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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/10266


    Title: High uric acid ameliorates indoxyl sulfate-induced endothelial dysfunction and is associated with lower mortality among hemodialysis patients
    Authors: Hsu, WL;Li, SY;Liu, JS;Huang, PH;Lin, SJ;Hsu, CC;Lin, YP;Tarng, DC
    Contributors: Division of Geriatric Research
    Abstract: High uric acid (UA) can act as a pro-oxidant in normal physiological conditions; however, emerging evidence is still debatable with regard to the association between high UA and poor outcomes among chronic hemodialysis (HD) patients. In the present study, 27,229 stable prevalent HD patients were enrolled and divided into four groups according to the quartiles of baseline UA concentration, and 5737 died during a median follow-up of 38 months. Multivariate Cox regression analysis showed that a UA level of <6.1 mg/dL was associated with a higher risk of all-cause mortality compared with a UA level of >8.1 mg/dL [HR, 1.20, 95% CI (1.10-1.31)] adjusting for baseline demographic and biochemical parameters. Moreover, a UA level of <6.1 mg/dL was associated with greater risks of cardiovascular mortality [HR, 1.26, 95% CI (1.13-1.41)] and stroke-related mortality [HR, 1.59, 95% CI (1.12-2.25)], respectively. In vitro experiments further showed an increase in oxidative stress and an inhibition nitric oxide synthesis by indoxyl sulfate (IS) in human aortic endothelial cells, which were significantly attenuated by UA in a dose-dependent manner. We concluded that higher UA in serum was associated with lower risk of all-cause and cardiovascular mortality among HD patients probably through its antioxidant property in ameliorating the IS-related vascular toxicity.
    Date: 2017-01-06
    Relation: Toxins. 2017 Jan 06;9(1):Article number 20.
    Link to: http://dx.doi.org/10.3390/toxins9010020
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2072-6651&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000392980000020
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85010332766
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