Two patients had transient deterioration of renal function during acute infectious states while receiving indomethacin. Neither patient was in septic shock; renal function deteriorated at a time when clinically the infection was improving and both patients improved when indomethacin was discontinued, with return of renal function to baseline. Indomethacin inhibits prostaglandin synthesis and has been shown to reduce glomerular filtration and alter renal hemodynamic autoregulation. In susceptible patients these effects may be clinically significant. Careful monitoring of renal function in such patients requiring indomethacin therapy is warranted.