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The threat of microplastics to human kidney health: Mechanisms of nephrotoxicity and future research directions
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This review examines the growing evidence that microplastics can reach and damage human kidneys, where they were first detected in 2023. Short-term exposure triggers oxidative stress and inflammation, while long-term exposure may lead to kidney scarring through a process called ferroptosis, a type of cell death linked to iron buildup. The authors propose that microplastics may also activate the immune system in kidneys through a gut-kidney connection, highlighting that kidney health is an important but overlooked concern in microplastic research.
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.
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Mice exposed to polystyrene microplastics in their drinking water for six months developed kidney scarring (fibrosis) driven by a type of cell death called ferroptosis. The microplastics triggered iron-dependent damage in kidney cells, which then released signals causing surrounding tissue to scar over. This long-term study reveals a new mechanism by which chronic microplastic exposure could lead to progressive kidney disease in humans.
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