Platelet activation and the formation of neutrophil extracellular traps (NETs) contribute to renal ischaemia–reperfusion injury (IRI), say researchers. Jansen et al. show that in mice, renal IRI led to activation of platelets in the proximity of necrotic cell casts. The antiplatelet agent clopidogrel reduced IRI-induced cell necrosis and inflammation. Further investigations indicated that the platelets were activated by extracellular DNA released by necrotic tubular epithelial cells, and that this activation in turn led to increased platelet–granulocyte interactions, the formation of NETs, renal inflammation and tissue injury.