Mansour SG, Martin TG, Obeid W, et al. - Using a prospective cohort of runners in the 2017 Hartford Marathon, researchers investigated volume and thermoregulatory responses as possible mechanisms in runners’ AKI in order to exmaine the etiology. Following accounting for consumption, runners had a net negative sodium and volume balance at the end of the race. During the race from their baseline, the majority of runners had increases in core body temperature to 38.4 (35.8–41)°C. AKI was developed in 55% of runners, however, 74% had positive urine microscopy for acute tubular injury. In comparison with those with lesser experience, runners with more running experience and more participation in prior marathons developed an elevation in creatinine. In runners with AKI vs non-AKI, sweat sodium losses were greater. Sweat volume losses were greater in runners with AKI vs non-AKI. Copeptin was significantly greater in runners with AKI compared with those without. Estimated temperature was not significantly distinct. Hence, all runners encountered a substantial rise in copeptin and body temperature along with salt and water loss because of sweating. Sodium and volume loss through sweat as well as plasma copeptin concentrations were related to AKI in runners.