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Abstract
Delayed graft function is a form of acute renal failure resulting in post-transplantation
oliguria, increased allograft immunogenicity and risk of acute rejection episodes,
and decreased long-term survival. Factors related to the donor and prerenal, renal,
or postrenal transplant factors related to the recipient can contribute to this condition.
From experimental studies, we have learnt that both ischaemia and reinstitution of
blood flow in ischaemically damaged kidneys after hypothermic preservation activate
a complex sequence of events that sustain renal injury and play a pivotal part in
the development of delayed graft function. Elucidation of the pathophysiology of renal
ischaemia and reperfusion injury has contributed to the development of strategies
to decrease the rate of delayed graft function, focusing on donor management, organ
procurement and preservation techniques, recipient fluid management, and pharmacological
agents (vasodilators, antioxidants, anti-inflammatory agents). Several new drugs show
promise in animal studies in preventing or ameliorating ischaemia-reperfusion injury
and possibly delayed graft function, but definitive clinical trials are lacking. The
goal of monotherapy for the prevention or treatment of is perhaps unattainable, and
multidrug approaches or single drug targeting multiple signals will be the next step
to reduce post-transplantation injury and delayed graft function.