The complex pathogenesis of ischemia reperfusion injury (IRI) includes endothelial
expression of adhesion molecules, leukocyte recruitment and activation, reactive oxygen
species production, and apoptotic and necrotic cell death. A role for complement in IRI of
different organs, including kidney, has been proposed on the basis of results of experiments
that used pharmacologic inhibitors as well as animals that were deficient in individual
complement proteins. Here, renal IRI in mice was examined. Animals that were deficient in …