Abstract Environment‐induced heat stress (EIHS) results from sustained body temperature elevation owing to prolonged exposure to heat and humidity. We hypothesized that EIHS would cause kidney injury and cellular dysfunction. To test this hypothesis, female C57 mice were exposed to EIHS ( n = 14; 37.6°C, 42.0% relative humidity) or thermoneutral (TN) conditions ( n = 12; 31.2°C, 35.0% relative humidity) for 24 h. EIHS increased rectal temperature by 2.1°C ( p < 0.001), decreased body mass by 10% ( p = 0.036), decreased absolute kidney mass by 10% ( p = 0.026), increased renal water content by 19% ( p < 0.007) and increased blood urea nitrogen by 102% ( p < 0.001) compared with TN. Histological analysis revealed that EIHS caused proximal tubule vacuolation ( p = 0.001) and alterations in glomerular structure, supported by markers of lipid accumulation, tubular injury and inflammatory signalling. EIHS increased relative protein abundance of heat shock proteins 70 (48%, p = 0.002), 90 (37%, p = 0.001) and 60 (36%, p = 0.026), in addition to heat shock factor 1 (2‐fold, p = 0.020) compared with TN. In addition, there was biochemical evidence of mitochondrial remodelling, increased autophagic flux and robust activation of endoplasmic reticulum stress in kidneys from EIHS mice compared with TN mice. Collectively, these data suggest that 24 h of EIHS is sufficient to cause histological injury and cellular dysfunction, which might undermine renal health and function.
Roths et al. (Thu,) studied this question.
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