Official reprint from UpToDate®
www.uptodate.com ©2016 UpToDate®

Overview of the management of acute kidney injury (acute renal failure)

Mark D Okusa, MD
Mitchell H Rosner, MD
Section Editor
Paul M Palevsky, MD
Deputy Editor
Alice M Sheridan, MD


Acute renal failure (ARF) is an abrupt and usually reversible decline in the glomerular filtration rate (GFR). This results in an elevation of serum blood urea nitrogen (BUN), creatinine, and other metabolic waste products that are normally excreted by the kidney.

The term acute kidney injury (AKI), rather than ARF, is increasingly used by the nephrology community to refer to the acute loss of kidney function. This term also highlights that injury to the kidney that does not result in "failure" is also of great clinical significance. In this topic review, the acute loss of kidney function will be referred to as AKI.

The initial assessment of patients with AKI and management of the major complications of AKI are discussed here. The incidence, causes, diagnosis, and prevention of AKI are presented separately. (See "Diagnostic approach to the patient with subacute kidney injury in an outpatient setting" and "Renal and patient outcomes after acute tubular necrosis" and "Possible prevention and therapy of postischemic (ischemic) acute tubular necrosis".)


AKI has multiple possible etiologies. Among hospitalized patients, AKI is most commonly due to acute tubular necrosis (ATN) from ischemia, nephrotoxin exposure, or sepsis [1]. The pathogenesis of ATN is discussed elsewhere. (See "Pathogenesis and etiology of postischemic (ischemic) acute tubular necrosis" and "Pathogenesis, clinical features, and diagnosis of contrast-induced nephropathy".)

Other frequent causes of AKI among either ambulatory or hospitalized patients include volume depletion, urinary obstruction, rapidly progressive glomerulonephritis, and acute interstitial nephritis. The pathogeneses of these disorders are also discussed elsewhere. (See "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury (acute renal failure)" and "Clinical manifestations and diagnosis of urinary tract obstruction and hydronephrosis" and "Overview of the classification and treatment of rapidly progressive (crescentic) glomerulonephritis" and "Clinical manifestations and diagnosis of acute interstitial nephritis".)


Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: Sep 2016. | This topic last updated: Jan 15, 2016.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2016 UpToDate, Inc.
  1. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis 2002; 39:930.
  2. Bagshaw SM, Bellomo R, Kellum JA. Oliguria, volume overload, and loop diuretics. Crit Care Med 2008; 36:S172.
  3. Grams ME, Estrella MM, Coresh J, et al. Fluid balance, diuretic use, and mortality in acute kidney injury. Clin J Am Soc Nephrol 2011; 6:966.
  4. Goldstein SL, Somers MJ, Baum MA, et al. Pediatric patients with multi-organ dysfunction syndrome receiving continuous renal replacement therapy. Kidney Int 2005; 67:653.
  5. Payen D, de Pont AC, Sakr Y, et al. A positive fluid balance is associated with a worse outcome in patients with acute renal failure. Crit Care 2008; 12:R74.
  6. Bouchard J, Soroko SB, Chertow GM, et al. Fluid accumulation, survival and recovery of kidney function in critically ill patients with acute kidney injury. Kidney Int 2009; 76:422.
  7. Kraut JA, Kurtz I. Use of base in the treatment of severe acidemic states. Am J Kidney Dis 2001; 38:703.
  8. Marsh JD, Margolis TI, Kim D. Mechanism of diminished contractile response to catecholamines during acidosis. Am J Physiol 1988; 254:H20.
  9. Mitchell JH, Wildenthal K, Johnson RL Jr. The effects of acid-base disturbances on cardiovascular and pulmonary function. Kidney Int 1972; 1:375.
  10. Teplinsky K, O'Toole M, Olman M, et al. Effect of lactic acidosis on canine hemodynamics and left ventricular function. Am J Physiol 1990; 258:H1193.
  11. Orchard CH, Kentish JC. Effects of changes of pH on the contractile function of cardiac muscle. Am J Physiol 1990; 258:C967.
  12. Mathieu D, Neviere R, Billard V, et al. Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study. Crit Care Med 1991; 19:1352.
  13. Orchard CH, Cingolani HE. Acidosis and arrhythmias in cardiac muscle. Cardiovasc Res 1994; 28:1312.
  14. Kraut JA, Madias NE. Treatment of acute metabolic acidosis: a pathophysiologic approach. Nat Rev Nephrol 2012; 8:589.
  15. MB, HMG. Metabolic Acidosis. In: Fluid, Electrolyte and Acid-Base Physiology, WB Saunders, Philadelphia 1993.
  16. Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296.
  17. Cooper DJ, Walley KR, Wiggs BR, Russell JA. Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective, controlled clinical study. Ann Intern Med 1990; 112:492.
  18. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med 2001; 344:264.
  19. Massry SG, Stein R, Garty J, et al. Skeletal resistance to the calcemic action of parathyroid hormone in uremia: role of 1,25 (OH)2 D3. Kidney Int 1976; 9:467.
  20. Massry SG, Arieff AI, Coburn JW, et al. Divalent ion metabolism in patients with acute renal failure: studies on the mechanism of hypocalcemia. Kidney Int 1974; 5:437.
  21. Tohme JF, Bilezikian JP. Diagnosis and treatment of hypocalcemic emergencies. The Endocrinologist 1996; 6:10.
  22. Fiaccadori E, Cremaschi E. Nutritional assessment and support in acute kidney injury. Curr Opin Crit Care 2009; 15:474.
  23. Krishnan JA, Parce PB, Martinez A, et al. Caloric intake in medical ICU patients: consistency of care with guidelines and relationship to clinical outcomes. Chest 2003; 124:297.
  24. Bellomo R, Seacombe J, Daskalakis M, et al. A prospective comparative study of moderate versus high protein intake for critically ill patients with acute renal failure. Ren Fail 1997; 19:111.
  25. Fouque D, Kalantar-Zadeh K, Kopple J, et al. A proposed nomenclature and diagnostic criteria for protein-energy wasting in acute and chronic kidney disease. Kidney Int 2008; 73:391.
  26. McClave SA, Martindale RG, Vanek VW, et al. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr 2009; 33:277.
  27. Fiaccadori E, Maggiore U, Giacosa R, et al. Enteral nutrition in patients with acute renal failure. Kidney Int 2004; 65:999.
  28. Li Y, Tang X, Zhang J, Wu T. Nutritional support for acute kidney injury. Cochrane Database Syst Rev 2010; :CD005426.
  29. Lameire N, Van Biesen W, Vanholder R. Acute renal failure. Lancet 2005; 365:417.