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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 245253, 8 pages
Clinical Study

The Role of Xanthine Oxidase in Hemodialysis-Induced Oxidative Injury: Relationship with Nutritional Status

1Institute of Biochemistry, Medical Faculty Pristina, 38220 Kosovska Mitrovica, Serbia
2Internal Clinic, Medical Faculty Pristina, 38220 Kosovska Mitrovica, Serbia
3Department of Informatics, State University of Novi Pazar, 36300 Novi Pazar, Serbia
4Institute of Pharmacology, Medical Faculty Pristina, 38220 Kosovska Mitrovica, Serbia

Received 31 January 2013; Accepted 17 May 2013

Academic Editor: Kota V. Ramana

Copyright © 2013 Dijana Miric et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 ( , 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 ( ) whilst decreasing in the group with GNRI > 90 ( ). In a multiple regression analysis, post-HD serum XOD activity was independently associated with GNRI ≤ 90 (β  ± SE: 0.398 ± 0.151; ) and HD vintage (β  ± SE: −0.349 ± 0.139; ). 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.