Acute renal failure (ARF) or acute kidney injury (AKI), defined as a measurable increase in the serum creatinine (Cr) concentration (usually relative increase of 50% or absolute increase by 44–88 µmol/L [0.5–1.0 mg/dL]), occurs in ∼5–7% of hospitalized pts. It is associated with a substantial increase in in-hospital mortality and morbidity. AKI can be anticipated in some clinical circumstances (e.g., after radiocontrast exposure or major surgery), and there are no specific pharmacologic therapies proven helpful at preventing or reversing the condition. It is important to recognize that AKI is a clinical diagnosis and not a structural one. A pt may have AKI with or without injury to the kidney parenchyma. AKI can range in severity from asymptomatic and transient changes in laboratory parameters of glomerular filtration rate (GFR), to overwhelming and rapidly fatal derangements in effective circulating volume regulation and electrolyte and acid-base composition of the plasma. Maintaining optimal renal perfusion and intravascular volume is critical in most clinical circumstances; important cofactors in AKI include hypovolemia and drugs that interfere with renal perfusion and/or glomerular filtration (nonsteroidal anti-inflammatory drugs [NSAIDs], angiotensin-converting enzyme [ACE] inhibitors, and angiotensin receptor blockers).