Ischemia reperfusion injury occurs in the kidney when blood supply is interrupted in clinical settings such as kidney transplantation or nephron sparing surgery for renal tumors. These lesions lead to acute kidney injury (AKI) a detrimental situation associated with impaired short-term allograft function (delayed graft function or primary non function) but also long-term transplant survival through the onset of chronic allograft nephropathy. The present review details the cellular and molecular consequences of ischemia reperfusion in a native kidney as well as in a kidney graft after cold ischemia time, giving a comprehensive description of biological pathways involved during the phase of ischemia and during the reperfusion period where the rapid return to normoxia leads to a large burst of reactive oxygen species along with a dramatic reduction in antioxidant defenses. This work also focuses on the distinct susceptibilities of kidney cells to ischemia (endothelial vs epithelial) and the outcome of acute kidney injury.
Keywords: Acute Kidney Injury; Chronic allograft nephropathy; Immunité innée; Innate Immune Response; Ischemia-reperfusion injury; Ischémie-reperfusion; Nécrose tubulaire aigue; Néphropathie chronique; Radicaux libres; Reactive oxygen species; Stress oxydatif.
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