Abstract
Ischemia-reperfusion-induced renal injury due to profound decrease of renal blood flow followed by restoration of renal perfusion is frequent in critically ill patients. Ischemic-induced microcirculatory dysfunction and perfusion defects persist after reperfusion leading to extension of initial renal damage, renal fibrosis, and acute or chronic renal failure. Renal ischemia-reperfusion should not be regarded as a sole ischemic injury with acute tubular necrosis but involves renal inflammation with infiltration of immune cells with tubular necrosis and apoptosis. Despite numerous promising pre-clinical therapeutic interventions protecting the kidney from ischemic injury, such strategies have been mostly unsuccessful in the clinical setting. Multiplicity of factors involved with complexes mechanisms of injury in most clinical scenarios may explain such discrepancy.
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