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      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Vascular Calcification and Cardiovascular Outcome in Dialysis Patients: The Role of Gene Polymorphisms

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          Abstract

          Vascular calcification and accelerated atherosclerosis are major causes of death in hemodialysis (HD) patients. Epigenetic mechanisms of gene regulation may be crucial determinants of cellular behavior in uremic conditions, determining an increased risk of cardiovascular morbidity and mortality. The common polymorphisms on different gene promoters have been related to increased coronary artery calcification and associated with cardiovascular outcome in HD population. In this review, we reported the gene polymorphisms of different proteins as negative prognostic risk factors for all-cause mortality in HD patients, independent of traditional risk factors. These data may have important implications for better understanding the pathogenesis of the increased mortality in this population.

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          Clinical epidemiology of cardiovascular disease in chronic renal disease.

          RN Foley, PS Parfrey, MJ Sarnak (1998)
          Article 0 comments Cited 643 times – based on 0 reviews     Review now
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            Association of low fetuin-A (AHSG) concentrations in serum with cardiovascular mortality in patients on dialysis: a cross-sectional study.

            Markus Ketteler, Philipp Bongartz, Ralf Westenfeld … (2003)
            Vascular calcification is the most prominent underlying pathological finding in patients with uraemia, and is a predictor of mortality in this population. Fetuin-A (alpha2-Heremans Schmid glycoprotein; AHSG) is an important circulating inhibitor of calcification in vivo, and is downregulated during the acute-phase response. We aimed to investigate the hypothesis that AHSG deficiency is directly related to uraemic vascular calcification. We did a cross-sectional study in 312 stable patients on haemodialysis to analyse the inter-relation of AHSG and C-reactive protein (CRP) and their predictive effect on all-cause and cardiovascular mortality, over a period of 32 months. Subsequently, we tested the capacity of serum to inhibit CaxPO4 precipitation in patients on long-term dialysis (n=17) with apparent soft-tissue calcifications, and in those on short-term dialysis (n=8) without evidence of calcifications and cardiovascular disease. AHSG concentrations in serum were significantly lower in patients on haemodialysis (mean 0.66 g/L [SD 0.28]) than in healthy controls (0.72 [0.19]). Low concentrations of the glycoprotein were associated with raised amounts of CRP and with enhanced cardiovascular (p=0.031) and all-cause mortality (p=0.0013). Sera from patients on long-term dialysis with low AHSG concentrations showed impaired ex-vivo capacity to inhibit CaxPO4 precipitation (mean IC50: 9.0 microL serum [SD 3.1] vs 7.5 [0.8] in short-term patients and 6.4 [2.6] in controls). Reconstitution of sera with purified AHSG returned this impairment to normal. Interpretation AHSG deficiency is associated with inflammation and links vascular calcification to mortality in patients on dialysis. Activated acute-phase response and AHSG deficiency might account for accelerated atherosclerosis in uraemia.
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              High expression of genes for calcification-regulating proteins in human atherosclerotic plaques.

              N Cary, Roger P Weissberg, J. Metcalfe … (1994)
              Calcification is common in atheromatous plaques and may contribute to plaque rupture and subsequent thrombosis. However, little is known about the mechanisms which regulate the calcification process. Using in situ hybridization and immunohistochemistry we show that two bone-associated proteins, osteopontin (OP) and matrix Gla protein (MGP), are highly expressed in human atheromatous plaques. High levels of OP mRNA and protein were found in association with necrotic lipid cores and areas of calcification. The predominant cell type in these areas was the macrophage-derived foam cell, although some smooth muscle cells could also be identified. MGP was expressed uniformly by smooth muscle cells in the normal media and at high levels in parts of the atheromatous intima. Highest levels of this matrix-associated protein were found in lipid-rich areas of the plaque. The pattern of expression of these two genes contrasted markedly with that of calponin and SM22 alpha, genes expressed predominantly by differentiated smooth muscle cells and whose expression was generally confined to the media of the vessel. The postulated function of OP and MGP as regulators of calcification in bone and the high levels and colocalization of both in atheromatous plaques suggest they have an important role in plaque pathogenesis and stability.
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                Author and article information

                Journal
                Journal ID (publisher-id): BPU
                Journal ID (nlm-ta): Blood Purif
                Journal ID (doi): 10.1159/issn.0253-5068
                Title: Blood Purification
                Publisher: S. Karger AG
                ISSN (Print): 0253-5068
                ISSN (Electronic): 1421-9735
                Publication date Subscription-year: 2010
                Publication date (Print): June 2010
                Publication date (Electronic): 31 March 2010
                Volume: 29
                Issue: 4
                Pages: 347-351
                Affiliations
                aRenal Division and bInfective Molecular Diagnostic, S. Paolo Hospital, cDepartment of Medicine, Surgery and Dentistry, University of Milan School of Medicine, dRenal Division, S. Carlo Hospital, Milan, Italy
                Article
                Publisher ID: 302722 Other ID: Blood Purif 2010;29:347–351
                DOI: 10.1159/000302722
                PubMed ID: 20357434
                SO-VID: 019671ef-e229-4707-bf2c-e6e844db0a8c
                Copyright © © 2010 S. Karger AG, Basel
                License:

                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.

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                Page count
                Figures: 1, References: 38, Pages: 5
                Categories
                Subject: In-Depth Review

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Atherosclerosis,Vascular calcification,Hemodialysis,Gene polymorphism
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Atherosclerosis, Vascular calcification, Hemodialysis, Gene polymorphism

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