0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Sign in to save

Micro- and Nanoplastic Pollution and Renal Health: Human Evidence, Mechanisms, and Clinical Implications

Journal of Xenobiotics 2026
Aris Tsalouchos, Pietro Claudio Dattolo

Summary

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.

Body Systems
Models

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 demonstrate renal access and urinary detection, but estimates are strongly method-dependent and do not yet define 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.

Share this paper