Oxidative stress, antioxidant imbalance, and Na⁺–K⁺–ATPase dysfunction in patients with kidney stone disease

Background: Kidney stone disease is a multifactorial disorder linked to oxidative stress, impaired antioxidant defense, and altered membrane enzyme activity. Reactive oxygen species can cause renal tubular injury, promoting crystal formation. Na⁺–K⁺–ATPase, a key membrane-bound enzyme, is essential for ion homeostasis, and its dysfunction may contribute to nephrolithiasis. Aims and Objectives: This study aimed to measure Na⁺–K⁺–ATPase enzyme activity in erythrocyte membranes, assess oxidative stress by measuring plasma malondialdehyde (MDA) levels, and evaluate antioxidant defense by measuring superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase activities in patients with kidney stones. Materials and Methods: A total of 40 patients with kidney stones (28 males and 12 females; mean age, 39.6±8.2 years) and 40 matched controls were recruited. Blood samples were collected, and erythrocyte membranes and plasma were prepared for biochemical assays. MDA, SOD, GPx, and catalase levels were measured using spectrophotometric methods, and Na⁺–K⁺–ATPase activity was determined by inorganic phosphate liberation. Data are expressed as mean±standard deviation, and analyzed using Student’s t-test, with P<0.05 considered significant. Results: Patients with kidney stones exhibited significantly higher MDA (3.13±1.20 nmol) and GPx activity (126.47±93.08 U/g hemoglobin [Hb]), along with reduced SOD (763.45±46.58 U/g Hb), catalase (14.46±2.05 U/g Hb), and Na⁺–K⁺–ATPase activity (0.97±0.43 μmol Pi/mg protein/h) compared to controls. Conclusion: Oxidative stress, altered antioxidant defense, and reduced Na⁺–K⁺–ATPase activity are associated with kidney stone pathogenesis, highlighting biochemical targets for prevention and therapy.