Abstract Plastics are hydrophobic carbon polymers with a half-life of approximately 500 years. The widespread production and environmental accumulation of plastics pose significant toxicity concerns. Humans are routinely exposed to micro- and nanoplastics (MNPs), which can enter rate the bloodstream and reach various organs, including the kidneys. Here, we review research on nephrotoxic effects of plastics and the underlying mechanisms. The results of several studies of kidneys in mammals and kidney cells from humans suggest that MNPs induce renal toxicity. Although the underlying mechanisms remain to be characterized in detail, the current body of evidence suggests that MNPs promote the production of reactive oxygen species and thus trigger local (renal) and systemic inflammatory responses. These processes enhance cytotoxicity and may drive MNP-induced kidney damage. This toxicity results in histopathological changes in renal tissues (including glomerular and tubular damage and fibrosis) and modifications in key biomarkers of renal function (such as the glomerular filtration rate, albuminuria, and the blood urea nitrogen level). Moreover, MNPs have been shown to induce cardiovascular damage, which may contribute to the progression of chronic kidney disease (CKD) - potentially via the activation of aryl hydrocarbon receptors. Notably, the nephrotoxic effects of MNPs appear to be exacerbated by co-exposure to other environmental contaminants and uremic toxins. CKD can impair the kidneys' ability to eliminate MNP. Furthermore, dialyzed patients are substantially exposed to MNPs during dialysis sessions, which potentially compounds their vulnerability. With a view to better understanding the effects of MNPs on renal health and the impact of CKD and dialysis on levels of exposure to plastics, further studies are essential.
Augey et al. (Tue,) studied this question.