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.

Highlights

  • Oxidative stress and malnutrition-inflammation complex syndrome often coexist in critically ill patients and have recently came into a focus as nontraditional risk factors of cardiovascular morbidity and overall mortality in patients with end-stage renal disease (ESRD) [1,2,3,4,5]

  • The major finding was that elevation of xanthine oxidase (XOD) activity during a single HD session was positively correlated with serum hydroperoxides and advanced oxidation protein products (AOPP) and independently associated with Geriatric nutritional risk index (GNRI) ≤ 90, as an indicator of poor nutritional status

  • Given that concentration of serum albumin is included in calculation of GNRI score, these results suggest that XOD can be implicated in protein oxidative injury during HD treatment

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Summary

Introduction

Oxidative stress and malnutrition-inflammation complex syndrome often coexist in critically ill patients and have recently came into a focus as nontraditional risk factors of cardiovascular morbidity and overall mortality in patients with end-stage renal disease (ESRD) [1,2,3,4,5]. The reasons underlying chronically disturbed oxidant homeostasis in ESRD may include various factors, such as progressive deterioration of renal metabolic activities, inflammation, uremic toxins, and restrictive diets [1, 6, 7]. Unlike XDH that generates mostly superoxide anion radicals, XOD more efficiently catalyzes the formation of hydrogen peroxide, which is less reactive but long-lived oxidant. Serum XOD activity was found to be markedly elevated in HD and peritoneal dialysis patients, independently of dialysis modality [13]

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