P2RX7 and glomerulonephritis: 2006). This contrasts with the predominant glomerular P2X7 expression seen in a glomerulonephritis model, which was also protected by genetic deletion or by P2X7 receptor antagonism (Taylor et al. 2009). The close association between the site of renal injury and the presence of P2X7, along with the protective effect of a P2X7 antagonist or genetic deletion, strongly supports a role for P2X7 in AKI pathogenesis.