8-Hydroxydeoxyguanosine Urine and Total Nitric Oxide Serum in Chronic Kidney Disease
- Oxidative markers 8-Hydroxydeoxyguanosine and Nitric Oxide was found high in hemodialysis and non-hemodialysis chronic kidney disease patients.
- There is no correlation between 8-Hydroxydeoxyguanosine and Nitric Oxide in hemodialysis and non-hemodialysis chronic kidney disease patients.
Oxidative stress is essential to chronic kidney disease (CKD). Several markers include 8-Hydroxydeoxyguanosine (8-OHdG) and Nitric Oxide (NO). Reactive oxygen species (ROS) and Reactive Nitrogen Species (RNS) increased in CKD and had a role in renal impairment progressivity. There are some controversies regarding oxidative markers in CKD patients in several studies. This study aimed to understand oxidative markers 8-OHdG and NO and explained the correlation of both markers in hemodialysis and non-hemodialysis CKD patients. Twenty hemodialysis patients and forty-nine non-hemodialysis patients were enrolled in this cross-sectional study. Urine patients were collected to measure 8-OHdG using the enzyme-linked immunoassay (ELISA) method, and NO was measured from serum patients using the Griss Saltzman method. Based on Bivariate Pearson analysis, there was no significant correlation between 8-OHdG urine and total NO serum in the hemodialysis group (p= 0,510, p>0.05) and in the non-hemodialysis group (p= 0.801, p>0,05). In this study, DNA oxidative marker, 8-OHdG, was not correlated with NO in CKD patients.
Alsagaff M, Pikir B, Thaha M, et al (2020). Correlations between total antioxidant capacity and 8-hydroxydeoxyguanosine with carotid-femoral pulse wave velocity in chronic kidney disease. Indones. Biomed. J. 12, 267–274.
Baylis C (2006). Arginine, arginine analogs and nitric oxide production in chronic kidney disease. Nat. Clin. Pract. Nephrol. 2, 209–220.
Dai L, Watanabe M, Qureshi A, et al (2019). Serum 8-hydroxydeoxyguanosine, a marker of oxidative DNA damage, is associated with mortality independent of inflammation in chronic kidney disease. Eur. J. Intern. Med. 68, 60–65.
Duni A, Liakopoulos V, Rapsomanikis K-P, et al (2017). Chronic kidney disease and disproportionately increased cardiovascular damage: Does oxidative stress explain the burden? Oxid. Med. Cell. Longev. 2017, 1–15.
Duni A, Liakopoulos V, Roumeliotis S, et al (2019). Oxidative stress in the pathogenesis and evolution of chronic kidney disease: Untangling ariadne’s thread. Int J Mol Sci 20, 1–17.
Ghanayem N, Badr E, Elmadbouh I, et al (2017). Urinary 8-hydroxy-2′-deoxyguanosine as an oxidative DNA damage biomarker in chronic heart failure. Menoufia Med. J. 30, 1072.
Hill N, Fatoba S, Oke J, et al (2016). Global prevalence of chronic kidney disease - A systematic review and meta-analysis. PLoS One 11, 1–18.
Hsu C, Tain Y (2021). Developmental origins of kidney disease: Why oxidative stress matters? Antioxidants 10, 1–18.
Luyckx V, Tonelli M, Stanifer J (2018). The global burden of kidney disease and the sustainable development goals. Bull. World Health Organ. 96, 414–422.
Meenaski S, Agarwal R (2013). Nitric oxide levels in patients with chronic renal disease. J. Clin. Diagnostic Res. 7, 1288–1290.
Putri A, Thaha M (2014). Role of oxidative stress on chronic kidney disease progression. Acta Med. Indones. 46, 244–252.
Ravarotto V, Simioni F, Pagnin E, et al (2018). Oxidative stress – chronic kidney disease – cardiovascular disease: A vicious circle. Life Sci. 210, 125–131.
Roumeliotis S, Mallamaci F, Zoccali C (2020). Endothelial dysfunction in chronic kidney disease, from biology to clinical outcomes: A 2020 update. J. Clin. Med. 9, 1–27.
Sung C-C, Hsu Y-C, Chen C-C (2013). Oxidative stress and nucleic acid oxidation in patients with chronic kidney disease. Oxid. Med. Cell. Longev. 2013, 1–15.
Toualbi L, Adnane M, Abderrezak K, et al (2020). Oxidative stress accelerates the carotid atherosclerosis process in patients with chronic kidney disease. Arch Med Sci Atheroscler Dis 14, 245–254.
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