eMedicine Specialties > Nephrology > Hypertension and the Kidney

Renal Artery Stenosis: Treatment & Medication

Author: Bruce S Spinowitz, MD, FACP, Clinical Professor of Medicine, Weill Medical College of Cornell University; School of Medicine; Associate Chairman, Associate Director and Attending Physician, Department of Medicine, Division of Nephrology, New York Hospital Medical Center Queens; Associate, Nephrology Associates, PC
Coauthor(s): Joanna Rodriguez, MD, Fellow, Department of Internal Medicine, Division of Nephrology, New York Hospital-Queens
Contributor Information and Disclosures

Updated: Jul 15, 2009

Treatment

Medical Care

All patients with significant (>80%) bilateral stenosis and stenosis in a solitary functioning kidney are candidates for revascularization, regardless of whether they have renal insufficiency. When renal insufficiency is present, patients with unilateral stenosis are also possible candidates for revascularization. The criteria are slightly different depending on the presence or absence of renal insufficiency.

  • When renal function is normal or nearly normal (prevention of renal insufficiency), specialists recommend revascularization if the patient meets the following criteria:
    • The degree of stenosis is more than 80-85%.
    • The degree of stenosis is 50-80%, and captopril-enhanced scintigraphy findings demonstrate an activation of intrarenal renal artery stenosis.
  • Conversely, physicians can choose observation instead of revascularization (serial control every 6 mo with duplex scanning, accurate correction of dyslipidemia, use of drugs that block platelet aggregation) when the patient meets the following criteria:
    • Stenosis is 50-80%, and scintigraphy findings are negative.
    • The degree of stenosis is less than 50%.
  • When renal insufficiency is present and the objective is recovery of renal function together with prevention of further renal function impairment, the prerequisites for revascularization are as follows:
    • The serum creatinine level is lower than 4 mg/dL.
    • The serum creatinine level is higher than 4 mg/dL but with a possible recent renal artery thrombosis.
    • When these conditions are satisfied, the authors propose revascularization if the following apply:
      • The degree of stenosis is more than 80%.
      • The serum creatinine level is increased after administration of ACE inhibitors.
      • The degree of stenosis is 50-80%, and the scintigraphy findings are positive.
  • Restrict conservative treatment in patients with an established diagnosis of IRD to those with absolute contraindications to surgery or angioplasty or to patients who are likely to succumb due to other comorbid conditions before advancing to end-stage renal disease because of IRD. Clinicians must rely on pharmacologic agents (eg, combination of calcium channels blockers to control blood pressure and optimize renal perfusion), accepting the high probability of deterioration in renal function and shortened survival.

Surgical Care

In 1962, Morris et al compiled the first report on a surgical treatment for occlusion of the renal arteries.15 They described 8 patients with renal failure who underwent revascularization. Six of these patients returned to essentially normal renal function.

Reports from retrospective studies clearly document that surgical revascularization can improve renal function in patients with ischemic nephropathy. In 1993, Rimmer and Gennari reported postoperative improvement (ie, 20% decrease in serum creatinine concentration) in more than half the patients in 9 studies.16

Bypass procedures include aortorenal, hepatorenal, splenorenal, and ileorenal conduits constructed with autologous saphenous veins, autologous arteries, or prosthetic material. For atherosclerotic disease, surgeons can also perform atherectomy to improve renal blood flow. In persons with nonatheromatous renal artery disease, surgeons can reconstruct the renal arteries ex vivo and then can reimplant the revascularized kidney. Reilly and coworkers reported an operative mortality rate of only 6% and immediate improvement in the serum creatinine level of 32% of surgical bypass procedures in 35 patients with solitary kidneys.17 In the last few years, researchers report that the results are more consistent. The largest series suggests that the GFR improved postoperatively in 49-80% of patients with underlying renal failure.

  • Revascularization
    • One unresolved issue is how to determine whether revascularization will salvage renal function from a kidney in which the artery is totally occluded.
    • Features that may predict successful restoration of renal function include the following:
      • Collateral circulation and nephrogram on angiography findings
      • Renal length longer than 9 cm
      • Lateralization of renin secretion
      • Differential concentration of urine on split-function study results
      • Spontaneous back-bleeding findings after arteriotomy during surgery
      • Viable nephrons after biopsy tissue examination
    • Specialists suggest nephrectomy as a modality of treatment in persons with unilateral RVD; one study compared nephrectomy versus revascularization in 95 patients and 190 kidneys, and revascularization showed a greater response, better management in blood pressure, and a significant improvement in the GFR.
  • Angioplasty
    • Angioplasty is effective for treating renovascular hypertension associated with atheromatous lesions. Indicative of this is the decreased rate of referrals for surgical renovascularization of atheromatous renovascular hypertensive nephropathy by the early 1980s (from 41% to 26%). In practical terms, angioplasty can usually limit hospitalization, avoid general anesthesia, and minimize tissue trauma.
    • In 1987, Ziegelbaum et al compared the outcomes of angioplasty and surgical bypass.18 The researchers studied 70 elderly patients with atheromatous disease and found that angioplasty caused major complications, including 2 deaths. Renal function improved (ie, >20% decrease in serum creatinine level) in 57.5% of surgery patients but in only 15.8% of angioplasty patients. After 48 months of follow-up, the unassisted patency rate was only 69% in the angioplasty group compared to 100% in the surgical group.
    • Erdoes et al examined the results of 58 surgical and 18 percutaneous revascularizations in nonrandomized patients.19 These 2 approaches showed similar operation risk (mortality rate 4.8-5.3%); however, functional improvement (ie, blood pressure, serum creatinine level) and patency of the renal artery were dramatically better in the surgical group compared to the revascularization group after nearly 4 years of follow-up.
    • van Jaarsveld et al reported the results of a multicenter trial designed to evaluate the relative benefit of angioplasty versus medical therapy for hypertension associated with RVD.20 They found that both groups had similar decreases in blood pressure, although the patients who underwent angioplasty used one fewer hypertensive medication. While renal function was improved at 3 months in those undergoing angioplasty, the function at 12 months was similar. They concluded that restricting angioplasty to those with atherosclerotic renovascular hypertension persisting despite use of 3 or more antihypertensive medications was prudent. Note that the patients in this trial did not undergo angioplasty with stent placement. In addition, 9% of patients in the medical therapy–only group experienced total occlusion of the affected renal artery on 12-month follow-up angiography.
    • A randomized study by van de Ven et al that compared percutaneous transluminal angioplasty (PTA) for ostial ATH with PTA with stent (PTAS) showed that PTAS is a better technique compared to PTA to achieve vessel patency in ostial atherosclerotic renal artery stenosis.21 The primary success rate was 57% for PTA compared with 88% for PTAS. The restenosis rate after a successful primary procedure was 48% for PTA compared to 14% for PTAS. In the last few years, the use of PTAS in patients with ostial stenosis or early restenosis has led to a considerable reduction in the restenosis rate.

      However, controversy still surrounds the best approach to patients with atherosclerotic renovascular disease, as reviewed by Ives et al, Textor, and Plouin.22,23,24 In a study of patients with atherosclerotic renal artery stenosis, Bax et al found that renal artery stenting had no clear effect on renal function impairment in the patients and led to significant complications in some of them.25 The multicenter trial included 140 patients with creatinine clearance of less than 80 mL/min per 1.73 m2 and renal artery stenosis of 50% or greater. All patients received medical treatment with antihypertensive agents, a statin, and aspirin. Although 64 patients were randomized to stent placement, only 46 had the procedure; in many patients, assessment of renal artery stenosis by noninvasive imaging was inaccurate and stenting was in fact not indicated.

      In the study, progression of renal dysfunction, as indicated by a decrease in creatinine clearance of 20% or greater, occurred in 16% of patients in the stent placement group and in 22% of patients in the medication group (hazard ratio, 0.73 [95% confidence interval [CI], 0.33-1.61]). Serious complications in the stent group included 2 procedure-related deaths.
    • In some institutions, PTAS is the first-step approach in patients with IRD, and practitioners reserve surgery for the technical failure of percutaneous maneuvers. However, surgery remains the first choice of treatment under certain conditions, including the following:
      • Simultaneous abdominal aorta aneurysm
      • Renal artery aneurysm
      • Renal artery occlusion (with unsuccessful thrombolysis)
      • Renal artery rupture
      • Renal artery stenosis secondary to kinking
      • Peripheral multifocal stenosis
      • Unsuccessful angioplasty
    • A small, retrospective review of 20 patients who underwent a revascularization procedure (ie, surgery, PTA, PTAS) revealed a high complication rate (increased serum creatinine level in 25%, eosinophilia in 5%, atheroemboli in 15%, renal artery dissection in 5%) despite achieving improved serum creatine values in only 25%.26 Fifty percent of patients had stable azotemia. The authors and others conclude that a prospective, randomized trial of medical management with or without PTAS is warranted for this complex clinical problem.

Consultations

The optimal approach to therapeutic interventions should be developed in consultation with an interventional radiologist and vascular surgeon to determine the relative expertise of these subspecialists at the individual medical center.

Medication

The general approach to therapy of ischemic nephropathy involves control of hypertension, preferably with ACE inhibitors or angiotensin II antagonists. Unfortunately, these 2 classes of drugs may lead to increased serum creatine levels and hyperkalemia, limiting their utility. In this case, calcium channel blockers are likely the most useful and best-tolerated agents. Initiate strict control of serum cholesterol, which usually requires the use of HMG-CoA reductase inhibitors, as with all conditions associated with ATH. A study by Bianchi et al (2003) suggests that statins, in addition to ACE inhibitors and angiotensin receptor blockers (ARBs), may reduce proteinuria and slow the progression of kidney disease.27

Angiotensin-converting enzyme inhibitors

These agents decrease aldosterone secretion.


Captopril (Capoten)

Parent compound of this class of medications. Sulfhydryl group associated with proteinuria and neutropenia when used at high doses. 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
CrCl 10-50 mL/min: 75% of starting dose
CrCl <10 mL/min: 50% of starting dose

Pediatric

6.25-12.5 mg 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

Category D in second and third trimesters of pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure


Enalapril (Vasotec)

One example of this class of compounds. Similar precautions to captopril with respect to potential increase in potassium and creatinine. Major adverse effect is dry cough. Newer and, occasionally, better tolerated than parent compound. Many variations that allow for once-daily dosing and better tissue ACE inhibition.

Adult

2.5-5 mg/d PO (increase prn)
Dosing range: 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

Category D in second and third trimesters of pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure

Angiotensin II receptor antagonists

Useful for hypertension and heart failure in patients who are intolerant of ACE inhibitors. Many alternative compounds exist with few significant clinical differences.


Losartan (Cozaar)

Initial compound in class to gain approval. Useful for treatment of hypertension and heart failure in patients who are intolerant of ACE inhibitors. Many alternative compounds exist with few significant clinical differences. Nonpeptide angiotensin II receptor antagonist that blocks the vasoconstricting 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 divided in 1-2 doses

Pediatric

Not established

Ketoconazole, sulfaphenazole, and phenobarbital may decrease effects; cimetidine and monoxidine may increase effects

Pregnancy

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

Precautions

Follow-up serum potassium and creatinine levels in 1-2 wk; caution in patients with unilateral or bilateral RAS

HMG-CoA reductase inhibitors

Adjunct to diet to reduce total and LDL cholesterol in patients with hypercholesterolemia. Also lower triglycerides.


Atorvastatin (Lipitor)

One of many compounds with comparable efficacy and adverse effect profiles. Inhibits HMG-CoA reductase, which, in turn, inhibits cholesterol synthesis and increases cholesterol metabolism.

Adult

10 mg PO qd; titrate to a maximum 80 mg/d prn

Pediatric

Not established

Toxicity increases when coadministered with triazole antifungals, CNS depressants, macrolide antibiotics, mibefradil, fibric acid derivatives

Documented hypersensitivity; significant hepatic impairment; pregnancy, breastfeeding

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Liver toxicity and rhabdomyolysis; monitor lipid levels, LFTs, and CK 4-6 wk after initiation of therapy; do not exceed daily dose; caution in patients receiving drugs that prolong QRS or Q-T interval

More on Renal Artery Stenosis

Overview: Renal Artery Stenosis
Differential Diagnoses & Workup: Renal Artery Stenosis
Treatment & Medication: Renal Artery Stenosis
Follow-up: Renal Artery Stenosis
References

References

  1. De Bruyne B, Manoharan G, Pijls NH, et al. Assessment of renal artery stenosis severity by pressure gradient measurements. J Am Coll Cardiol. Nov 7 2006;48(9):1851-5. [Medline].

  2. Crowley JJ, Santos RM, Peter RH, et al. Progression of renal artery stenosis in patients undergoing cardiac catheterization. Am Heart J. Nov 1998;136(5):913-8. [Medline].

  3. Holley KE, Hunt JC, Brown AL Jr, et al. Renal artery stenosis. A clinical-pathologic study in normotensive and hypertensive patients. Am J Med. Jul 1964;37:14-22.

  4. Levey AS, Bosch JP, Lewis JB, et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med. Mar 16 1999;130(6):461-70. [Medline].

  5. Radermacher J, Chavan A, Bleck J, et al. Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis. N Engl J Med. Feb 8 2001;344(6):410-7. [Medline].

  6. Olbricht CJ, Paul K, Prokop M, et al. Minimally invasive diagnosis of renal artery stenosis by spiral computed tomography angiography. Kidney Int. Oct 1995;48(4):1332-7. [Medline].

  7. Broome DR, Girguis MS, Baron PW, et al. Gadodiamide-associated nephrogenic systemic fibrosis: why radiologists should be concerned. AJR Am J Roentgenol. Feb 2007;188(2):586-92. [Medline].

  8. Loubeyre P, Trolliet P, Cahen R, et al. MR angiography of renal artery stenosis: value of the combination of three-dimensional time-of-flight and three-dimensional phase-contrast MR angiography sequences. AJR Am J Roentgenol. Aug 1996;167(2):489-94. [Medline].

  9. Vasbinder GB, Nelemans PJ, Kessels AG, et al. Accuracy of computed tomographic angiography and magnetic resonance angiography for diagnosing renal artery stenosis. Ann Intern Med. Nov 2 2004;141(9):674-82; discussion 682. [Medline].

  10. Gilfeather M, Yoon HC, Siegelman ES, et al. Renal artery stenosis: evaluation with conventional angiography versus gadolinium-enhanced MR angiography. Radiology. Feb 1999;210(2):367-72. [Medline].

  11. Gross CM, Kramer J, Weingartner O, et al. Determination of renal arterial stenosis severity: comparison of pressure gradient and vessel diameter. Radiology. Sep 2001;220(3):751-6.

  12. Cooper CJ, Murphy TP. Is renal artery stenting the correct treatment of renal artery stenosis? The case for renal artery stenting for treatment of renal artery stenosis. Circulation. Jan 16 2007;115(2):263-9; discussion 270. [Medline].

  13. Dworkin LD, Jamerson KA. Is renal artery stenting the correct treatment of renal artery stenosis? Case against angioplasty and stenting of atherosclerotic renal artery stenosis. Circulation. Jan 16 2007;115(2):271-6; discussion 276. [Medline].

  14. Levin A, Linas S, Luft FC, et al. Controversies in renal artery stenosis: a review by the American Society of Nephrology Advisory Group on Hypertension. Am J Nephrol. 2007;27(2):212-20. [Medline].

  15. Morris GC, DeBakey ME, Cooley DA. Surgical Treatment of renal failure of renovascular origin. JAMA. 1962;182:609-12.

  16. Rimmer JM, Gennari FJ. Atherosclerotic renovascular disease and progressive renal failure. Ann Intern Med. May 1 1993;118(9):712-9. [Medline].

  17. Reilly JM, Rubin BG, Thompson RW, et al. Revascularization of the solitary kidney: a challenging problem in a high risk population. Surgery. Oct 1996;120(4):732-6; discussion 736-7. [Medline].

  18. Ziegelbaum M, Novick AC, Hayes J, et al. Management of renal arterial disease in the elderly patient. Surg Gynecol Obstet. Aug 1987;165(2):130-4. [Medline].

  19. Erdoes LS, Berman SS, Hunter GC, et al. Comparative analysis of percutaneous transluminal angioplasty and operation for renal revascularization. Am J Kidney Dis. Apr 1996;27(4):496-503. [Medline].

  20. van Jaarsveld BC, Krijnen P, Pieterman H, et al. The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group. N Engl J Med. Apr 6 2000;342(14):1007-14. [Medline].

  21. van de Ven PJ, Kaatee R, Beutler JJ, et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomised trial. Lancet. Jan 23 1999;353(9149):282-6. [Medline].

  22. Ives NJ, Wheatley K, Stowe RL, et al. Continuing uncertainty about the value of percutaneous revascularization in atherosclerotic renovascular disease: a meta-analysis of randomized trials. Nephrol Dial Transplant. Feb 2003;18(2):298-304. [Medline].

  23. Textor SC. Ischemic nephropathy: where are we now?. J Am Soc Nephrol. Aug 2004;15(8):1974-82. [Medline].

  24. Plouin PF. Stable patients with atherosclerotic renal artery stenosis should be treated first with medical management. Am J Kidney Dis. Nov 2003;42(5):851-7. [Medline].

  25. [Best Evidence] Bax L, Woittiez AJ, Kouwenberg HJ, et al. Stent placement in patients with atherosclerotic renal artery stenosis and impaired renal function: a randomized trial. Ann Intern Med. Jun 16 2009;150(12):840-8, W150-1. [Medline][Full Text].

  26. Dejani H, Eisen TD, Finkelstein FO. Revascularization of renal artery stenosis in patients with renal insufficiency. Am J Kidney Dis. Oct 2000;36(4):752-8. [Medline].

  27. Bianchi S, Bigazzi R, Caiazza A, et al. A controlled, prospective study of the effects of atorvastatin on proteinuria and progression of kidney disease. Am J Kidney Dis. Mar 2003;41(3):565-70. [Medline].

  28. Schreiber MJ, Pohl MA, Novick AC. The natural history of atherosclerotic and fibrous renal artery disease. Urol Clin North Am. Aug 1984;11(3):383-92. [Medline].

  29. Greco BA, Breyer JA. Atherosclerotic ischemic renal disease. Am J Kidney Dis. Feb 1997;29(2):167-87. [Medline].

  30. Jacobson HR. Ischemic renal disease: an overlooked clinical entity?. Kidney Int. Nov 1988;34(5):729-43. [Medline].

  31. Krijnen P, Van Jaarsveld BC, Deinum J, et al. Which patients with hypertension and atherosclerotic renal artery stenosis benefit from immediate intervention?. J Hum Hypertens. Feb 2004;18(2):91-6. [Medline].

  32. Mailloux LU, Napolitano B, Bellucci AG, et al. Renal vascular disease causing end-stage renal disease, incidence, clinical correlates, and outcomes: a 20-year clinical experience. Am J Kidney Dis. Oct 1994;24(4):622-9. [Medline].

  33. Main J. When should atheromatous renal artery stenosis be considered? A guide for the general physician. Clin Med. Nov-Dec 2003;3(6):520-5. [Medline].

  34. Middleton JP. Ischemic disease of the kidney: how and why to consider revascularization. J Nephrol. May-Jun 1998;11(3):123-36. [Medline].

  35. Novick AC. Options for therapy of ischemic nephropathy: role of angioplasty and surgery. Semin Nephrol. Jan 1996;16(1):53-60. [Medline].

  36. Pedersen EB. New tools in diagnosing renal artery stenosis. Kidney Int. Jun 2000;57(6):2657-77. [Medline].

  37. Porter GA. Experimental contrast-associated nephropathy and its clinical implications. Am J Cardiol. Oct 26 1990;66(14):18F-22F. [Medline].

  38. Reilly LM, Cunningham CG, Maggisano R, et al. The role of arterial reconstruction in spontaneous renal artery dissection. J Vasc Surg. Oct 1991;14(4):468-77; discussion 477-9. [Medline].

  39. Safian RD, Textor SC. Renal-artery stenosis. N Engl J Med. Feb 8 2001;344(6):431-42. [Medline].

  40. Wilcox CS. Ischemic nephropathy: noninvasive testing. Semin Nephrol. Jan 1996;16(1):43-52. [Medline].

  41. Zuccala A, Zucchelli P. Ischemic nephropathy: diagnosis and treatment. J Nephrol. Nov-Dec 1998;11(6):318-24. [Medline].

  42. Zucchelli PC. Hypertension and atherosclerotic renal artery stenosis: diagnostic approach. J Am Soc Nephrol. Nov 2002;13 Suppl 3:S184-6. [Medline].

Further Reading

Keywords

renal artery stenosis, RAS, renovascular disease, ischemic nephropathy, atherosclerotic renovascular disease, renovascular hypertension, chronic renal insufficiency, end-stage renal disease, ESRD, atherosclerosis, ATH, RVD, renal artery occlusion, renal disease, kidney disease, ischemic renal disease, renal artery lesions

Contributor Information and Disclosures

Author

Bruce S Spinowitz, MD, FACP, Clinical Professor of Medicine, Weill Medical College of Cornell University; School of Medicine; Associate Chairman, Associate Director and Attending Physician, Department of Medicine, Division of Nephrology, New York Hospital Medical Center Queens; Associate, Nephrology Associates, PC
Bruce S Spinowitz, MD, FACP is a member of the following medical societies: American College of Physicians, American Society of Nephrology, International Society for Peritoneal Dialysis, International Society of Nephrology, and Renal Physicians Association
Disclosure: AMAG Pharmaceuticals Grant/research funds Independent contractor; Roche Grant/research funds Independent contractor; Amgen Grant/research funds Independent contractor; Affymax Grant/research funds Independent contractor; Ortho Biotech Grant/research funds Independent contractor

Coauthor(s)

Joanna Rodriguez, MD, Fellow, Department of Internal Medicine, Division of Nephrology, New York Hospital-Queens
Disclosure: Nothing to disclose.

Medical Editor

Donald A Feinfeld, MD, FACP, FASN, Consulting Staff, Division of Nephrology & Hypertension, Beth Israel Medical Center
Donald A Feinfeld, MD, FACP, FASN is a member of the following medical societies: American Academy of Clinical Toxicology, American Society of Hypertension, American Society of Nephrology, and National Kidney Foundation
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

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.

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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