Although marked alterations in temperature often accompany ischemic, acute renal failure (ARF), the effects of altered temperature on renal structure and function have received little attention. In the present investigation, isolated rat kidneys perfused at 41°C had extensive tubular damage and decreased function compared to kidneys perfused at 37°C. In contrast, kidneys perfused at 30°C had less tubular damage, and better function, than kidneys perfused at 37°C. Increased temperature caused a 50% reduction in renal ATP (0.46±0.04 μM/100mg tissue protein. 37°C, vs. 0.26 ± 0.03 μM/100 mg tissue protein. 41°C: P<0.05). The decreased ATP occurred despite reduced sodium rcabsorption (129 ± 8 μM/min/g. 37°C, vs. 65 ± 12 μM/min/g, 41°C. P<0.05) and normal renal oxygen consumption (QO2). These results suggest that increased temperature may cause an uncoupling of QO2 and sodium chloride transport, and an increase in nontransport mediated, basal metabolic rate may result in depleted cellular ATP levels and renal tubular cell death.