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      The Pattern of Inflammation and a Potential New Clinical Meaning and Usefulness of C-Reactive Protein in End-Stage Renal Failure Patients

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          Abstract

          Inflammatory indexes are frequently elevated in end-stage renal failure (ESRF) patients. It seems that the pattern of inflammation is particular in this population. In the presence of a higher than normal microinflammatory background (CRP, C-reactive protein, values between 0.1 and 10–15 mg/l) that varies with time, waves of ‘true’ inflammation (CRP > 10–15 mg/l), mainly due to infections, are added periodically. To accurately assess the average microinflammation in these patients, multiple CRP measurements are required. As recent experimental studies showed that inflammation and particularly elevated CRP levels may be risk factors and not just a risk index for atherosclerosis, in this case, the characteristic inflammation pattern might be of importance in the evolution of this disease in ESRF patients. The causes of the inflammatory state in ESRF patients are multiple: renal insufficiency per se and its complications, coexisting diseases, established atherosclerosis, the consequences of renal replacement treatment, and frequent infections are potentially the main ones. The fluctuating inflammatory pattern is probably due to destabilization or changes in time of the above-mentioned parameters. Thus, the clinical meaning of the average microinflammation in these patients, as assessed by CRP measurements, seems to be that of an index indicative of the grade of their health aggravation by the multiple factors implicated in the inflammation formation. CRP is a sensitive, but not specific, risk index of the overall morbidity and mortality in these patients. The manipulation of the inflammation in ESRF patients should include follow-up and treatment of all the factors that contribute to this state and probably medications such as the statins. If inflammation and CRP in particular definitely prove to be risk factors for atherosclerosis, intensification of this treatment will be necessary.

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          Most cited references 35

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          Explaining how "high-grade" systemic inflammation accelerates vascular risk in rheumatoid arthritis.

          There is intense interest in mechanisms whereby low-grade inflammation could interact with conventional and novel vascular risk factors to promote the atheromatous lesion. Patients with rheumatoid arthritis (RA), who by definition manifest persistent high levels of inflammation, are at greater risk of developing cardiovascular disease. Mechanisms mediating this enhanced risk are ill defined. On the basis of available evidence, we argue here that the systemic inflammatory response in RA is critical to accelerated atherogenesis operating via accentuation of established and novel risk factor pathways. By implication, long-term suppression of the systemic inflammatory response in RA should be effective in reducing risk of coronary heart disease. Early epidemiological observational and clinical studies are commensurate with this hypothesis. By contrast, risk factor modulation with conventional agents, such as statins, may provide unpredictable clinical benefit in the context of uncontrolled systemic inflammatory parameters. Unraveling such complex relationships in which exaggerated inflammation-risk factor interactions are prevalent may elicit novel insights to effector mechanisms in vascular disease generally.
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            Association of low fetuin-A (AHSG) concentrations in serum with cardiovascular mortality in patients on dialysis: a cross-sectional study.

            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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              Are there two types of malnutrition in chronic renal failure? Evidence for relationships between malnutrition, inflammation and atherosclerosis (MIA syndrome).

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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
                2005
                December 2004
                11 January 2005
                : 28
                : 1
                : 55-61
                Affiliations
                Department of Nephrology, General Hospital of Athens, Athens, Greece
                Article
                82165 Kidney Blood Press Res 2005;28:55–61
                10.1159/000082165
                15550763
                © 2005 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: 1, Tables: 3, References: 51, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/82165
                Categories
                Review Article

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