This article summarizes the pathophysiology of acute renal failure from both experimental and clinical points of view. Prerenal acute renal failure is an appropriate physiologic response to renal hypoperfusion and can complicate any disease characterized by either true hypovolemia or a reduction in the effective circulating volume. In acute tubular necrosis, the abrupt fall in glomerular filtration rate is thought to be caused by interplay of hemodynamic and tubular abnormalities. The postischemic kidney also shows a dramatic capacity for recovery. The molecular mechanisms and the effect of growth factors are also summarized.