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Background and objectives Marathon runners develop transient AKI with urine sediments and injury biomarkers suggesting nephron damage. Design, setting, participants, 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. Podcast This article contains a podcast at https: //www. asn-online. org/media/podcast/CJASN/2019₀8₁3CJASNPodcast₁9₀9_. mp3
Mansour et al. (2019) studied this question.