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Multi-omics and genetic prioritization identify candidate molecular links between micro- and nanoplastics-associated signatures and chronic kidney disease
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Scientists used advanced computer modeling and lab tests to explore how tiny plastic particles (microplastics) found in our bodies might contribute to chronic kidney disease. They identified specific genes and biological pathways linking plastic exposure to kidney damage, and confirmed in lab-grown kidney cells that polystyrene microplastics can trigger changes linked to kidney scarring. While this is early-stage research that doesn't prove plastics directly cause kidney disease in people, it offers promising leads for understanding—and potentially preventing—environmentally-driven kidney damage.
Micro- and nanoplastics (MNPs) have been detected in human renal and urinary tissues and are increasingly recognized as potential environmental contributors to kidney injury and chronic kidney disease (CKD), but the molecular signatures connecting MNP-associated toxicogenomic signals with CKD remain poorly understood. In this study, we employed an integrative analytical framework combining toxicity prediction, toxicogenomic target analysis, transcriptomic analysis, machine learning, transcriptome-wide Mendelian randomization, single-nucleus RNA sequencing, and targeted in vitro expression validation to investigate candidate molecular links between MNP-associated toxicogenomic signatures and CKD. Among MNP monomers with available SMILES notations, PVC, PMMA, PP, and PS showed moderate predicted nephrotoxicity, whereas PE showed a borderline score and PET showed a lower predicted score. We identified 58 shared candidate genes between MNP-associated targets and CKD-related genes, which were mainly enriched in inflammatory and oxidative stress-related pathways. A machine learning model based on these features showed discriminative performance in training and external validation CKD datasets. Transcriptome-wide MR analyses prioritized several genes, including TGFB1, CTNNB1, PF4, and NR3C2, whose genetically predicted expression was associated with CKD risk, although colocalization evidence was limited. Single-nucleus analysis highlighted proximal tubular, endothelial, podocyte, and monocyte-lineage cells as CKD-relevant renal compartments. Exploratory molecular docking provided computational binding hypotheses between selected MNP monomeric units and candidate proteins. Targeted qRT-PCR validation further showed that PS-MP exposure increased the expression of profibrotic markers and altered the expression of selected candidate genes in proximal tubular epithelial cells. Overall, this study provides an integrative, systems-level characterization of candidate molecular links between MNP-associated toxicogenomic signatures and CKD. These findings highlight candidate genes, pathways, and CKD-relevant renal cell types, offering hypothesis-generating insights into environmentally related kidney injury and providing preliminary expression-level experimental support for selected prioritized genes.
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This study used computer-based methods, including gene databases and molecular docking, to examine how PET plastic particles might affect chronic kidney disease. The analysis identified seven genes that both PET microplastics and kidney disease may affect, often related to immune, inflammation, and energy processes. No animals or human volunteers were tested directly.
Network toxicology and bioinformatics analysis reveal the molecular mechanisms of polyethylene terephthalate microplastics in exacerbating diabetic nephropathy
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This computational study used bioinformatics to explore how polyethylene terephthalate (PET) microplastics might worsen diabetic kidney disease. The analysis identified key genes and inflammatory pathways that are affected by both PET microplastics and kidney damage in diabetes. The findings suggest that microplastic exposure could accelerate kidney problems in people who already have diabetes, though lab and clinical studies are needed to confirm this.
Micro- and nanoplastics and the kidney: exposure pathways, toxicokinetics, and pathophysiological insights
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Tiny plastic particles from our air, water, and food—called micro- and nanoplastics—can enter our bodies and travel to the kidneys, where studies show they may cause cell damage, inflammation, and scarring over time. This review pulls together existing research on how these plastics get into our system and harm kidney tissue, suggesting that everyday plastic exposure could be an overlooked risk factor for kidney disease. More research is needed, but this is an early signal that reducing plastic exposure might matter for long-term kidney health.
Micro- and Nanoplastic Pollution and Renal Health: Human Evidence, Mechanisms, and Clinical Implications
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Tiny plastic particles have been found in human blood, urine, and even kidney tissue, and lab studies show they can stress kidney cells and potentially contribute to inflammation and scarring. This review pulls together what scientists currently know, but it's clear we still don't have solid proof that microplastics actually cause kidney disease in people, more research is needed, especially for those already dealing with kidney problems or dialysis, before we can say how worried to be.
Unveiling the molecular toxicity of plasticizers derived from microplastics (DMP and DEP) in diabetic kidney disease: integrative insights from network toxicology and multi-omics analysis
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Scientists found that two chemicals commonly released from microplastics (used to make plastics flexible) can damage kidney cells in lab tests, and this damage got worse when combined with high blood sugar levels similar to those seen in diabetes. This early-stage research points to specific genes that may explain how these plastic chemicals harm kidney health, but the findings come from cell studies, not humans, so more research is needed before we know if this applies to real-world diabetic kidney disease. Still, it raises important questions about whether everyday plastic exposure could compound health risks for people with diabetes.
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