Environmental micro and nanoplastics (MNPs) have emerged as pervasive contaminants with growing implications for systemic toxicity and organ-specific pathophysiological outcomes. Among vulnerable organs, the kidney represents a critical target due to its high perfusion rate, filtration function and continuous exposure to circulating xenobiotics. This review provides a renal-focused integrative synthesis of current experimental and mechanistic evidence examining the potential association between environmental MNPs exposure to nephrotoxicity. A structured literature search was conducted across major scientific databases to identify studies describing toxicokinetic behavior, molecular signaling responses and renal functional outcomes associated with MNP exposure. Mechanistically, MNPs exposure has been associated with oxidative stress amplification, inflammatory signaling activation, mitochondrial dysfunction, endoplasmic reticulum stress, autophagy dysregulation and profibrotic remodeling, collectively contributing to nephron structural alterations and renal functional impairment. Comparative evidence from experimental models further suggest that renal toxicity may be influenced by exposure route, dose and physicochemical particle transformation, highlighting the complexity of real-world environmental risk assessment. Advances in analytical toxicology have enabled improved detection of MNPs in biological matrices; however, methodological limitations related to contamination control, nanoscale sensitivity and standardized biomonitoring protocols remain significant challenges. By integrating environmental exposure dynamics with renal pathophysiological endpoints, this review proposes a conceptual framework that may help explain how molecular signaling hierarchies to clinically relevant kidney injury progression. Understanding these interconnected mechanisms may facilitate identification of early diagnostic biomarkers, refinement of exposure assessment strategies, and development of targeted therapeutic interventions aimed at mitigating environmentally mediated renal disease risk.
Verma et al. (Tue,) studied this question.