Role of oxidative stress and reactive oxygen species in calcium oxalate kidney stone pathogenesis

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.