ReviewJournal of xenobiotics2026
Micro- and Nanoplastic Pollution and Renal Health: Human Evidence, Mechanisms, and Clinical Implications.
Review in Journal of xenobiotics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
2 authors.
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Abstract
Micro- and nanoplastics (MNPs) are reported in blood, urine, and tissues, including the kidney, raising concern that the urinary system may be both a target and a route of elimination. This narrative review integrates analytical, toxicokinetic, experimental, epidemiological, and dialysis-related evidence on MNPs and renal health. Human studies report polymer-confirmed particles or polymer-associated signals in blood, urine, and kidney-related specimens, supporting systemic presence and compatibility with renal exposure; however, estimates are strongly method-dependent and do not establish anatomical localization, tissue dose, clearance, or a disease threshold. Cell, kidney-organoid, and animal studies consistently identify oxidative and mitochondrial stress, endoplasmic-reticulum dysfunction, inflammation, altered autophagy, regulated cell death, senescence, and fibrotic remodelling. Effects vary with polymer, size, shape, surface ageing, route, dose, and chemical co-exposures, and many experiments remain difficult to map to typical human exposure. Direct human outcome evidence is limited to cross-sectional or exploratory studies; plasticizer epidemiology is informative for chemical co-exposure but cannot establish particle-specific toxicity. Patients with chronic kidney disease may be more susceptible, while kidney dysfunction may also alter measured blood or urinary concentrations. Dialysis introduces an additional, incompletely quantified exposure system. MNP-related renal injury is biologically plausible, but causal contribution to human kidney disease and clinical actionability remain unproven. Standardized methods, paired-matrix kinetics, prospective cohorts, and complete dialysis mass-balance studies are priorities.
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