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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      Estimation of Oxidative Stress Markers in Chronic Kidney Disease

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          Abstract

          Changes mediated by oxidative stress are thought to be involved with atherosclerosis in patients with chronic kidney disease (CKD). The purpose of this study was to analyze the markers of oxidative damage and the activity of antioxidative enzymes as well as the total antioxidant capability in patients with different stages of CKD, both conventionally treated and dialyzed. We evaluated the oxidative modification of lipids (by oxidized low-density lipoprotein and malonodialdehyde levels) and proteins (by advanced oxidation protein products level). We also assessed the activity of paraoxonase-1 and glutathione peroxidases and total antioxidant status. Compared with the control group, the uremic patients, both dialyzed and nondialyzed, had higher levels of all studied plasma oxidative stress markers and decreased activity of antioxidative enzymes. Our results lead us to conclude that oxidative stress seems to be related rather to the uremic state than to the dialysis treatment. We also showed that estimating total antioxidant status in a simple test is unreliable for assessing the antioxidant ability of patients with CKD.

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          Most cited references29

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          The elephant in uremia: oxidant stress as a unifying concept of cardiovascular disease in uremia.

          Cardiovascular disease is the leading cause of mortality in uremic patients. In large cross-sectional studies of dialysis patients, traditional cardiovascular risk factors such as hypertension and hypercholesterolemia have been found to have low predictive power, while markers of inflammation and malnutrition are highly correlated with cardiovascular mortality. However, the pathophysiology of the disease process that links uremia, inflammation, and malnutrition with increased cardiovascular complications is not well understood. We hereby propose the hypothesis that increased oxidative stress and its sequalae is a major contributor to increased atherosclerosis and cardiovascular morbidity and mortality found in uremia. This hypothesis is based on studies that conclusively demonstrate an increased oxidative burden in uremic patients, before and particularly after renal replacement therapies, as evidenced by higher concentrations of multiple biomarkers of oxidative stress. This hypothesis also provides a framework to explain the link that activated phagocytes provide between oxidative stress and inflammation (from infectious and non-infections causes) and the synergistic role that malnutrition (as reflected by low concentrations of albumin and/or antioxidants) contributes to the increased burden of cardiovascular disease in uremia. We further propose that retained uremic solutes such as beta-2 microglobulin, advanced glycosylated end products (AGE), cysteine, and homocysteine, which are substrates for oxidative injury, further contribute to the pro-atherogenic milieu of uremia. Dialytic therapy, which acts to reduce the concentration of oxidized substrates, improves the redox balance. However, processes related to dialytic therapy, such as the prolonged use of catheters for vascular access and the use of bioincompatible dialysis membranes, can contribute to a pro-inflammatory and pro-oxidative state and thus to a pro-atherogenic state. Anti-oxidative therapeutic strategies for patients with uremia are in their very early stages; nonetheless, early studies demonstrate the potential for significant efficacy in reducing cardiovascular complications.
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            Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis.

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              Glutathione antioxidant system as a marker of oxidative stress in chronic renal failure

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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2011
                January 2011
                11 November 2010
                : 34
                : 1
                : 12-19
                Affiliations
                Departments of aClinical Chemistry, bInternal Diseases, Connective Tissue Diseases and Geriatrics, and cNephrology, Transplantology and Internal Medicine, Medical University of Gdańsk, Gdańsk, Poland
                Author notes
                *Agnieszka Kuchta, Department of Clinical Chemistry, Medical University of <under>Gdańsk</under>, <under>Dębinki 7, PL–</under>80-220 <under>Gdańsk</under> (Poland), Tel. +48 58 349 27 95, Fax +48 58 346 15 38, E-Mail agastencel@gumed.edu.pl
                Article
                321508 Kidney Blood Press Res 2011;34:12–19
                10.1159/000321508
                21071957
                ecd1b690-4654-47d9-87e0-e64095736ff1
                © 2010 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 02 February 2010
                : 24 September 2010
                Page count
                Figures: 3, Tables: 3, References: 40, Pages: 8
                Categories
                Original Paper

                Cardiovascular Medicine,Nephrology
                Chronic kidney disease,Oxidized low-density lipoprotein,Paraoxonase-1

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