The role of volume regulation and thermoregulation in aki during marathon running

Background and objectives Marathon runners develop transient AKI with urine sediments and injury biomarkers suggesting nephron damage. Design, setting, participants, & measurements To investigate the etiology, we examined volume and thermoregulatory responses as possible mechanisms in runners’ AKI using a prospective cohort of runners in the 2017 Hartford Marathon. Vitals, blood, and urine samples were collected in 23 runners 1 day premarathon and immediately and 1 day postmarathon. We measured copeptin at each time point. Continuous core body temperature, sweat sodium, and volume were assessed during the race. The primary outcome of interest was AKI, defined by AKIN criteria. Results Runners ranged from 22 to 63 years old; 43% were men. Runners lost a median (range) of 2.34 (0.50–7.21) g of sodium and 2.47 (0.36–6.81) L of volume via sweat. After accounting for intake, they had a net negative sodium and volume balance at the end of the race. The majority of runners had increases in core body temperature to 38.4 (35.8–41)°C during the race from their baseline. Fifty-five percent of runners developed AKI, yet 74% had positive urine microscopy for acute tubular injury. Runners with more running experience and increased participation in prior marathons developed a rise in creatinine as compared with those with lesser experience. Sweat sodium losses were higher in runners with AKI versus non-AKI (median, 3.41 [interquartile range (IQR), 1.7–4.8] versus median, 1.4 [IQR, 0.97–2.8] g; P=0.06, respectively). Sweat volume losses were higher in runners with AKI versus non-AKI (median, 3.89 [IQR, 1.49–5.09] versus median, 1.66 [IQR, 0.72–2.84] L; P=0.03, respectively). Copeptin was significantly higher in runners with AKI versus those without (median, 79.9 [IQR, 25.2–104.4] versus median, 11.3 [IQR, 6.6–43.7]; P=0.02, respectively). Estimated temperature was not significantly different. Conclusions All runners experienced a substantial rise in copeptin and body temperature along with salt and water loss due to sweating. Sodium and volume loss via sweat as well as plasma copeptin concentrations were associated with AKI in runners.