The pathogenesis of acute renal failure has been attributed to persistent vasoconstriction and leukocyte-endothelial interactions, resulting in inflammation and compromise of local blood flow to the outer medulla, the loss of tubular epithelial cell polarity with multiple functional sequelae, necrosis or apoptosis of epithelial cells, and the de-differentiation, migration and proliferation of surviving cells. In this paper, the authors present their views of pathophysiology of ischemic acute renal failure.