Abstract During the COVID‐19 pandemic, heat stress (HS) was a serious occupational risk for health‐care workers (HCWs) wearing personal protective equipment, which limits heat dissipation and increases the risk of kidney injury. In this exploratory study, we assessed HS‐related changes in the urinary metabolites of 38 HCWs working at mobile COVID‐19 screening units in Taiwan and their possible role in incident kidney injury (IKI). Urine samples were collected before and after their shifts. Nuclear magnetic resonance‐based metabolomics was applied to measure urinary metabolic perturbations associated with HS, and these findings were subsequently correlated with clinical markers of IKI. Data were analyzed through multivariate and univariate analyses. We found that HS‐related changes in taurine and trimethylamine N‐oxide (TMAO) levels showed a trend associated with postshift IKI. Preshift urinary citrate, acetone, and 4‐hydroxybenzoate levels tended to be higher in the IKI population than the non‐IKI population. Compared to the non‐IKI population, the IKI population exhibited a trend toward lower postshift levels of glutarate and valine, but higher postshift levels of citrate, taurine, TMAO, and histidine. Metabolites whose levels were altered after HS included creatine, methylguanidine, formate, methylmalonate, 4‐hydroxybenzoate, adenine, hippurate, and tryptophan. Our preliminary findings suggest that higher postshift urinary taurine levels in the IKI population are potentially related to oxidative stress. In contrast, elevated TMAO levels possibly indicate disturbances in the gut‐kidney axis affecting renal health. Higher baseline urinary citrate and acetone may suggest increased susceptibility to HS‐related IKI. Finally, elevated urinary glutarate in the non‐IKI population may represent a protective metabolic response.
Ting et al. (Mon,) studied this question.