Serum Extracellular Superoxide Dismutase Concentration in Type 2 Diabetic Patients with Nephropathy: An Investigation of the Relationship
Main Article Content
Keywords
Extracellular Super Oxide Dismutase, SOD3, Diabetic Nephropathy, Oxidative Stress
Abstract
Diabetic nephropathy (DN) is a leading cause of end-stage renal disease and is characterized by complex pathogenic mechanisms involving oxidative stress. Antioxidant enzymes play a crucial role in combating oxidative stress and potentially slowing down the progression of DN. Extracellular superoxide dismutase (EcSOD) is an important enzyme located in the extracellular spaces that scavenges the superoxide anion, a key contributor to oxidative stress.
Methods: In this study, we enrolled a total of 167 diabetic patients, with 101 patients without nephropathy serving as the control group. The DN group consisted of 66 patients, who were further categorized into subgroups based on their albumin creatinine ratio (ACR): microalbuminuria (ACR 30-300 mg/g) and macroalbuminuria (ACR > 300 mg/g). EcSOD enzyme concentrations were measured using the Enzyme-Linked Immuno-Sorbent Assay (ELISA) technique.
Results: The mean EcSOD concentration in the DN group was 166.18 ng/mL (±66.02), slightly higher than the diabetic-only group (157.68 ng/mL ±66.67), but this difference was not statistically significant (P value = 0.420). Within the DN group, the microalbuminuria subgroup exhibited an EcSOD concentration of 166.95 ng/mL (±68.83), while the macroalbuminuria subgroup showed a concentration of 159.73 ng/mL (±36.96). However, the comparison between these subgroups did not yield a statistically significant difference (P = 0.787).
Conclusions: Based on our findings, the concentration of EcSOD does not appear to be significantly associated with the development of nephropathy in Type 2 diabetic patients. Further investigations are warranted to explore other potential mechanisms contributing to the pathogenesis of diabetic nephropathy and to determine the role of EcSOD in this context
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