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Prevention and treatment of heme pigment-induced acute kidney injury (acute renal failure)

Joseph A Eustace, MB, MHS, MRCPI
Section Editor
Paul M Palevsky, MD
Deputy Editor
Alice M Sheridan, MD


Acute kidney injury (AKI) can occur in patients who have rhabdomyolysis and, less commonly, in patients with hemolysis [1,2]. In both groups of patients, AKI is caused by the nonprotein heme pigment that is released from either myoglobin or hemoglobin and is toxic to the kidney.

The prevention and treatment of heme pigment-induced AKI due to nontraumatic rhabdomyolysis or hemolysis will be reviewed here. The clinical features and diagnosis of this disorder, AKI due to traumatic muscle injury, overviews of rhabdomyolysis and hemolysis, and the general management of oliguric acute renal failure (ARF) and its complications are discussed elsewhere. (See "Clinical features and diagnosis of heme pigment-induced acute kidney injury (acute renal failure)" and "Crush-related acute kidney injury (acute renal failure)" and "Clinical manifestations and diagnosis of rhabdomyolysis" and "Diagnosis of hemolytic anemia in the adult" and "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Recovery of renal function and effect of hemodialysis membrane".)


In addition to treating the underlying rhabdomyolysis or hemolysis, the general goals for preventive therapy in all patients at risk for heme pigment-induced AKI are twofold:

Correction of volume depletion if present

Prevention of intratubular cast formation


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Literature review current through: Sep 2016. | This topic last updated: Nov 16, 2015.
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