Microplastics and the Kidney: A Narrative Review of Human Evidence, Molecular Mechanisms of Cell Injury, and Future Directions

Abstract

Microplastics (MPs) are widespread environmental contaminants, but their potential effects on kidney health remain poorly defined. As an organ continuously exposed to circulating particles and involved in their urinary elimination, the kidney may represent both a target of MP toxicity and a route of excretion. In this narrative review, we examine current evidence linking MPs to kidney injury, integrating experimental, mechanistic, and human data. Particular attention is given to the early events governing particle–cell interactions. After exposure, micro- and nanoplastics acquire an eco- and biomolecular corona that modifies their surface properties, cellular recognition, uptake, and biodistribution. Following internalization through phagocytic and endocytic pathways, particles may accumulate within endolysosomal compartments and interact with intracellular structures, disrupting cellular homeostasis. In renal cells, these events converge on mitochondrial dysfunction, reactive oxygen species generation, endoplasmic reticulum stress, inflammatory signaling, altered autophagy, and regulated cell death. Several interconnected pathways have been implicated, including Keap1–Nrf2/ARE and NF-κB signaling, MAPK and IRE1/XBP1-mediated stress responses, ACSL4–GPX4-related ferroptosis, and TGF-β1-related profibrotic signaling. Human studies have detected MPs in urine and kidney tissue and provide preliminary evidence linking MP burden with early markers of kidney damage, although current findings remain limited by small study populations and substantial methodological heterogeneity. Patients with chronic kidney disease, particularly those receiving dialysis, may represent a population of special interest because potentially altered renal handling may coexist with repeated exposure to polymer-based medical devices and dialysis fluids. Despite this potential relevance, data on MP exposure and accumulation in CKD and dialysis patients remain remarkably scarce. We finally discuss the limitations of current experimental models and analytical methods and the need for standardized biomonitoring, more environmentally relevant particles and exposure concentrations, and detection strategies capable of reaching the nanoscale, including artificial intelligence-assisted analysis. Overall, available evidence provides a mechanistic basis for MP-induced kidney injury, but its clinical relevance and contribution to human kidney disease remain to be established.