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热应激通过哪些病理生理机制潜在诱导甘蔗工人的肾脏炎症和慢性肾脏病。

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

机构信息

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.

出版信息

Nutrients. 2020 Jun 2;12(6):1639. doi: 10.3390/nu12061639.

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.

摘要

背景

非传统来源的慢性肾病(CKDnt)在中美洲甘蔗工人中很常见。反复的热应激和脱水是一个主要的假说。有证据表明炎症起着关键作用。

方法

我们从运动和热生理学文献开始,提出了一个理论框架,说明剧烈的热环境工作如何导致肾脏炎症。我们描述了从渗漏的肠道和/或受伤的肌肉中单独或与肾小管果糖和尿酸一起释放的促炎物质,以及由肾血流量减少和肾小管代谢需求增加引起的炎症加重。然后,我们分析了 800 多名甘蔗收割工人的纵向数据,并回顾了 CKDnt 的文献,以评估理论框架的经验支持。

结果

炎症(CRP 升高和发热)和高尿酸血症与肾脏损伤密切相关。用含糖液体和 NSAID 再水化增加了肾脏损伤的风险,而电解质溶液的摄入则具有保护作用。低钾血症和低镁血症与肾脏损伤有关。

讨论

热应激、肌肉损伤、肾血流量减少和果糖代谢可能导致肾脏炎症,而日常反复的促炎触发因素可能会影响炎症的成功解决。我们概述了进一步的描述性、实验性和干预性研究,以解决本研究中确定的因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4df6/7352879/87c25d503cfb/nutrients-12-01639-g001.jpg

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