Acute Tubular Necrosis
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Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI) in the renal category (that is, AKI in which the pathology lies within the kidney itself). [1] See the ATN image below.
ATN follows a well-defined three-part sequence of initiation, maintenance, and recovery (see Pathophysiology). The initiation phase is characterized by an acute decrease in glomerular filtration rate (GFR) to very low levels, with a sudden increase in serum creatinine and blood urea nitrogen (BUN) concentrations.
The maintenance phase is characterized by a sustained severe reduction in GFR that persists for a variable length of time, most commonly 1-2 weeks. Because the filtration rate is so low during the maintenance phase, the creatinine and BUN levels continue to rise.
The recovery phase, in which tubular function is restored, is characterized by an increase in urine volume (if oliguria was present during the maintenance phase) and by a gradual decrease in BUN and serum creatinine to their preinjury levels.
The tubule cell damage and cell death that characterize ATN usually result from an acute ischemic or toxic event. Nephrotoxic mechanisms of ATN include direct drug toxicity, intrarenal vasoconstriction, and intratubular obstruction (see Pathophysiology and Etiology). Most of the pathophysiologic features of ischemic ATN are shared by the nephrotoxic forms. [2]
The history, physical examination, and laboratory findings, especially the renal ultrasonogram and the urinalysis, are particularly helpful in identifying the cause of ATN (see Presentation and Workup).
Therapeutic mainstays are prevention, avoidance of further kidney damage, treatment of underlying conditions, and aggressive treatment of complications (see Treatment and Medication).
Go to Pediatric Acute Tubular Necrosis for complete information on this topic. For patient education information, see the Diabetes Center, as well as Acute Kidney Failure.
Acute tubular necrosis (ATN) follows a well-defined three-part sequence of initiation, maintenance, and recovery (see below). The tubule cell damage and cell death that characterize ATN usually result from an acute ischemic or toxic event. Most of the pathophysiologic features of ischemic ATN, as described below, are shared by the nephrotoxic forms.
Ischemic ATN is often described as a continuum of prerenal azotemia. Indeed, the causes of the two conditions are the same. Ischemic ATN results when hypoperfusion overwhelms the kidney’s autoregulatory defenses. Under these conditions, hypoperfusion initiates cell injury that often, but not always, leads to cell death.
Injury of tubular cells is most prominent in the straight portion of the proximal tubules and in the thick ascending limb of the loop of Henle, especially as it dips into the relatively hypoxic medulla. The reduction in the glomerular filtration rate (GFR) that occurs from ischemic injury is a result not only of reduced filtration due to hypoperfusion but also of casts and debris obstructing the tubule lumen, causing back-leak of filtrate through the damaged epithelium (ie, ineffective filtration).
The earliest changes in the proximal tubular cells are apical blebs and loss of the brush border membrane followed by a loss of polarity and integrity of the tight junctions. This loss of epithelial cell barrier can result in the above-mentioned back-leak of filtrate.
Another change is relocation of Na+/K+-ATPase pumps and integrins to the apical membrane. Cell death occurs by both necrosis and apoptosis. Sloughing of live and dead cells occurs, leading to cast formation and obstruction of the tubular lumen (see the image below). Activation of the renal immune system—with damage to tubular cells stimulating local secretion of proinflammatory cytokines—in turn induces further necrosis. [3]
In addition, ischemia leads to decreased production of vasodilators (ie, nitric oxide, prostacyclin [prostaglandin I2, or PGI2]) by the tubular epithelial cells, leading to further vasoconstriction and hypoperfusion.
On a cellular level, ischemia causes depletion of adenosine triphosphate (ATP), an increase in cytosolic calcium, free radical formation, metabolism of membrane phospholipids, and abnormalities in cell volume regulation. The decrease or depletion of ATP leads to many problems with cellular function, not the least of which is active membrane transport.
With ineffective membrane transport, cell volume and electrolyte regulation are disrupted, leading to cell swelling and intracellular accumulation of sodium and calcium. Typically, phospholipid metabolism is altered, and membrane lipids undergo peroxidation. In addition, free radical formation is increased, producing toxic effects. Damage inflicted by free radicals apparently is most severe during reperfusion.
Maintenance phase
The maintenance phase of ATN is characterized by a stabilization of GFR at a very low level, and it typically lasts 1-2 weeks. Complications (eg, uremic and others; see Complications) typically develop during this phase.
The mechanisms of injury described above may contribute to continued nephron dysfunction, but tubuloglomerular feedback also plays a role. Tubuloglomerular feedback in this setting leads to constriction of afferent arterioles by the macula densa cells, which detect an increased salt load in the distal tubules.
The recovery phase of ATN is characterized by regeneration of tubular epithelial cells. [4] During recovery, an abnormal diuresis sometimes occurs, causing salt and water loss and volume depletion. The mechanism of the diuresis is not completely understood, but it may in part be due to the delayed recovery of tubular cell function in the setting of increased glomerular filtration. In addition, continued use of diuretics (often administered during initiation and maintenance phases) may also add to the problem.
This is a condition that develops in patients without an overt severe hypotensive episode. These patients have low-normal blood pressure but still have severe ATN. The most common reason for this condition is renal susceptibility to the lower blood pressure because of impairment of autoregulatory function of the kidney. Normally, the afferent arteriole dilates (via prostaglandins) and efferent arteriole constricts (via angiotensin-II) to maintain the glomerular capillary pressure. Factors that impair this autoregulatory mechanisms include the following [5] :
Sepsis is a recognized cause of ATN. However, the hypothesis that ATN develops in these cases when sepsis-related hypotension leads to a reduction in renal blood flow has been challenged by several animal and human studies. Those studies have indicated that in fact, renal blood flow may increase in that setting, due to a mechanism leading to efferent arteriolar vasodilatation. [6]
Other suspected contributors to ATN in sepsis include the following:
ATN is generally caused by an acute event, either ischemic or toxic.
Ischemic ATN may be considered part of the spectrum of prerenal azotemia, and indeed, ischemic ATN and prerenal azotemia have the same causes and risk factors. Specifically, these include the following:
Hypovolemic states: Hemorrhage, volume depletion from gastrointestinal (GI) or renal losses, burns, fluid sequestration
Low cardiac output states: Heart failure and other diseases of myocardium, valvulopathy, arrhythmia, pericardial diseases, tamponade
Systemic vasodilation: Sepsis, anaphylaxis
Disseminated intravascular coagulation
The kidney is a particularly vulnerable target for toxins, both exogenous and endogenous. Not only does it have a rich blood supply, receiving 25% of cardiac output, but it also helps in the excretion of these toxins by glomerular filtration and tubular secretion.
Exogenous nephrotoxins that cause ATN
Aminoglycoside-related toxicity occurs in 10-30% of patients receiving aminoglycosides, even when blood levels are in apparently therapeutic ranges. Risk factors for ATN in these patients include the following:
Amphotericin B nephrotoxicity risk factors include the following:
Radiographic contrast media can cause contrast-induced nephropathy (CIN) or radiocontrast nephropathy (RCN); this commonly occurs in patients with several risk factors, such as elevated baseline serum creatinine, preexisting renal insufficiency, underlying diabetic nephropathy, chronic heart failure [CHF], or high or repetitive doses of contrast media, as well as volume depletion and concomitant use of diuretics, ACE inhibitors, or ARBs. The 2011 UKRA guidelines recommend that patients at risk of CIN should have a careful evaluation of volume status and receive volume expansion with 0.9% sodium chloride or isotonic sodium bicarbonate before the procedure. [7]
Other exogenous nephrotoxins that can cause ATN include the following:
Cyclosporine and tacrolimus (calcineurin inhibitors)
Cisplatin
Ifosfamide
Foscarnet
Pentamidine, which is used to treat Pneumocystis jiroveci infection in immunocompromised individuals (risk factors for nephrotoxicity include volume depletion and concomitant use of other nephrotoxic antibiotic agents, such as aminoglycosides, which is common practice in the immunosuppressed)
Sulfa drugs
Acyclovir and indinavir
Mammalian target of rapamycin (mTOR) inhibitors (eg, everolimus, temsirolimus) [8]
Endogenous nephrotoxins that cause ATN
In myoglobinuria, rhabdomyolysis is the most common cause of heme pigment–associated acute kidney injury (AKI) and can result from traumatic or nontraumatic injuries. Most cases of rhabdomyolysis are nontraumatic, such as those related to alcohol abuse or drug-induced muscle toxicity (eg, statins alone or in combination with fibrates).
In hemoglobinuria, AKI is a rare complication of hemolysis and hemoglobinuria, and most often is associated with transfusion reactions (in contrast to myoglobin, hemoglobin has no apparent direct tubular toxicity, and AKI in this setting is probably related to hypotension and decreased renal perfusion). [8]
Acute crystal-induced nephropathy occurs when crystals are generated endogenously due to high cellular turnover (ie, uric acid, calcium phosphate), as observed in certain malignancies or the treatment of malignancies. However, this condition is also associated with ingestion of certain toxic substances (eg, ethylene glycol) or nontoxic substances (eg, vitamin C). Choudhry et al reported a case of AKI caused by ingestion of excessive quantities of calcium-containing antacids. [9]
In multiple myeloma, renal impairment results from the accumulation and precipitation of light chains, which form casts in the distal tubules that cause renal obstruction. In addition, myeloma light chains have a direct toxic effect on proximal renal tubules. [10]
For patients with ATN, the in-hospital survival rate is approximately 50%, with about 30% of patients surviving for 1 year. Factors associated with an increased mortality rate include the following:
The mortality rate in patients with ATN is probably related more to the severity of the underlying disease than to ATN itself. For example, the mortality rate in patients with ATN after sepsis or severe trauma is much higher (about 60%) than the mortality rate in patients with ATN that is nephrotoxin related (about 30%). The mortality rate is as high as 60-70% with patients in a surgical setting. If multiorgan failure is present, especially severe hypotension or acute respiratory distress syndrome, the mortality rate ranges from 50 to 80%.
Patients with oliguric ATN have a worse prognosis than patients with nonoliguric ATN. This probably is related to more severe necrosis and more significant disturbances in electrolyte balance. In addition, a rapid increase in serum creatinine (ie, >3 mg/dL) probably also indicates a poorer prognosis. Again, this probably reflects a more serious underlying disease.
Of the survivors of ATN, approximately 50% have some impairment of renal function. Some (about 5%) continue to undergo a decline in renal function. About 5% never recover kidney function and require dialysis.
A review of United States Renal Data System data (n = 1,070,490) for 2001 through 2010 found that although the incidence of end-stage renal disease (ESRD) attributed to ATN increased during that period, the prospects for renal recovery and survival also increased. Recovery of renal function was more likely in patients with ATN than in matched controls (cumulative incidence 23% vs. 2% at 12 weeks, 34% vs. 4% at 1 year), as was death (cumulative incidence 38% vs. 27% at 1 year). Hazards ratios for death declined in stepwise fashion to 0.83 in 2009-2010. [11]
For post AKI hospitalization outcomes and monitoring see Treatment/Long-Term Monitoring
The landmark PICARD (Program to Improve Care in Acute Renal Disease) study was an observational study of a cohort of 618 patients with acute kidney injury in the intensive care units of 5 academic centers in the United States. Ischemic ATN was the presumed etiology for 50% of all patients with renal failure, an additional ~12% due to unresolved pre-renal factors, and ~25% from nephrotoxic ATN. [12] These data were similar to those from the Madrid Acute Renal Failure Study Group. [13]
Hanif MO, Ramphul K. Renal Tubular Necrosis, Acute. 2018 Jan. [Medline]. [Full Text].
Lee HT, Kim JY, Kim M, Wang P, Tang L, Baroni S, et al. Renalase protects against ischemic AKI. J Am Soc Nephrol. 2013 Feb. 24(3):445-55. [Medline]. [Full Text].
Kundert F, Platen L, Iwakura T, Zhao Z, Marschner JA, Anders HJ. Immune mechanisms in the different phases of acute tubular necrosis. Kidney Res Clin Pract. 2018 Sep. 37 (3):185-196. [Medline]. [Full Text].
Verghese E, Ricardo SD, Weidenfeld R, et al. Renal primary cilia lengthen after acute tubular necrosis. J Am Soc Nephrol. 2009 Jul 16. [Medline]. [Full Text].
Abuelo JG. Normotensive ischemic acute renal failure. N Engl J Med. 2007 Aug 23. 357 (8):797-805. [Medline].
Wan L, Langenberg C, Bellomo R, May CN. Angiotensin II in experimental hyperdynamic sepsis. Crit Care. 2009. 13 (6):R190. [Medline].
[Guideline] Lewington A, Kanagasundaram S. Renal Association Clinical Practice Guidelines on acute kidney injury. Nephron Clin Pract. 2011. 118 Suppl 1:c349-90. [Medline]. [Full Text].
Izzedine H, Escudier B, Rouvier P, Gueutin V, Varga A, Bahleda R, et al. Acute tubular necrosis associated with mTOR inhibitor therapy: a real entity biopsy-proven. Ann Oncol. 2013 Sep. 24(9):2421-5. [Medline].
Choudhry WM, Nori US, Nadasdy T, Satoskar AA. An unexpected cause of acute kidney injury in a patient with ANCA associated vasculitis. Clin Nephrol. 2016 May. 85 (5):289-95. [Medline].
Dimopoulos MA, Kastritis E, Rosinol L, Bladé J, Ludwig H. Pathogenesis and treatment of renal failure in multiple myeloma. Leukemia. 2008 Aug. 22 (8):1485-93. [Medline]. [Full Text].
Foley RN, Sexton DJ, Reule S, Solid C, Chen SC, Collins AJ. End-stage renal disease attributed to acute tubular necrosis in the United States, 2001-2010. Am J Nephrol. 2015. 41 (1):1-6. [Medline].
Mehta RL, Pascual MT, Soroko S, Savage BR, Himmelfarb J, Ikizler TA, et al. Spectrum of acute renal failure in the intensive care unit: the PICARD experience. Kidney Int. 2004 Oct. 66 (4):1613-21. [Medline].
Liaño F, Pascual J. Epidemiology of acute renal failure: a prospective, multicenter, community-based study. Madrid Acute Renal Failure Study Group. Kidney Int. 1996 Sep. 50 (3):811-8. [Medline].
Al-Jaghbeer M, Kellum JA. Acid-base disturbances in intensive care patients: etiology, pathophysiology and treatment. Nephrol Dial Transplant. 2015 Jul. 30 (7):1104-11. [Medline].
Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004 Aug. 8(4):R204-12. [Medline]. [Full Text].
Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007. 11(2):R31. [Medline]. [Full Text].
American College of Radiology. ACR Appropriateness Criteria: Renal Failure. Available at http://bit.ly/ewIXV5. Accessed: September 10, 2010.
Perdiz LB, Furtado GH, Linhares MM, et al. Incidence and risk factors for surgical site infection after simultaneous pancreas-kidney transplantation. J Hosp Infect. 2009 Aug. 72(4):326-31. [Medline].
Mattoso R, Khouri N, de Jesus L, et al. Risk factors for graft dysfunction in the late period of renal transplantation. Transplant Proc. 2009 Jun. 41(5):1594-8. [Medline].
Devarajan P. Emerging biomarkers of acute kidney injury. Contrib Nephrol. 2007. 156:203-12. [Medline].
Belcher JM, Sanyal AJ, Peixoto AJ, Perazella MA, Lim J, Thiessen-Philbrook H, et al. Kidney biomarkers and differential diagnosis of patients with cirrhosis and acute kidney injury. Hepatology. 2014 Aug. 60(2):622-32. [Medline]. [Full Text].
Koyner JL, Davison DL, Brasha-Mitchell E, Chalikonda DM, Arthur JM, Shaw AD, et al. Furosemide Stress Test and Biomarkers for the Prediction of AKI Severity. J Am Soc Nephrol. 2015 Aug. 26 (8):2023-31. [Medline]. [Full Text].
Chawla LS, Davison DL, Brasha-Mitchell E, Koyner JL, Arthur JM, Shaw AD, et al. Development and standardization of a furosemide stress test to predict the severity of acute kidney injury. Crit Care. 2013 Sep 20. 17 (5):R207. [Medline]. [Full Text].
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2:1-138.
Maxwell RA, Bell CM. Acute Kidney Injury in the Critically Ill. Surg Clin North Am. 2017 Dec. 97 (6):1399-1418. [Medline].
Jones D, Bellomo R. Renal-dose dopamine: from hypothesis to paradigm to dogma to myth and, finally, superstition?. J Intensive Care Med. 2005 Jul-Aug. 20 (4):199-211. [Medline].
Bhatt GC, Das RR. Early versus late initiation of renal replacement therapy in patients with acute kidney injury-a systematic review & meta-analysis of randomized controlled trials. BMC Nephrol. 2017 Feb 28. 18 (1):78. [Medline].
Faubel S, Shah PB. Immediate Consequences of Acute Kidney Injury: The Impact of Traditional and Nontraditional Complications on Mortality in Acute Kidney Injury. Adv Chronic Kidney Dis. 2016 May. 23 (3):179-85. [Medline].
Nagler EV, Vanmassenhove J, van der Veer SN, Nistor I, Van Biesen W, Webster AC, et al. Diagnosis and treatment of hyponatremia: a systematic review of clinical practice guidelines and consensus statements. BMC Med. 2014 Dec 11. 12:1. [Medline].
Prins JM, Büller HR, Kuijper EJ, Tange RA, Speelman P. Once versus thrice daily gentamicin in patients with serious infections. Lancet. 1993 Feb 6. 341 (8841):335-9. [Medline].
Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med. 2002 Feb 11. 162(3):329-36. [Medline].
Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA. 2004 May 19. 291(19):2328-34. [Medline].
Tepel M, van der Giet M, Schwarzfeld C, et al. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med. 2000 Jul 20. 343(3):180-4. [Medline].
Weisbord SD, Gallagher M, Jneid H, Garcia S, Cass A, Thwin SS, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine. N Engl J Med. 2017 Nov 12. [Medline].
Coca SG, Singanamala S, Parikh CR. Chronic kidney disease after acute kidney injury: a systematic review and meta-analysis. Kidney Int. 2012 Mar. 81 (5):442-8. [Medline].
Pannu N, James M, Hemmelgarn B, Klarenbach S, Alberta Kidney Disease Network. Association between AKI, recovery of renal function, and long-term outcomes after hospital discharge. Clin J Am Soc Nephrol. 2013 Feb. 8 (2):194-202. [Medline].
Silver SA, Siew ED. Follow-up Care in Acute Kidney Injury: Lost in Transition. Adv Chronic Kidney Dis. 2017 Jul. 24 (4):246-252. [Medline].
Wijewickrama ES, Gooneratne L, De Silva C, Lanarolle RL. Acute tubular necrosis in a patient with paroxysmal nocturnal hemoglobinuria. Saudi J Kidney Dis Transpl. 2013 Jan. 24(1):105-8. [Medline].
Dent CL, Ma Q, Dastrala S, et al. Plasma neutrophil gelatinase-associated lipocalin predicts acute kidney injury, morbidity and mortality after pediatric cardiac surgery: a prospective uncontrolled cohort study. Crit Care. 2007. 11(6):R127. [Medline].
du Cheyron D, Daubin C, Poggioli J, et al. Urinary measurement of Na+/H+ exchanger isoform 3 (NHE3) protein as new marker of tubule injury in critically ill patients with ARF. Am J Kidney Dis. 2003 Sep. 42(3):497-506. [Medline].
Han WK, Bailly V, Abichandani R, et al. Kidney Injury Molecule-1 (KIM-1): a novel biomarker for human renal proximal tubule injury. Kidney Int. 2002 Jul. 62(1):237-44. [Medline].
Hirsch R, Dent C, Pfriem H, et al. NGAL is an early predictive biomarker of contrast-induced nephropathy in children. Pediatr Nephrol. 2007 Dec. 22(12):2089-95. [Medline].
Mishra J, Dent C, Tarabishi R, et al. Neutrophil gelatinase-associated lipocalin (NGAL) as a biomarker for acute renal injury after cardiac surgery. Lancet. 2005 Apr 2-8. 365(9466):1231-8. [Medline].
Mishra J, Ma Q, Kelly C, et al. Kidney NGAL is a novel early marker of acute injury following transplantation. Pediatr Nephrol. 2006 Jun. 21(6):856-63. [Medline].
Mishra J, Mori K, Ma Q, et al. Amelioration of ischemic acute renal injury by neutrophil gelatinase-associated lipocalin. J Am Soc Nephrol. 2004 Dec. 15(12):3073-82. [Medline].
Parikh CR, Jani A, Melnikov VY, et al. Urinary interleukin-18 is a marker of human acute tubular necrosis. Am J Kidney Dis. 2004 Mar. 43(3):405-14. [Medline].
van Timmeren MM, Vaidya VS, van Ree RM, et al. High urinary excretion of kidney injury molecule-1 is an independent predictor of graft loss in renal transplant recipients. Transplantation. 2007 Dec 27. 84(12):1625-30. [Medline]. [Full Text].
Wagener G, Jan M, Kim M, et al. Association between increases in urinary neutrophil gelatinase-associated lipocalin and acute renal dysfunction after adult cardiac surgery. Anesthesiology. 2006 Sep. 105(3):485-91. [Medline].
Zhou H, Hewitt SM, Yuen PS, et al. Acute kidney injury biomarkers – needs, present status, and future promise. Nephrol Self Assess Program. 2006 Mar. 5(2):63-71. [Medline]. [Full Text].
Hickson LJ, Chaudhary S, Williams AW, Dillon JJ, Norby SM, Gregoire JR, et al. Predictors of outpatient kidney function recovery among patients who initiate hemodialysis in the hospital. Am J Kidney Dis. 2015 Apr. 65 (4):592-602. [Medline].
Finding
Prerenal Azotemia
ATN and/or Intrinsic Renal Disease
Urine osmolarity
(mOsm/kg)
>500
< 350
Urine sodium
(mmol/d)
< 20
>40
Fractional excretion of sodium (FENa)
(%)
< 1
>2
Fractional excretion of urea
(%)
< 35
>50
Urine sediment
Bland and/or nonspecific
May show muddy brown granular casts
Nikhil A Shah, MBBS, DNB(Neph) Clinical Research Fellow in Home Dialysis, Nephrologist, University of Alberta Faculty of Medicine and Dentistry, Canada
Nikhil A Shah, MBBS, DNB(Neph) is a member of the following medical societies: American Society of Nephrology, American Society of Transplantation, Canadian Medical Protective Association, Canadian Society of Nephrology, Indian Society of Nephrology, International Society of Nephrology
Disclosure: Nothing to disclose.
Mahendra Agraharkar, MD, MBBS, FACP, FASN Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology
Mahendra Agraharkar, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology, National Kidney Foundation
Disclosure: Nothing to disclose.
Brent Kelly, MD Assistant Professor, Department of Dermatology, University of Texas Medical Branch, Galveston, Texas
Brent Kelly, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association
Disclosure: Nothing to disclose.
Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF Clinical Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Research Director, Internal Medicine Training Program, Advocate Christ Medical Center; Consulting Staff, Associates in Nephrology, SC
Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF 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, Society of General Internal Medicine
Disclosure: Author for: UpToDate, ACP Smart Medicine, Elsevier, McGraw-Hill, Wolters Kluwer.
Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology, Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.
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.
F John Gennari, MD Associate Chair for Academic Affairs, Robert F and Genevieve B Patrick Professor, Department of Medicine, University of Vermont College of Medicine
F John Gennari, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
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