Abstract

Renal toxicity represents a major clinical and public health challenge, contributing substantially to the global burden 
of acute kidney injury and its frequent progression to chronic kidney disease. A growing body of research identifies 
oxidative stress and redox imbalance as central drivers of renal damage, modulating inflammation, tubular cell death, 
mitochondrial dysfunction, and maladaptive repair. During toxicant-induced kidney injury, excessive reactive 
oxygen species production overwhelms antioxidant systems, producing structural and functional alterations that 
often persist long after the initial insult. Recent technological advances in molecular profiling have revealed a new 
generation of biomarkers capable of detecting early oxidative injury, predicting disease trajectory, and 
differentiating reversible from progressive forms of renal impairment. These biomarkers include those derived from 
oxidative stress pathways, mitochondrial damage, inflammation, tubular epithelial injury, and epigenetic 
modifications. This review synthesizes emerging evidence on mechanisms linking redox dysregulation to the 
transition from acute kidney injury to chronic kidney disease and highlights the most promising biomarkers for 
early diagnosis, risk stratification, and therapeutic monitoring. Understanding these mechanistic and diagnostic 
breakthroughs is crucial for guiding targeted interventions aimed at preventing kidney disease progression.