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      Association of Anticardiolipin Antibodies with Vascular Access Occlusion in Hemodialysis Patients: Cause or Effect?

      Nephron

      S. Karger AG

      Anticardiolipin antibody, Antiphospholipid antibody, Vascular occlusion, Arteriovenous access, Hemodialysis

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          Abstract

          Background: Uremic patients on hemodialysis (HD) often display occlusive disorders despite their uremic thromboasthenia. The role of anticardiolipin antibodies (aCL) and the recently identified anti-β<sub>2</sub>-glycoprotein I antibodies (aβGPI) in these phenomena is unknown. Methods: The prevalence of IgG and IgM aCL and aβGPI was documented in 54 HD patients and 19 nondialyzed patients with chronic renal failure (CRF). The HD patients were further divided into arteriovenous (AV) access occluders and nonoccluders. Results: HD patients had a higher mean IgG aCL level than CRF patients (14.68 ± 3 vs. 2.96 ± 1 IU/ml, respectively, p < 0.0007). IgM aCL did not differ significantly. AV access occluders had a higher mean IgG and IgM aCL levels than nonoccluders (24.47 and 8.39 IU/ml in occluders vs. 8.45 and 3.59 IU/ml in nonoccluders, p < 0.0226 and p < 0.05, respectively). IgM and IgG aβGPI antibody levels were below the cutoff point and did not differ significantly between the various groups. Cardiovascular episodes were not correlated with the titer of aCL or aβGPI. Conclusion: These results indicate that HD, especially in patients with recurrent access occlusion episodes, is associated with elevated levels of IgG aCL, and that IgG aCL level may predict the occlusive status of HD patients.

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          Most cited references 4

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          The mosaic of autoimmunity.

          The term 'autoimmune' is applied to a wide spectrum of diseases, which, although they may differ in pathology, share many factors. In their review, portrayed as a mosaic, Yehuda Shoenfeld and David Isenberg illustrate the complexity of these conditions, outlining the many pieces, genetic, hormonal, immunological and environmental that contribute to auto-immunity, and show how their varying combinations lead to diverse diseases.
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            Immunization with anticardiolipin cofactor (beta-2-glycoprotein I) induces experimental antiphospholipid syndrome in naive mice.

             D Faden,  M. Blank,  A Tincani (1994)
            Beta-2-GPI is a 50 kDa glycoprotein which is known to be a serum co-factor, with a role in determining the binding of pathogenic anticardiolipin antibodies to phospholipids. Immunization of naive mice with beta-2-GPI resulted in elevated levels of antibodies directed against negatively charged phospholipids (cardiolipin, phosphotidylserine, phosphatidylinositol). The presence of increased titres of antiphospholipid antibodies in the sera of the mice was later followed by prolonged activated partial thromboplastin time (APTT), thrombocytopenia, and when the mice were mated, by a high percentage of fetal resorptions in the uterus. These data point to the ability of beta-2-GPI to induce pathogenic anti-cardiolipin antibodies following active immunization.
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              • Abstract: not found
              • Article: not found

              Crossreaction between antibodies to oxidised low-density lipoprotein and to cardiolipin in systemic lupus erythematosus

               O Vaarala,  K Aho,  T Palosuo (1993)
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2000
                December 2000
                01 December 2000
                : 86
                : 4
                : 447-454
                Affiliations
                Nephrology and Hypertension Services, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
                Article
                45833 Nephron 2000;86:447–454
                10.1159/000045833
                11124593
                © 2000 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: 5, References: 48, Pages: 8
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/45833
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                Original Paper

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