Kidney disease is a growing global public health challenge that accounts for substantial morbidity, premature mortality, and rising healthcare costs. Although diabetes mellitus and hypertension remain the principal clinical risk factors for renal injury, accumulating evidence indicates that environmental pollution represents an independent and globally pervasive contributor to kidney disease burden. Long-term exposure to environmental toxicants, including heavy metals, ambient air pollutants, persistent organic pollutants, and endocrine-disrupting chemicals, has been consistently associated with acute kidney injury, an accelerated decline in renal function, and progression to end-stage kidney disease. The kidney is characterized by a high perfusion rate, specialized tubular transport systems, and a central role in xenobiotic metabolism and excretion, which confer heightened vulnerability to environmental insults. Experimental and epidemiological studies have demonstrated that pollutant exposure across the life course converges on shared pathogenic mechanisms, including oxidative stress, inflammatory signaling, mitochondrial dysfunction, fibrogenesis, and persistent epigenetic alterations. Importantly, environmental toxicants not only initiate renal injury, but they also impair intrinsic repair processes, exacerbating susceptibility to chronic and progressive kidney disease. This Review integrates population-based epidemiological data with experimental mechanistic evidence to define environmental exposures, renal cellular targets, and convergent molecular pathways underlying pollutant-induced nephrotoxicity, and aims to translate this knowledge into actionable strategies for kidney disease prevention, clinical risk stratification, and evidence-informed environmental policy.
Lee et al. (2026) studied this question.