ArticleOxidative medicine and cellular longevity2013
The role of xanthine oxidase in hemodialysis-induced oxidative injury: relationship with nutritional status.
Article in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Implication of changes in xanthine oxidase activity following hemodialysis.BMC nephrology · 2023Article
- Xanthine oxidoreductase activity in platelet-poor and rich plasma as a oxidative stress indicator in patients required renal replacement therapy.BMC nephrology · 2022Article
- Oxidative Stress in Patients with Advanced CKD and Renal Replacement Therapy: The Key Role of Peripheral Blood Leukocytes.Antioxidants (Basel, Switzerland) · 2021Article
- Association between Serum Uric Acid Levels, Nutritional and Antioxidant Status in Patients on Hemodialysis.Nutrients · 2020Article
- Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Role of Myeloperoxidase in Patients with Chronic Kidney Disease.Oxidative medicine and cellular longevity · 2016Review
- Influence of vitamin C supplementation on oxidative stress and neutrophil inflammatory response in acute and regular exercise.Oxidative medicine and cellular longevity · 2015Article
- The cytotoxic role of intermittent high glucose on apoptosis and cell viability in pancreatic beta cells.Journal of diabetes research · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of xanthine oxidase (XOD) in patients undergoing chronic hemodialysis treatment (HD) is poorly understood. Geriatric nutritional risk index (GNRI) ≤ 90 could be linked with malnutrition-inflammation complex syndrome. This study measured XOD, myeloperoxidase (MPO), superoxide dismutase (SOD), lipid hydroperoxides, total free thiol groups, and advanced oxidation protein products (AOPP) in 50 HD patients before commencing (pre-HD) and immediately after completion of HD session (post-HD) and in 22 healthy controls. Pre-HD serum hydroperoxides, AOPP, XOD, and SOD were higher and total thiol groups were lower in patients than in controls (P < 0.05, resp.). Compared to baseline values, serum MPO activity was increased irrespective of GNRI status. Serum XOD activity was increasing during HD treatment in the group with GNRI ≤ 90 (P = 0.030) whilst decreasing in the group with GNRI > 90 (P = 0.002). In a multiple regression analysis, post-HD serum XOD activity was independently associated with GNRI ≤ 90 ( β ± SE: 0.398 ± 0.151; P = 0.012) and HD vintage ( β ± SE: -0.349 ± 0.139; P = 0.016). These results indicate that an upregulated XOD may be implicated in HD-induced oxidative injury contributing to accelerated protein damage in patients with GNRI ≤ 90.
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