Pathophysiological impact of nano- and microplastics on the kidney and their potential role in blood pressure regulation

Nanoplastics (NPs) and microplastics (MPs) have recently been identified in human blood, kidney tissue, and urine, reflecting systemic exposure to environmental plastic contamination. As plastic particles can induce cellular damage, particle-related impairment of renal perfusion and filtration can be considered a hypothetical mechanism that could influence systemic blood pressure. The aim of this review was to evaluate current evidence on the effects of plastic particles on renal function and their potential implications for systemic blood pressure. For this purpose, current evidence from in vitro experiments, mouse and rat studies, and emerging human data on the nephrotoxic effects of NPs and MPs was examined, and potential mechanistic pathways linking renal injury to blood pressure regulation were discussed. Across experimental models, exposure to NPs and MPs induces oxidative stress, inflammatory responses, and structural damage to renal cells. These alterations may impair glomerular filtration and contribute to glomerulosclerosis and interstitial fibrosis. In adenine-induced chronic kidney disease (CKD) rat models, prolonged MP exposure has been associated with elevated serum creatinine and urea concentrations, albuminuria, histological evidence of fibrosis, and exacerbation of arterial hypertension. Renal localization and persistence of plastic particles depend on particle size, shape, surface chemistry, and exposure dose. In human kidney tissue and urine, plastic particles in the micrometer range have been detected across multiple studies. However, a direct association between their presence and any functional renal impairment has not yet been demonstrated in humans. Although a direct causal link between environmental plastic exposure, renal impairment, and hypertension has not yet been demonstrated in humans, current experimental evidence points to biological processes such as oxidative stress, inflammation, and vascular dysfunction. Long-term low-level exposure may therefore represent a hypothetical contributing factor to subtle changes in kidney function and blood pressure, though this remains to be demonstrated in humans.