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      Plasma Homocysteine, Vitamin B 6, Vitamin B 12 and Folic Acid in End-Stage Renal Disease during Low-Dose Supplementation with Folic Acid

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          Abstract

          In order to see whether conventional low-dose folic acid supplement along with vitamin B<sub>6</sub> and B<sub>12</sub> reduces hyperhomocysteinemia in patients with ESRD, we compared the levels of homocysteine, vitamin B<sub>6</sub>, B<sub>12</sub> and folic acid among 3 groups of patients: 44 ESRD patients on hemodialysis with replacement of folic acid, vitamin B<sub>6</sub>, and B<sub>12</sub> (dialysis group); 27 chronic renal failure patients without vitamin replacement (predialysis group); and 17 hypertensive patients without vitamin replacement (control group). Mean plasma total homocysteine concentration was higher in the dialysis (15.5 ± 6.6 µmol/l) and the predialysis groups (15.7 ± 4.2 µmol/l) than in the control group (6.2 ± 1.5 µmol/l) (p < 0.001). However, there was no difference in homocysteine concentrations between the dialysis and predialysis groups. In the control and predialysis groups, the homocysteine concentration showed a reverse correlation with the concentrations of folic acid (r = 0.584, p = 0.014 for the control group; r = 0.431, p = 0.247 for the predialysis group) and vitamin B<sub>12</sub> (r = 0.485, p = 0.049 for the control group; r = –0.562, p = 0.023 for the predialysis group) but not with vitamin B<sub>6</sub>. In conclusion, plasma folic acid concentrations were 3–4 times higher in the dialysis than in the predialysis group. But these levels of folic acid are not enough to reduce hyperhomocysteinemia in ESRD.

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          Homocysteine and coronary atherosclerosis.

          Homocysteine is increasingly recognized as a risk factor for coronary artery disease. An understanding of its metabolism and of the importance of vitamins B6 and B12 and folate as well as enzyme levels in its regulation will aid the development of therapeutic strategies that, by lowering circulating concentrations, may also lower risk. Possible mechanisms by which elevated homocysteine levels lead to the development and progression of vascular disease include effects on platelets, clotting factors and endothelium. This review presents the clinical and basic scientific evidence supporting the risk and mechanisms of vascular disease associated with elevated homocysteine concentrations as well as the results of preliminary therapeutic trials.
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            Author and article information

            Journal
            AJN
            Am J Nephrol
            10.1159/issn.0250-8095
            American Journal of Nephrology
            S. Karger AG
            0250-8095
            1421-9670
            1998
            October 1998
            10 September 1998
            : 18
            : 5
            : 367-372
            Affiliations
            Departments of a Internal Medicine, and b Chemistry, Soonchunhyang University, Chunan City, Korea
            Article
            13378 Am J Nephrol 1998;18:367–372
            10.1159/000013378
            9730558
            © 1998 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.

            Page count
            Figures: 3, Tables: 1, References: 23, Pages: 6
            Product
            Self URI (application/pdf): https://www.karger.com/Article/Pdf/13378
            Categories
            Clinical Study

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