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

Pathophysiological Mechanisms by which Heat Stress Potentially Induces Kidney Inflammation and Chronic Kidney Disease in Sugarcane Workers
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DOI:
10.3390/nu12061639
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发表时间:
2020-06-01
期刊:
影响因子:
5.9
通讯作者:
Wegman, David H.
Wegman, David H.
中科院分区:
医学2区
文献类型:
--
作者:
Hansson, Erik;Glaser, Jason;Wegman, David H.

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背景:慢性肾脏疾病的非传统来源(CKDnt)是常见的中美洲甘蔗工人。反复的热应激和脱水是一个主要的假设。证据表明炎症起着关键作用。方法:从运动和热病理生理学文献开始,我们建立了一个理论框架,说明高温下的剧烈工作如何诱发肾脏炎症。我们描述了从渗漏的肠道和/或受伤的肌肉中释放促炎物质,单独或与小管果糖和尿酸联合,肾血流量减少和小管代谢需求增加而加重。然后,我们分析了bb00800甘蔗切割机的纵向数据,并回顾了CKDnt文献,以评估理论框架的实证支持。结果:炎症(CRP升高、发热)和高尿酸血症与肾损伤密切相关。用含糖液体和非甾体抗炎药补充水分会增加肾脏损伤的风险,而电解质溶液的摄入则有保护作用。低钾血症和低镁血症与肾损伤有关。讨论:热应激、肌肉损伤、肾血流量减少和果糖代谢可引起肾脏炎症,每日重复的促炎触发因素可能会损害肾脏炎症的成功解决。我们概述了进一步的描述性、实验性和干预研究,以解决本研究中确定的因素。
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.