calgary Faculty of Medicine, Calgary Health Region
Contributor Information and Disclosures

Updated: Aug 19, 2009

Treatment

Medical Care

Evaluation normally is conducted on an outpatient basis unless the patient develops a complication of severe nephrotic syndrome. All patients with evidence of glomerular disease or any reduction in renal function should be referred to a nephrologist.

  • Medical care can be considered as having 2 components as follows:
    • Nonspecific treatment that is applicable irrespective of the underlying cause, assuming the patient has no contraindications to the therapy
    • Specific treatment that depends on the underlying renal or nonrenal cause
  • Nonspecific treatment
    • The degree of proteinuria depends on the integrity of the GCW (charge and size selectivity) and the intraglomerular pressure. Intraglomerular pressure is controlled by both the afferent arteriole, which transmits systemic blood pressure to the glomerulus, and the efferent arteriole.
    • Normalization of systemic blood pressure in a patient with hypertension should result in a reduction in intraglomerular pressure and a fall in albuminuria.
    • Some vasodilatory antihypertensives (eg, hydralazine and nifedipine) dilate the afferent arteriole, which may attenuate the reduction in intraglomerular pressure despite the fall in arterial blood pressure.
    • As a consequence, these agents may not reduce proteinuria to the same degree, particularly if systemic blood pressure is not adequately reduced at the same time the afferent arteriole is dilated. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin-receptor antagonists (AT1-ra) reduce intraglomerular pressure by inhibiting angiotensin–II-mediated efferent arteriolar vasoconstriction.
    • These groups of drugs have a proteinuria-reducing effect independent of their antihypertensive effect.
    • Other hemodynamic and nonhemodynamic effects of ACEIs may partly explain the renoprotective properties of this group of drugs, such as reduced breakdown of bradykinin (an efferent arteriolar vasodilator), restoration of size and charge selectivity to the GCW, and reduced production of cytokines that promote glomerulosclerosis and fibrosis, such as TGF-beta.
    • Target blood pressure is less than 125/75 mm Hg. The dose of ACEI should be increased as tolerated until this blood pressure is achieved.
    • Normotensive patients with proteinuria also should be given ACEIs because low doses usually are well tolerated and do not usually cause symptomatic hypotension.
    • Patients who develop adverse effects from ACEIs, such as cough, should be given an AT1-ra. Patients also may develop angioedema due to the increase in bradykinin levels that accompany the use of ACEIs. This adverse effect also warrants cessation of treatment. An AT1-ra may be used instead. Patients with mild hyperkalemia should receive dietary counseling. Those with significant hyperkalemia should have the medication immediately discontinued and should be administered a potassium-binding resin.
    • Patients with edema should have salt and water restrictions (see Diet).
    • Patients with fluid overload should be treated with diuretics. The use of diuretics in patients with nephrotic syndrome requires careful attention because patients may be refractory to normal doses of diuretics due to reduced delivery to the renal tubule (reduced albumin transport). Use a combination of diuretics acting at different sites of the nephron (eg, loop diuretic ± thiazide ± spironolactone). These patients, at the same time, may have intravascular volume depletion and, as a consequence, may be at risk of acute renal failure due to exacerbation of volume depletion.
    • The routine use of albumin infusion combined with diuretics is not advocated in patients with nephrotic syndrome. Most patients diurese with a loop diuretic or a combination of diuretics. The addition of albumin may improve natriuresis in patients with refractory salt and water retention, but the potential benefits must be offset against cost and risks of albumin infusion, including the possibility of exacerbating fluid overload.
    • No evidence-based recommendations are available for the treatment of hyperlipidemia associated with nephrotic syndrome, and, as such, this is a controversial topic.
      • The lipid abnormalities in these patients usually are not responsive to dietary measures.
      • In patients in whom proteinuria is reduced, by specific or nonspecific treatment, dyslipidemia usually improves.
      • In patients with persistent proteinuria and lipid abnormalities, many nephrologists now treat the secondary lipid abnormalities, particularly if these patients have other risk factors for vascular disease. Unfortunately, patients with severe nephrotic syndrome frequently are only partially responsive to lipid-lowering agents (eg, statin group).5
    • Recommendations on anticoagulation for patients with nephrotic syndrome also are not evidence-based and are equally controversial.
      • Due to urinary losses associated with coagulation inhibitors, such as antithrombin III and protein S and C, these patients are hypercoagulable.
      • The risk of thrombosis appears highest in patients with membranous glomerulonephritis. Numerous case reports have been published pertaining to the development of renal vein thrombosis (usually presents as acute onset of gross hematuria and back pain) in patients with membranous glomerulonephritis.
      • While some nephrologists advocate treating patients with Coumadin, most do not prophylactically anticoagulate these patients unless the patients have a second risk factor for venous thrombosis, such as immobility. Some nephrologists recommend the use of heparin (5000 U subcutaneously bid) as prophylactic anticoagulation in those patients with serum albumin levels of less than 2.5 mg/dL.
    • Patients with nephrotic syndrome are at increased risk of infection. The risk is greatest for bacterial infection (including spontaneous bacterial peritonitis) due to renal losses of immunoglobulin and complement components. No data, however, advocates the routine use of prophylactic antibiotics or immunoglobulin infusions.
  • Specific treatment
    • This depends on the nature of the underlying glomerular injury and, in particular, whether or not the injury is immune mediated.
    • For details on specific treatment for the various glomerular diseases, see the relevant eMedicine articles.

Consultations

  • Nephrologist

Diet

  • Patients with nephrotic syndrome and fluid overload should have a salt-restricted diet. A "no-added-salt" diet usually is sufficient, although some patients may need restrictions of up to 40 mmol/d.
  • The issue of dietary protein restrictions is controversial.
    • Evidence exists that indicates a protein restriction may slow down the rate of deterioration in the GFR in patients with glomerular diseases, including diabetic nephropathy. The presumed mechanism is a reduction in intraglomerular pressure.
    • However, concern exists that protein-restricted diets may increase the risk of protein malnutrition, and other methods of reducing intraglomerular pressure, such as the use of ACEIs, may be safer than protein restriction.
    • Most nephrologists recommend no restrictions or mild restriction in protein intake (0.8-1 g/kg/d).
  • The role of cholesterol restriction is discussed in Medical Care.

Medication

ACEIs are effective therapy for the reduction of proteinuria, regardless of whether it is associated with arterial hypertension.

ACE inhibitors

Reduce intraglomerular pressure and may restore size and charge integrity to the GCW. They also reduce level of profibrotic cytokines. ACEIs reduce proteinuria and also reduce rate of deterioration of renal function in patients with diabetic and nondiabetic renal disease associated with proteinuria.


Lisinopril (Zestril, Prinivil)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. Target blood pressure is <125/75 mm Hg in patients with proteinuria of > 1 g/d.
Patients who develop a cough, angioedema, bronchospasm, or other hypersensitivity reactions after starting ACEIs should receive an angiotensin-receptor blocker.

Adult

2.5 mg PO qd initially; increase dose as tolerated

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase levels; coadministration with diuretics increases hypotensive effects; hypotensive effects may be enhanced when given concurrently with diuretics and NSAIDs

Documented hypersensitivity; hyperkalemia (>5.5 mmol/L) prior to starting ACEIs despite a potassium-restricted diet

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 first trimester of pregnancy; check creatinine and electrolytes 1 week and 2 months after starting ACEIs; caution in renal impairment, valvular stenosis, or severe congestive heart failure


Ramipril (Altace)

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

Adult

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

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase levels; coadministration with diuretics increases hypotensive effects; hypotensive effects may be enhanced when given concurrently with diuretics and NSAIDs

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 first trimester of pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure


Captopril (Capoten)

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

Adult

12.5-25 mg PO bid/tid; may increase by 12.5-25 mg/dose at 1- to 2-wk intervals, not to exceed 50 mg tid

Pediatric

6.25-12.5 mg/dose PO q12-24h; not to exceed 6 mg/kg/d

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

Documented hypersensitivity; renal impairment

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 first trimester of pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure


Enalapril (Vasotec)

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

Adult

2.5-5 mg/d PO (increase prn)
10-40 mg/d PO in 1-2 divided doses
Alternatively, 1.25 mg/dose IV over 5 min q6h

Pediatric

Not established

NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects 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 first trimester of pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure

Angiotensin II receptor antagonists

Reduce intraglomerular pressure and may restore size and charge integrity to the GCW. They also reduce level of profibrotic cytokines. ACEIs reduce proteinuria and also reduce rate of deterioration of renal function in patients with diabetic and nondiabetic renal disease associated with proteinuria.


Candesartan (Atacand)

Blocks vasoconstriction and aldosterone-secreting effects of angiotensin II. 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. Use in patients unable to tolerate ACE inhibitors.
Angiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function and delaying onset of end-stage renal disease.

Adult

8-16 mg/d PO initially; not to exceed 32 mg/d

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase candesartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of candesartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing 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; caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium


Eprosartan (Teveten)

Nonpeptide angiotensin II receptor antagonist that blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II. 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.
For patients unable to tolerate ACE inhibitors. Angiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function and delaying onset of end-stage renal disease.

Adult

400-800 mg PO qd or divided bid

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase eprosartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of eprosartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; bilateral renal artery stenosis or renal insufficiency; significant aortic/mitral stenosis

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; avoid use or use lower dose in patients who are volume depleted (correct volume depletion first); renal deterioration can occur with initiation of therapy; caution in unilateral renal artery stenosis and preexisting renal insufficiency; caution in aortic/mitral stenosis


Irbesartan (Avapro)

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II at tissue receptor site. 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.

Adult

150 mg PO qd; not to exceed 300 mg/d

Pediatric

<6 years: Not established
6-12 years: 75 mg PO qd initially; may increase if needed, not to exceed 150 mg/d
>12 years: Administer as in adults

May increase digoxin, lithium, and allopurinol levels; probenecid may increase irbesartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of irbesartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; 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; caution in patients with unilateral or bilateral renal artery stenosis; decrease dose in volume- or salt-depleted patients


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. For patients unable to tolerate ACE inhibitors.

Adult

25-100 mg PO qd or divided bid

Pediatric

<6 years: Not established
>6 years: 0.7 mg/kg PO qd; not to exceed 50 mg/d if <50 kg or 100 mg/d if >50 kg

May increase digoxin, lithium, and allopurinol levels; probenecid may increase losartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of losartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing 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; caution in patients with unilateral or bilateral renal artery stenosis


Olmesartan (Benicar)

Blocks vasoconstrictor effects of angiotensin II by selectively blocking binding of angiotensin II to AT-1 receptor in vascular smooth muscle. Action is independent of pathways for angiotensin II synthesis.

Adult

20 mg PO qd initially; may increase to 40 mg/d after 2 wk if further blood pressure reduction required; lower dose in volume- or salt-depleted patients

Pediatric

Not established

Diuretics may enhance hypotensive effect

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; may cause injury or even death to a developing fetus due to effect on renin-angiotensin system if given in second or third trimesters of pregnancy; serum levels and AUC increase with renal and hepatic insufficiency, respectively; may cause oliguria, azotemia, and acute renal failure; facial edema, angioedema, or decreased hemoglobin or hematocrit occur rarely


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. For use in patients unable to tolerate ACE inhibitors.

Adult

80 mg/d PO; may increase to 160 mg/d if needed

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase valsartan levels; coadministration with diuretics, increase hypotensive effects; NSAIDs may reduce hypotensive effects of valsartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; severe hepatic insufficiency; biliary cirrhosis or obstruction; primary hyperaldosteronism; bilateral renal artery stenosis

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 hyperkalemia, suspected bilateral renal artery stenosis, or solitary kidney with unilateral RAS

Non-dihydropyridine calcium channel antagonists

May help reduce proteinuria.


Diltiazem (Cardizem, Dilacor)

During depolarization, inhibits the influx of extracellular calcium across myocardial and vascular smooth muscle cell membranes. Serum calcium levels remain unchanged. The resultant decrease in intracellular calcium inhibits the contractile processes of myocardial smooth muscle cells, resulting in dilation of the coronary and systemic arteries and improved oxygen delivery to the myocardial tissue.
Decreases conduction velocity in AV node. Also increases refractory period via blockade of calcium influx. This, in turn, stops reentrant phenomenon. Decreases myocardial oxygen demand by reducing peripheral vascular resistance, reducing heart rate by slowing conduction through SA and AV nodes, and reducing LV inotropy. Slows AV nodal conduction time and prolongs AV nodal refractory period, which may convert SVT or slow the rate in atrial fibrillation. Also has vasodilator activity but may be less potent than other agents. Total peripheral resistance, systemic blood pressure, and afterload are decreased.
Calcium channel blockers provide control of hypertension associated with less impairment of function of the ischemic kidney. Calcium channel blockers may have beneficial long-term effects, but this remains uncertain. Proteinuria reducing properties noted in patients with well-controlled hypertension.

Adult

Cardizem SR: 60-120 mg PO bid
Cardizem CD: Hypertension: 180-240 mg PO qd
Cardizem LA: Hypertension: 120-540 mg PO qd
Dilacor: Hypertension: 180-240 mg PO qd
Angina: 120 mg/d PO; titrate slowly over 7-14 d up to 480 mg/d prn; not exceed 540 mg/d

Pediatric

Not established

May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output; when given with beta-blockers may increase cardiac depression; cimetidine may increase diltiazem levels

Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

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 impaired renal or hepatic function; may increase LFT levels; hepatic injury may occur

More on Proteinuria

Overview: Proteinuria
Differential Diagnoses & Workup: Proteinuria
Treatment & Medication: Proteinuria
Follow-up: Proteinuria
References
Further Reading
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References

  1. Wu Y, Chen Y, Chen D, et al. Presence of foam cells in kidney interstitium is associated with progression of renal injury in patients with glomerular diseases. Nephron Clin Pract. Aug 12 2009;113(3):c155-c161. [Medline].

  2. Jackson CE, Solomon SD, Gerstein HC, et al. Albuminuria in chronic heart failure: prevalence and prognostic importance. Lancet. Aug 15 2009;374(9689):543-50. [Medline].

  3. Hladunewich MA, Troyanov S, Calafati J, et al. The natural history of the non-nephrotic membranous nephropathy patient. Clin J Am Soc Nephrol. Aug 6 2009;[Medline].

  4. Hebert LA, Birmingham DJ, Shidham G, et al. Random spot urine protein/creatinine ratio is unreliable for estimating 24-Hour proteinuria in individual systemic lupus erythematosus nephritis patients. Nephron Clin Pract. Aug 12 2009;113(3):c177-c182. [Medline].

  5. Nakamura T, Sato E, Fujiwara N, et al. Co-administration of ezetimibe enhances proteinuria-lowering effects of pitavastatin in chronic kidney disease patients partly via a cholesterol-independent manner. Pharmacol Res. Aug 7 2009;[Medline].

  6. Burton C, Harris KP. The role of proteinuria in the progression of chronic renal failure. Am J Kidney Dis. Jun 1996;27(6):765-75. [Medline].

  7. Giatras I, Lau J, Levey AS. Effect of angiotensin-converting enzyme inhibitors on the progression of nondiabetic renal disease: a meta-analysis of randomized trials. Angiotensin-Converting-Enzyme Inhibition and Progressive Renal Disease Study Group. ALYSIS. Sep 1 1997;127(5):337-45. [Medline].

  8. Klahr S, Levey AS, Beck GJ. The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease. Modification of Diet in Renal Disease Study Group. N Engl J Med. Mar 31 1994;330(13):877-84. [Medline].

  9. Lewis EJ, Hunsicker LG, Bain RP. The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. The Collaborative Study Group [published erratum appears in N Engl J Med 1993 Jan 13;330(2):152]. N Engl J Med. Nov 11 1993;329(20):1456-62. [Medline].

  10. Robinson RR. Isolated proteinuria in asymptomatic patients. Kidney Int. Sep 1980;18(3):395-406. [Medline].

  11. Ruggenenti P, Perna A, Mosconi L. Proteinuria predicts end-stage renal failure in non-diabetic chronic nephropathies. The "Gruppo Italiano di Studi Epidemiologici in Nefrologia" (GISEN). Kidney Int Suppl. Dec 1997;63:S54-7. [Medline].

  12. Springberg PD, Garrett LE Jr, Thompson AL Jr. Fixed and reproducible orthostatic proteinuria: results of a 20-year follow-up study. Ann Intern Med. Oct 1982;97(4):516-9. [Medline].

  13. Waugh NR, Robertson AM. Protein restriction in diabetic renal disease. In: The Cochrane Database of Systematic Reviews [serial CD-ROM]. Issue 4. 1999.

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Keywords

proteinuria, microalbuminuria, microalbumin, albuminuria, glomerulonephritis, nephrotic syndrome, diabetic nephropathy, albumin creatinine ratio, glomerulosclerosis, membranous glomerulonephritis, minimal-change disease, focal segmental glomerulosclerosis, glomerular proteinuria

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Contributor Information and Disclosures

Author

Edgar V Lerma, MD, Clinical Associate Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Consulting Staff, Associates in Nephrology, SC
Edgar V Lerma, MD is a member of the following medical societies: American Heart Association, American Medical Association, American Society of Hypertension, American Society of Nephrology, Chicago Medical Society, Illinois State Medical Society, National Kidney Foundation, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Kevin McLaughlin, MB, ChB, MSc, PhD, Associate Professor, Department of Medicine, University of Calgary Faculty of Medicine, Calgary Health Region
Kevin McLaughlin, MB, ChB, MSc, PhD is a member of the following medical societies: American Society of Nephrology, American Society of Transplantation, and College of Physicians and Surgeons of Alberta
Disclosure: Nothing to disclose.

Medical Editor

Frank C Brosius III, MD, Nephrology Program Director, Professor of Internal Medicine and Physiology, Department of Internal Medicine, Division of Nephrology, University of Michigan School of Medicine
Frank C Brosius III, MD is a member of the following medical societies: Alpha Omega Alpha, American Diabetes Association, American Society of Nephrology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

George R Aronoff, MD, Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine
George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation
Disclosure: Nothing to disclose.

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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