Ischaemia‐reperfusion injury is a complex interrelated sequence of events that classically involves the vascular endothelium and activated leucocytes. During the ischaemic phase the endothelium is primed both to produce free radicals and to secrete chemo attractants. The resultant neutrophil sequestration serves to amplify the injury, but damage is not confined to the postischaemic area and more generalized effects typically follow. The situation in the kidney is complex for, while isocheimal primes the tissue for reperfusion damage, it also causes early and irreversible tubular injury. Furthermore, it appears that relatively less importance should be attached to the involvement of neutrophils than at other sites, and relatively more to a local postiischaemic imbalance in the levels of nitric oxide and endothelin. Despite a greater understanding of the pathogenesis of isocheimal‐reperfusion injury, effective treatment remains elusive and research is hampered by apparent species and organ specific differences.