Tan Ru-Yu, She Qin-Ying, Ma Yun-Ci, Liu Ming-Hong, Li Li-Juan, Huang Li-Li, Zhong Yi-Wen, Bi Hui-Xin
Department of Nephrology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, 510900, China; Department of Nephrology, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China; Sichuan Clinical Research Center for Nephropathy, Chengdu, 610000, China.
Department of Nephrology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, 510900, China.
Environ Res. 2025 Oct 15;283:122124. doi: 10.1016/j.envres.2025.122124. Epub 2025 Jun 10.
Following the inadequacy of global plastic pollution control measures, microplastic (MP) pollution is posing new challenges to human health. In recent years, MPs have been detected in various human tissues, including their first identification in human kidneys in 2023. MPs can reach the kidneys through inhalation, oral ingestion, and intravascular injection, and they can be excreted via urine. Based on the latest research, this article reviews the nephrotoxicity of MPs and proposes a filtration-reabsorption-translocation hypothesis regarding the potential renal excretion mechanism of MPs. Short-term exposure to MPs can induce oxidative stress, resulting in endoplasmic reticulum (ER) stress, inflammatory responses, and lipid metabolism disorders, while long-term exposure may result in renal fibrosis mediated by ferroptosis. The nephrotoxicity of MPs is associated with particle size, though not in a linear manner. A specific size range appears to exhibit more significant kidney toxicity. Furthermore, oral exposure may activate the complement system in the kidneys through the gut-kidney axis, with the C5a/C5aR pathway playing an important role in this process. In conclusion, MPs present a substantial threat to human kidney health. Considering the existing research limitations, it is imperative to urgently investigate the effects of MPs at realistic environmental exposure concentrations on human kidneys and to explore strategies for mitigating their nephrotoxicity.
由于全球塑料污染控制措施的不足，微塑料（MP）污染正在对人类健康构成新的挑战。近年来，已在各种人体组织中检测到微塑料，包括2023年在人类肾脏中的首次发现。微塑料可通过吸入、口服摄入和血管内注射进入肾脏，并可通过尿液排出。基于最新研究，本文综述了微塑料的肾毒性，并提出了关于微塑料潜在肾脏排泄机制的滤过-重吸收-转运假说。短期接触微塑料可诱导氧化应激，导致内质网（ER）应激、炎症反应和脂质代谢紊乱，而长期接触可能导致铁死亡介导的肾纤维化。微塑料的肾毒性与颗粒大小有关，但并非呈线性关系。特定的尺寸范围似乎表现出更显著的肾脏毒性。此外，口服接触可能通过肠-肾轴激活肾脏中的补体系统，C5a/C5aR途径在此过程中起重要作用。总之，微塑料对人类肾脏健康构成了重大威胁。考虑到现有研究的局限性，迫切需要研究现实环境暴露浓度下微塑料对人类肾脏的影响，并探索减轻其肾毒性的策略。
