Acute renal failure, now referred to as acute kidney injury (AKI), complicates 5–10% of general hospital admissions and is associated with increased morbidity and mortality and prolonged hospitalizations. The definition of AKI varies, but it is usually defined as an increase in serum creatinine concentration of 25–50% above the baseline, a decline in estimated glomerular filtration rate (eGFR) of 25–50%, or the need for renal replacement therapy. It is now recognized that changes in GFR are delayed manifestations of renal injury, and the development of urinary biomarkers may help to identify AKI earlier in the course of injury. The major causes of AKI in hospitalized patients include prerenal causes (~40%), postrenal causes (~5–10%), and intrinsic diseases affecting blood vessels, glomeruli, or tubules. Of the intrinsic causes, tubular disorders (acute tubular necrosis and acute interstitial nephritis) are the most common etiologies, accounting for 40–50% of all causes of AKI. Acute glomerulonephritis and vascular disorders are rare etiologies of AKI in hospitalized patients (〈5%).