Renal Toxicity and Redox Imbalance: Novel Biomarkers Predicting Progression from Acute Kidney Injury to Chronic Kidney Disease

Nyambura Achieng M.

School of Natural and Applied Sciences Kampala International University Uganda

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.

Keywords: Acute kidney injury, chronic kidney disease, oxidative stress, redox imbalance, biomarkers

 CITE AS: Nyambura Achieng M. (2026). Renal Toxicity and Redox Imbalance: Novel Biomarkers Predicting Progression from

 Acute Kidney Injury to Chronic Kidney Disease.

IDOSR JOURNAL OF SCIENCE AND TECHNOLOGY 12(1):98-102. https://doi.org/10.59298/IDOSR/JST/26/113.98102