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Pathophysiological Mechanisms by which Heat Stress Potentially Induces Kidney Inflammation and Chronic Kidney Disease in Sugarcane Workers.

School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 414, 405 30 Gothenburg, Sweden. La Isla Network, 1441 L Street NW, Washington, DC 20005, USA. Faculty of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK. Occupational and Environmental Medicine, Sahlgrenska University Hospital, Box 414, 405 30 Gothenburg, Sweden. Institute of Environmental Medicine, Karolinska Institutet, Nobels väg 13, 171 65 Solna, Sweden. School of Sport, Exercise & Rehabilitation Sciences, University of Birmingham, 142 Edgbaston Park Rd, Birmingham B15 2TT, UK. Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 2 Medical Drive, MD9, National University of Singapore, Singapore 117593, Singapore. Global Asia Institute, National University of Singapore, 10 Lower Kent Ridge Rd, Singapore 119076, Singapore. N.1 Institute for Health, National University of Singapore, 28 Medical Dr, Singapore 117456, Singapore. Department of Laboratory Medicine, Division of Clinical Chemistry and Pharmacology, Lund University, 221 85 Lund, Sweden. Division of Renal Medicine, Department of Clinical Science Intervention and Technology, Karolinska Institutet, 141 86 Stockholm, Sweden. Division of Renal Diseases and Hypertension, School of Medicine, University of Colorado Denver, Aurora, CO 80045, USA. Department of Work Environment, University of Massachusetts Lowell, Lowell, MA 01845, USA.

Nutrients. 2020;(6)
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Abstract

BACKGROUND Chronic kidney disease of non-traditional origin (CKDnt) is common among Mesoamerican sugarcane workers. Recurrent heat stress and dehydration is a leading hypothesis. Evidence indicate a key role of inflammation. METHODS Starting in sports and heat pathophysiology literature, we develop a theoretical framework of how strenuous work in heat could induce kidney inflammation. We describe the release of pro-inflammatory substances from a leaky gut and/or injured muscle, alone or in combination with tubular fructose and uric acid, aggravation by reduced renal blood flow and increased tubular metabolic demands. Then, we analyze longitudinal data from >800 sugarcane cutters followed across harvest and review the CKDnt literature to assess empirical support of the theoretical framework. RESULTS Inflammation (CRP elevation and fever) and hyperuricemia was tightly linked to kidney injury. Rehydrating with sugary liquids and NSAID intake increased the risk of kidney injury, whereas electrolyte solution consumption was protective. Hypokalemia and hypomagnesemia were associated with kidney injury. DISCUSSION Heat stress, muscle injury, reduced renal blood flow and fructose metabolism may induce kidney inflammation, the successful resolution of which may be impaired by daily repeating pro-inflammatory triggers. We outline further descriptive, experimental and intervention studies addressing the factors identified in this study.