Overview of the management of acute kidney injury in adults
- Mark D Okusa, MD
Mark D Okusa, MD
- Professor of Medicine
- University of Virginia Health System
- Mitchell H Rosner, MD
Mitchell H Rosner, MD
- Professor of Medicine
- University of Virginia Health System
Acute kidney injury (AKI) 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 AKI, rather than acute renal failure (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 adult patients with subacute kidney injury in an outpatient setting" and "Kidney and patient outcomes after acute kidney injury in adults" and "Possible prevention and therapy of ischemic acute tubular necrosis".)
AKI has multiple possible etiologies. Among hospitalized patients, AKI is most commonly due to either prerenal etiologies (volume depletion, "third spacing," effective volume depletion from heart failure or cirrhosis) or acute tubular necrosis (ATN) from ischemia, nephrotoxin exposure, or sepsis . The pathogenesis of ATN is discussed elsewhere. (See "Pathogenesis and etiology of 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 in adults" 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".)To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- RISK SCORE FOR PREDICTION
- INITIAL EVALUATION AFTER DIAGNOSIS
- Immediate therapy
- Volume issues
- - Volume depletion
- - Volume overload
- Metabolic acidosis
- Bleeding disorders
- Indications for dialysis therapy
- SOCIETY GUIDELINE LINKS
- SUMMARY AND RECOMMENDATIONS