Approximately 10,000 people develop ARF each year. It has been estimated that 5% of hospital admissions, 30% of clients in critical care units, and 25% of all hospitalized patients develop ARF.

Acute tubular necrosis (ATN), one cause of ARF, occurs because of renal hypoperfusion or in response to nephrotoxic drugs, such as aminoglycosides, and chemicals, such as radiological dyes, which set up an inflammatory process leading to tubular edema, obstruction, and ischemia. Up to 12% of patients exposed to radiocontrast agents develop ATN. Other causes of ATN are major trauma, systemic infections, and muscle breakdown, which produces myoglobin, a substance that clogs renal tubules. Damaged tubules result in a decreased ability to maintain homeostasis. ATN usually resolves in about 8 weeks.

The factors that instigate prerenal ARF (i.e., factors that occur before blood being filtered by the kidneys) are caused by renal hypoperfusion and account for approximately 40-80% of ARF cases per year. Prerenal factors include those that cause decreased cardiac output such as shock and congestive heart failure, volume depletion from vomiting, or increased renal vascular resistance as occurs in renal artery stenosis. If perfusion can be restored in a short amount of time, permanent renal damage can be averted. In prerenal ARF, urine osmolality is high and urine sodium is low, because although renal perfusion is greatly decreased, renal tubular function is normal.

Intrarenal ARF results from injury to the kidney itself from emboli or ATN. Sodium cannot be conserved and urine cannot be concentrated because of glomerular damage. Postrenal or obstructive ARF results from urinary tract obstruction by renal calculi or prostatic enlargement; thus urine osmolarity and sodium levels are usually unaffected.