Acute renal failure remains a common, devastating complication of the postoperative period and in the critically ill patient. The most common cause is the progression of prerenal insufficiency to ATN. Despite improved understanding of the pathogenic mechanisms, including impaired hemodynamic autoregulation, medullary hypoxia, and proximal tubular obstruction and transtubular backleak, the treatment, to date, remains largely supportive. Avoidance by ensuring hemodynamic stability, with provision of adequate renal perfusion, provides the best means for minimizing the complications of this organ dysfunction.
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