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Acute renal failure (ARF), or acute kidney injury (AKI), as it is now referred to in the literature, is defined as an abrupt or rapid decline in renal filtration function. This condition is usually marked by a rise in serum creatinine concentration or by azotemia (a rise in blood urea nitrogen [BUN] concentration).

However, immediately after a kidney injury, BUN or creatinine levels may be normal, and the only sign of a kidney injury may be decreased urine production. (See History.)

A rise in the creatinine level can result from medications (eg, cimetidine, trimethoprim) that inhibit the kidney’s tubular secretion. A rise in the BUN level can occur without renal injury, resulting instead from such sources as GI or mucosal bleeding, steroid use, or protein loading, so a careful inventory must be taken before determining if a kidney injury is present.

Categories of AKI

AKI may be classified into 3 general categories, as follows:

Prerenal - as an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons

Intrinsic - in response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage

Postrenal - from obstruction to the passage of urine

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