Microplastics and the Kidney: A Narrative Review of Human Evidence, Molecular Mechanisms of Cell Injury, and Future Directions
9 affiliations
- 1UOC Nephrology, IRCCS Istituto Giannina Gaslini, 16147 Genoa, Italy
- 2UOC Nephrology, Guglielmo da Saliceto Hospital, AUSL Piacenza, 29121 Piacenza, Italy
- 3Department of Translational Medicine, IRCCS AOU “SS Antonio e Biagio e Cesare Arrigo” University Hospital, 15121 Alessandria, Italy
- 4INSTM Unit of Brescia, Department of Mechanical and Industrial Engineering, University of Brescia, 25123 Brescia, Italy
- 5CNR-ICMATE, Institute of Condensed Matter Chemistry and Technologies for Energy, National Research Council, 16149 Genoa, Italy
- 6Department of Internal Medicine, University of Genoa, 16132 Genoa, Italy
- 7Nephrology, Dialysis and Transplantation Unit, Department of Emergency-Urgency and Transplantation, University Hospital of Siena, 53100 Siena, Italy
- 8Department of Internal Medicine and Medical Specialties (DIMI), University of Genoa, 16132 Genoa, Italy
- 9Nephrology, Dialysis and Transplantation Unit, AOM—IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy
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.
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BibTeX
@article{porta2026microplastics,
title = {{Microplastics and the Kidney: A Narrative Review of Human Evidence, Molecular Mechanisms of Cell Injury, and Future Directions}},
author = {Edoardo La Porta and Micaela Gentile and Marco Quaglia and Serena Ducoli and Sara Massardo and Daniela Verzola and Nicoletta Mancianti and Pasquale Esposito},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27208978},
url = {https://www.mdpi.com/1422-0067/27/20/8978},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Microplastics and the Kidney: A Narrative Review of Human Evidence, Molecular Mechanisms of Cell Injury, and Future Directions
AU - Edoardo La Porta
AU - Micaela Gentile
AU - Marco Quaglia
AU - Serena Ducoli
AU - Sara Massardo
AU - Daniela Verzola
AU - Nicoletta Mancianti
AU - Pasquale Esposito
PY - 2026
DA - 2026/10/01
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27208978
UR - https://www.mdpi.com/1422-0067/27/20/8978
AB - 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.
SN - 1422-0067
ER -