Wet bulb temperatures (T(wet)) during extreme heat events are commonly 31°C. Recent predictions indicate that T(wet) will approach or exceed 34°C. Epidemiological data indicate that exposure to extreme heat events increases kidney injury risk. We tested the hypothesis that kidney injury risk is elevated to a greater extent during prolonged exposure to T(wet) = 34°C compared with T(wet) = 31°C. Fifteen healthy men rested for 8 h in T(wet) = 31 (0)°C and T(wet) = 34 (0)°C. Insulin-like growth factor-binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinase 2 (TIMP-2), and thioredoxin 1 (TRX-1) were measured from urine samples. The primary outcome was the product of IGFBP7 and TIMP-2 ([IGFBP7·TIMP-2]), which provided an index of kidney injury risk. Plasma interleukin-17a (IL-17a) was also measured. Data are presented at preexposure and after 8 h of exposure and as mean (SD) change from preexposure. The increase in [IGFBP7·TIMP-2] was markedly greater at 8 h in the 34°C [+26.9 (27.1) (ng/mL)(2)/1,000) compared with the 31°C [+6.2 (6.5) (ng/mL)(2)/1,000] trial (P < 0.01). Urine TRX-1, a marker of renal oxidative stress, was higher at 8 h in the 34°C [+77.6 (47.5) ng/min] compared with the 31°C [+16.2 (25.1) ng/min] trial (P < 0.01). Plasma IL-17a, an inflammatory marker, was elevated at 8 h in the 34°C [+199.3 (90.0) fg/dL; P < 0.01] compared with the 31°C [+9.0 (95.7) fg/dL] trial. Kidney injury risk is exacerbated during prolonged resting exposures to T(wet) experienced during future extreme heat events (34°C) compared with that experienced currently (31°C), likely because of oxidative stress and inflammatory processes.NEW AND NOTEWORTHY We have demonstrated that kidney injury risk is increased when men are exposed over an 8-h period to a wet bulb temperature of 31°C and exacerbated at a wet bulb temperature of 34°C. Importantly, these heat stress conditions parallel those that are encountered during current (31°C) and future (34°C) extreme heat events. The kidney injury biomarker analyses indicate both the proximal and distal tubules as the locations of potential renal injury and that the injury is likely due to oxidative stress and inflammation.