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Iranian Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran
Abstract:   (11 Views)
Introduction: Numerous factors contribute to the advancement of progressive kidney damage in chronic kidney disease (CKD). Among these, oxidative damage plays a significant role in the progression of CKD. The reactions involving free radicals are recognized as a crucial element that can exacerbate oxidative damage in patients with CKD. However, the precise mechanisms underlying oxidative damage remain incompletely understood. Consequently, this study aimed to explore oxidative and other associated biochemical parameters.
Materials and Methods: This case-control study included 38 male and 23 female patients, with mean ages of 58.9 ± 15.9 and 62.13 ± 13.43 years, respectively. At the same time, 40 healthy male and 22 healthy female individuals with an average age of 60.33 ± 10.62 and 59.3 ± 6.64, respectively, were selected as the control group who had no history of any diseases such as hypertension, diabetes, infection and kidney disease. Research variables including malondialdehyde (MDA), nitric oxide metabolites (nitrite/nitrate), and homocysteine (Hcy) concentration were measured in both case and control groups. Statistical analysis was done according to the obtained results.
Results: There was a significant increase in homocysteine concentration in CKD patients compared to the control (P = 0.001). Nitrite and nitrate metabolites exhibited a substantial reduction in patients when compared to the control group (P = 0.001). On the other hand, malondialdehyde (MDA) showed a significant increase in patients compared to controls (P = 0.01).
Conclusion: The findings indicate that homocysteine levels, lipid peroxidation, and alterations in nitric oxide may significantly contribute to the progression of oxidative damage in patients with chronic kidney disease (CKD) and may also influence the disease’s pathogenesis.
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Type of Study: Research | Subject: Biochemistry
Received: 2024/07/3 | Accepted: 2024/11/12

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