The pathogenesis of human acute ischemic renal failure is complex. Studies in animals have revealed a number of factors that could contribute to the injury associated with acute ischemic renal failure. Despite these discoveries, we have yet to devise a therapeutic regimen that will ameliorate or prevent acute renal failure in humans. Nevertheless we have made great strides in understanding mechanisms that contribute to acute ischemic renal failure. An important component is the contribution of the inflammatory cascade brought about by tissue reperfusion following an ischemic period. This review summarizes recent studies that implicate the inflammatory cells in the development of renal injury associated with acute ischemic renal failure. Because of the complex overlapping pathways involved in the inflammatory cascade, blocking single molecules is unlikely to be successful in reducing renal injury. Rather broadly abrogating the inflammatory cascade is likely to yield the greatest success in the treatment and prevention of acute ischemic renal failure.