Hamid Nasri
1 
, Paniz Pourpashang
2,3* 1 Department of Natural Sciences, The University of Georgia, Tbilisi, 0171, Georgia
2 Department of Pediatric Nephrology, Bahrami Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
3 Pediatric Chronic Kidney Disease Research Center, Gene, Cell and Tissue Research Institute, Tehran University of Medical Sciences, Tehran, Iran
Abstract
Oxidative stress and reactive oxygen species (ROS) generation are central drivers of calcium oxalate kidney stone pathogenesis by promoting renal tubular epithelial cell injury, inflammation, cell death, and extracellular matrix remodeling, which collectively create a renal environment conducive to crystal deposition, retention, and stone growth. Targeting oxidative stress pathways with antioxidants and modulators of ROS production presents a promising avenue for therapeutic intervention to prevent kidney stone recurrence and progression. This insights from molecular, cellular, and pathophysiological studies showing that calcium oxalate crystals set off a cascade of oxidative and inflammatory events that culminate in kidney stone formation, and also accentuates the importance of maintaining redox balance and renal cellular health in mitigating the burden of calcium oxalate nephrolithiasis.
Implication for health policy/practice/research/medical education:
Oxidative stress and reactive oxygen species (ROS) play an intricate role in the pathogenesis of calcium oxalate kidney stones, from initial cellular injury and inflammation to crystal adhesion and growth. The complex interplay of reactive oxygen species generation, antioxidant defenses, mitochondrial dysfunction, and endoplasmic reticulum stress collectively drives this pathological process.
Please cite this paper as: Nasri H, Pourpashang P. Role of oxidative stress and reactive oxygen species in calcium oxalate kidney stone pathogenesis. J Renal Inj Prev. 2026; 15(2): e38747. doi: 10.34172/jrip.2026.38747.