Increase of core temperature affected the progression of kidney injury by repeated heat stress exposure

American Journal of Physiology - Renal Physiology - Tập 317 Số 5 - Trang F1111-F1121 - 2019
Yuka Sato1,2, Carlos A. Roncal‐Jimenez1, Ana Andrés-Hernando1, Thomas Jensen1, Dean R. Tolan1, Laura Gabriela Sánchez‐Lozada3, Lee S. Newman4,5,6, Jaime Butler-Dawson4,5,6, Cecilia Sorensen4,7,5,6, Jason Glaser8,9, Makoto Miyazaki1, Henry F. Díaz10, Takuji Ishimoto11, Tomoki Kosugi11, Shoichi Maruyama11, Gabriela García1, Miguel A. Lanaspa1, Richard J. Johnson1
1Division of Renal Diseases and Hypertension, University of Colorado, Aurora, Colorado
2Japan Society for the Promotion of Science Overseas Research Fellow, Tokyo, Japan
3Laboratory of Renal Physiopathology, Department of Nephrology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico
4Center for Work, Health and Environment, Colorado School of Public Health, University of Colorado, Aurora, Colorado
5Department of Environmental and Occupational Health, Colorado School of Public Health, University of Colorado, Aurora, Colorado
6Department of Epidemiology, Colorado School of Public Health, University of Colorado, Aurora, Colorado
7Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, Colorado
8Department of Epidemiology, London School of Hygiene and Tropical Medicine, London, United Kingdom
9La Isla Network, Washington, District of Columbia
10Department of Geography and Environment, University of Hawai‘i at Mānoa, Honolulu, Hawai‘i
11Department of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan

Tóm tắt

An epidemic of chronic kidney disease of unknown etiology (Mesoamerican nephropathy) has emerged in hot regions of Central America. We have demonstrated that dehydration associated with recurrent heat exposure causes chronic kidney disease in animal models. However, the independent influence of core body temperature on kidney injury has not been explored. In the present study, we tested the hypothesis that kidney injury could be accelerated by increasing body temperature independent of external temperature. Wild-type mice were exposed to heat (39.5°C, 30 min, 2 times daily) with or without the mitochondrial uncoupling agent 2,4-dinitrophenol (DNP) for 10 days. Core temperature, renal function, proteinuria, and renal histological and biochemical analyses were performed. Isolated mitochondria markers of oxidative stress were evaluated from kidney tissue. DNP increased body core temperature in response to heat by 1°C (42 vs. 41°C), which was transient. The mild increase in temperature correlated with worsening albuminuria ( R = 0.715, P < 001), renal tubular injury, and interstitial infiltration of monocytes/macrophages. Tubular injury was marked in the outer medulla. This was associated with a reduction in kidney tissue ATP levels (nonheated control: 16.71 ± 1.33 nmol/mg and DNP + heat: 13.08 ± 1.12 nmol/mg, P < 0.01), reduced mitochondria, and evidence for mitochondrial oxidative stress. The results of the present study suggest that kidney injury in heat stress is markedly worsened by increasing core temperature. This is consistent with the hypothesis that clinical and subclinical heat stroke may play a role in Mesoamerican nephropathy.

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American Journal of Physiology - Renal Physiology

Tập 317 Số 5

F1111-F1121

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