Kidney injury induced by micro- and nanoplastic exposure: molecular mechanisms and clinical consequences (a state-of-the-art review)

Abstract

This review systematizes current data on the routes by which micro- and nanoplastics enter the body, their systemic distribution and accumulation in the organs of the urinary system, including exposure patterns during renal replacement therapy (RRT), and summarizes the evidence of in vitro, in vivo, and human studies addressing the nephrotoxic effects of micro- and nanoplastics (MNPs). The principal mechanisms of MNP-induced kidney injury include oxidative stress, inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress. MNP exposure is also accompanied by activation of autophagy, cellular senescence, various forms of cell death, and fibrogenesis, which may contribute to the development and progression of chronic kidney disease (CKD). MNP toxicity depends on particle size, the level and duration of exposure, as well as physicochemical properties. It may be further enhanced by the ability of MNP surfaces to adsorb various chemical contaminants, including heavy metals. Thus, MNPs may be considered a new potential risk factor for the development of kidney diseases. However, further studies are needed to clarify their mechanisms of action, assess the degree of toxicity and clinical relevance, and determine the contribution of different types of MNPs to the development of kidney pathology.