Clinical Study on Delaying the Progression of Diabetic Kidney Disease by Inhibiting Excessive Reactive Oxygen Species Production through Alleviating Renal Inflammation and Fibrosis

Abstract

Objective: To investigate the intervention effect of inhibiting excessive reactive oxygen species (ROS) production on renal inflammation, fibrosis, and disease progression in patients with diabetic kidney disease (DKD). Methods: Thirty DKD patients treated at the Department of Nephrology, Hebei University Affiliated Hospital from April 2025 to April 2026 were enrolled as the DKD group. Thirty non-DKD patients from the same period served as the control group. General characteristics and clinical indicators were collected for both groups, including complete blood count, liver and kidney function, electrolytes, blood glucose, and 24-hour urine protein quantification. Serum NLRP3 inflammasome and inflammatory factors (IL-1β, IL-18, TNF-α, IL-6) were measured using ELISA. Transforming growth factor-β (TGF-β) was assessed to evaluate fibrosis severity. Estimated glomerular filtration rate (eGFR) was calculated using the CKD-EPI formula. Differences in indicators between groups were compared, and correlations between ROS-related pathway markers and renal function/disease progression endpoints were analyzed. Primary endpoint: eGFR decline ≥ 40% or initiation of dialysis. Secondary endpoints: doubling of random urine albumin-to-creatinine ratio (UACR) or occurrence of cardiovascular events. Results: Patients in the DKD group exhibited significantly higher serum levels of NLRP3, IL-1β, IL-18, TNF-α, IL-6, and TGF-β compared to the control group (p < 0.05). Their eGFR was significantly lower than the control group (p < 0.05), while 24-hour urine protein quantification and UACR were significantly higher than the control group (p < 0.05). Correlation analysis revealed that NLRP3 and TGF-β levels were negatively correlated with eGFR (r = −0.682, −0.715, p < 0.05) and positively correlated with 24-hour urine protein quantification (r = 0.654, 0.691, p < 0.05). During follow-up, the incidence of primary endpoint events in the DKD group was 26.67% (8/30), and that of secondary endpoint events was 36.67% (11/30), both significantly higher than in the control group (p < 0.05). Conclusion: Excessive ROS production may promote renal inflammation and fibrosis by activating the NLRP3 inflammasome pathway. Inhibiting excessive ROS production holds promise as an effective intervention target for delaying DKD progression.