Using a murine model of septic AKI, Privratsky et al. find that F4/80hi kidney macrophages are necessary to attenuate the severity of septic AKI through elaboration of anti-inflammatory mediators, namely a receptor antagonist for IL-1 (also called IL1rn), which curbs IL-6 expression in endothelial cells. Here, IL1B is linked to acute kidney injury.