During the acute phase of burn inju

During the acute phase of burn injury, renal blood
flow and glomerular filtration rate (GFR), as measured
by creatinine clearance, decrease. In the hypermetabolic
phase, creatinine clearance is increased, indicating that
both blood flow and GFR are raised; however, tubular
function is impaired (44). Diminished blood volume and
cardiac output cause a post burn decrease in renal blood
flow and glomerular filtration rate. If untreated, the
resulting oliguria may progress to acute renal failure.
The incidence of acute renal failure (ARF) in severely
burned patients ranges from 1.3 to 38% and this
complication has always been associated with high
mortality rates (73 to 100%). The pathophysiologicmechanism may be related to filtration failure or tubular
dysfunction (45). Two different forms of acute renal
failure have been described in burned patients, differing
in terms of their time of onset (45-51). The first occurs
during the first few days after the injury and is related
to hypovolemia with low cardiac output and systemic
vasoconstriction during the resuscitation period or to
myoglobinuria, which damages the tubular cells
(45,46,50,51). Elevated levels of stress hormones like
catecholamines, angiotensin, aldosterone and
vasopressin have been reported to be implicated in the
pathogenesis of this form of ARF (50). Although this
form of ARF has become less frequent than before with
aggressive fluid resuscitation, it still is a life-threatening
complication in patients with extensive deep burns or
with electro-trauma (46,47,51). The other form of ARF
develops later and has a more complex pathogenesis.
This form has been reported to be related to sepsis and
multiorgan failure and is most often fatal. It has been
said to occur more often in patients with inhalation
injury and is considered the most frequent cause of renal
insufficiency in burn patients (49,51). In addition to
these mechanisms that support the pathogenesis, we
have recently shown that the kidney damage induced by
burn injury is dependent upon the formation of oxygen
radicals, as evidenced by increased lipid and protein
oxidation with a concomitant decrease in renal
antioxidant (glutathione) levels