Declining Antioxidant Defense Correlates with Albuminuric Injury in Chronic Kidney Disease

Background: Chronic kidney disease (CKD) is characterized by progressive loss of renal function and high cardiovascular risk. Microalbuminuria reflects glomerular and endothelial injury and is widely used for risk stratification. Oxidative stress has been implicated in CKD progression, yet the relationship between systemic antioxidant defenses and microalbuminuria across CKD stages requires clearer clinical characterization. Objective: To evaluate stage-wise changes in antioxidant biomarkers and to determine their association with microalbuminuria among CKD patients. Methods: This observational cross-sectional study included 60 CKD patients spanning stages 1–5. Participants were grouped as early CKD (stages 1–2), moderate CKD (stage 3), and advanced CKD (stages 4–5). Enzymatic antioxidants—superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx)—and total antioxidant capacity (TAC) were assessed. Microalbuminuria was measured using the urinary albumin–creatinine ratio (ACR). Stage-wise comparisons, correlation analysis, and multivariate linear regression were performed, adjusting for age, diabetes mellitus, and CKD stage. Results: Antioxidant biomarkers showed a significant progressive decline with advancing CKD stage (all p < 0.001), while ACR increased markedly across stages (p < 0.001). TAC demonstrated the strongest inverse correlation with ACR (r = −0.50, p < 0.001), followed by GPx (r = −0.48, p < 0.001). In multivariate regression analysis, TAC (β = −0.40, p < 0.001) and GPx (β = −0.35, p = 0.002) remained independent negative predictors of microalbuminuria, whereas CKD stage (β = +0.45, p < 0.001) and diabetes mellitus (β = +0.20, p = 0.01) were positive predictors. Conclusion: Declining antioxidant defense is independently associated with microalbuminuria in CKD, supporting oxidative imbalance as a mechanistic contributor to albuminuric renal injury.