Elevations in sweat sodium concentration following ischemia‐reperfusion injury during heat stress

Abstract

INTRODUCTIONAcute kidney injury is a major cause of excess hospitalizations during heat waves. The etiology of this acute kidney injury is likely contributed to by renal ischemia‐reperfusion (IR) injury. Renal IR injury results in damage to the renal tubules and a subsequent impairment in sodium reabsorption. Fractional excretion of sodium is often used as an indirect marker of damage to the renal tubules and increases of >1% reflect ischemic acute kidney injury. Mechanistic studies, which are limited to rodent IR models, have reported that impairments in sodium reabsorption following ischemic acute kidney injury are mediated by a reduction in active transporters for sodium reabsorption in the renal tubules. However, similar in vivo studies are not possible in humans. The eccrine sweat glands have been proposed as a model of the nephrons given the anatomical and physiological similarities (e.g., sodium reabsorption).PURPOSETest the hypothesis that sweat sodium concentrations are elevated following IR injury during passive heat stress.METHODSFifteen healthy adults (10 women; age: 25±3 y; body mass index: 23.7±3.5 kg·m‐2) completed a cross‐body design experiment consisting of ~160 min of passive heat stress (core body temperature: +1.5±0.2°C) utilizing a suit perfused with 50°C water. At 60 min of whole‐body heating, one upper arm (randomized) was occluded (220 mmHg) for 20 min followed by reperfusion. Sweat was collected from the ventral aspect of each forearm via an absorbent patch (~77 cm2) pre‐ and post‐IR for 24±4 and 30±6 min, respectively. Sweat sodium concentration (mmol·L‐1) was measured in duplicate via electrolyte analyzer (EasyLyte® Plus). Local sweat rate was measured on the distal aspect of the dorsal forearm continuously via hygrometry (mL·min‐1·cm‐2). Comparisons were made between the experimental (IR) and control arms. Data are reported as mean±SD.RESULTSLocal sweat rate increased during whole‐body passive heating (p<0.001) and was not different between the experimental and control arms at any timepoint except during ischemia (0.45±0.53 vs.1.31±0.43 mL·min‐1·cm‐2, respectively; p<0.001). Sweat sodium concentration did not change from pre‐ to post‐IR in the control arm (pre: 54.9±32.2 mmol·L‐1 and post: 58.7±25.6 mmol·L‐1; p=0.99), but increased from pre‐ to post‐IR in the experimental arm (pre: 48.4±23.3 mmol·L‐1 and post: 63.8±30.9 mmol·L‐1; p=0.02). Furthermore, the change from pre‐IR in sweat sodium concentration was different between experimental and control arms post‐IR (+12.5±14.70 mmol·L‐1 versus ‐0.3±20.5 mmol·L‐1, respectively; p=0.05).CONCLUSIONIn support of our hypothesis, sweat sodium concentration was elevated following IR injury and does not appear to be mediated by alterations in sweat rate. These observations are in‐line with rodent renal IR models demonstrating impaired sodium reabsorption. While these findings appear to support the use of eccrine sweat glands as a model, further testing is required to verify its use to understand impaired sodium handling following IR injury in humans.