Pathophysiology of acute renal failure

Acute renal failure (ARF) is a common renal disease affecting up to 5% of all hospitalized patients, with a higher prevalence of 10-30% in patients in critical care units (1-3). Despite advances in the management of critically ill patients and technological advances in renal replacement therapy, the high mortality of patients with ARF has not changed over the last decades and remains above 50% (4-6). Moreover, as a consequence of more advanced medical therapy and more complicated surgical interventions in older and multimorbid patients, the number of patients with ARF is increasing (1, 4, 5). Moreover, ARF itself increases the risk to develop additional complications that can be deleterious. Recently, an independent association between ARF and mortality has been shown in patients following administration of radiocontrast media in an intensive care unit and in patients following cardiac surgery (6, 7). Following radiocontrast media the mortality of patients with ARF was increased five fold and following cardiac surgery sixteen-fold as compared to patients with the same underlying disease without ARF. The pathophysiology of ischemic ARF is reviewed with the emphasis on the following mechanisms: Increased fractional excretion of sodium, Activation of tubuloglomerular feedback, Cytoskeletal disruption, Tubular obstruction, Vascular mechanisms. The following mediators will also be discussed: Calcium, Cysteine proteases, Nitric oxide, Adhesion receptors and integrins.