Acute renal failure (ARF) is a common renal disease affecting up to 5% of a
ll hospitalized patients, with a higher prevalence of 10-30% in patients in
critical care units (1-3). Despite advances in the management of criticall
y 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 me
dical therapy and more complicated surgical interventions in older and mult
imorbid 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 radioc
ontrast media in an intensive care unit and in patients following cardiac s
urgery (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 path
ophysiology of ischemic ARF is reviewed with the emphasis on the following
mechanisms: Increased fractional excretion of sodium, Activation of tubulog
lomerular feedback, Cytoskeletal disruption, Tubular obstruction, Vascular
mechanisms. The following mediators will also be discussed: Calcium, Cystei
ne proteases, Nitric oxide, Adhesion receptors and integrins.