Keisuke Nakayama1, Hiroyuki Terawaki2, Masaaki Nakayama2, Masashi Iwabuchi3, Toshinobu Sato3, Sadayoshi Ito2. 1. Research Division of Dialysis and Chronic Kidney Disease, Tohoku University Graduate School of Medicine, 1-1 Seiryo machi aoba-ku, Sendai, 980-8574, Japan. nkeisuke@ac.cyberhome.ne.jp. 2. Research Division of Dialysis and Chronic Kidney Disease, Tohoku University Graduate School of Medicine, 1-1 Seiryo machi aoba-ku, Sendai, 980-8574, Japan. 3. Department of Blood Purification, Tohoku University Graduate School of Medicine, Sendai, Japan.
Abstract
BACKGROUND: Hemodialysis (HD) is thought to exacerbate oxidative stress (OS). The purpose of this study was to assess patients' oxidative status during and after HD, and to clarify the relation between oxidative status and antioxidant solutes such as uric acid (UA) and ascorbic acid (AsA). METHODS: Serum diacron-reactive oxygen metabolites (d-ROM), and biological antioxidant potential (BAP), as well as serum concentrations of UA, AsA, urea nitrogen (UN), and creatinine (Cre) were measured in eight HD patients at six time points during and after HD. Inflow and outflow dialyzer blood was evaluated during HD or sham HD (no dialysate flow). Further, BAP was evaluated by adding UA or AsA to post-HD serum. RESULTS: No changes were found in d-ROM over time, whereas BAP was significantly decreased by HD. No differences were found in d-ROM during HD or sham HD, or between inflow and outflow blood. During HD, significantly lower BAP levels were found in outflow blood than in inflow blood. Serum UA and AsA levels were decreased by HD; however, no increases were observed in BAP levels after the addition of these molecules to post-HD serum. CONCLUSION: These data indicate that HD reduces serum antioxidative capacity, and the loss of dialyzable molecules may be involved. However, this reduction in capacity does not seem to be caused by the loss of UA or AsA.
BACKGROUND: Hemodialysis (HD) is thought to exacerbate oxidative stress (OS). The purpose of this study was to assess patients' oxidative status during and after HD, and to clarify the relation between oxidative status and antioxidant solutes such as uric acid (UA) and ascorbic acid (AsA). METHODS: Serum diacron-reactive oxygen metabolites (d-ROM), and biological antioxidant potential (BAP), as well as serum concentrations of UA, AsA, ureanitrogen (UN), and creatinine (Cre) were measured in eight HDpatients at six time points during and after HD. Inflow and outflow dialyzer blood was evaluated during HD or sham HD (no dialysate flow). Further, BAP was evaluated by adding UA or AsA to post-HD serum. RESULTS: No changes were found in d-ROM over time, whereas BAP was significantly decreased by HD. No differences were found in d-ROM during HD or sham HD, or between inflow and outflow blood. During HD, significantly lower BAP levels were found in outflow blood than in inflow blood. Serum UA and AsA levels were decreased by HD; however, no increases were observed in BAP levels after the addition of these molecules to post-HD serum. CONCLUSION: These data indicate that HD reduces serum antioxidative capacity, and the loss of dialyzable molecules may be involved. However, this reduction in capacity does not seem to be caused by the loss of UA or AsA.
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