Acute kidney injury (AKI), also known as acute renal failure, is a rapidly progressive loss of renal function, which is characterized by oliguria (decreased urine production, quantified as less than 400 mL per day in adults, less than 0.5 mL/kg/h in children or less than 1 mL/kg/h in infants); body water and body fluids disturbances; and electrolyte derangement. AKI can result from a variety of causes, generally classified as prerenal, intrinsic, and postrenal. An underlying cause must be identified and treated to arrest the progress, and dialysis may be necessary to bridge the time gap required for treating these fundamental causes.
Acute kidney injury can be caused by damage to the glomeruli, renal tubules, or interstitium. Common causes of each are glomerulonephritis, acute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively. Other causes of acute kidney injury can be decrease effective blood flow to the kidney. These include low blood volume, low blood pressure, and heart failure. Changes to the blood vessels supplying the kidney can also lead to prerenal AKI. These include renal artery stenosis, which is a narrowing of the renal artery that supplies the kidney, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney.
The treatment of acute kidney injury is the treatment of the underlying cause of this condition. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, and others. Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.