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      C-Reactive Protein Predicts Vascular Access Thrombosis in Hemodialysis Patients

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          Abstract

          Background: Vascular access thrombosis (VAT) is one of the most common morbidity in hemodialysis patients. The development of arteriovenous fistula thrombosis is associated with vascular intimal hyperplasia. Some studies suggested that serum C-reactive protein (CRP) predicts the development of vascular intima hyperplasia that conduces vascular access stenosis and thrombosis. This study aimed to access the clinical usefulness of CRP in predicting VAT in hemodialysis patients. Methods: We retrospectively reviewed all prevalent hemodialysis patients with native arteriovenous fistula (nAVF) between November 2001 and November 2004. The CRP levels and relation to the development of VAT was analyzed with Kaplan-Meier analysis in four groups of patients divided according to their serum CRP levels. Besides serum CRP levels, other factors possibly influencing vascular access thrombosis were also considered: gender, age, diabetes, aspirin, smoking, statin, serum albumin, hematocrit, cholesterol >200 mg/dl, Calcium-phosphate product, and intact parathyroid hormone >200 pg/ml. Results: We retrospectively reviewed 223 chronic hemodialysis patients. 198 patients with forearm nAVF and 25 with upper arm nAVF were included. Of the above 223 patients, 51 experienced one or more VAT episodes. In Kaplan-Meier survival analysis, patients with serum CRP levels >0.8 mg/dl were prone to develop VAT (log-rank, p < 0.001). In a multivariate Cox regression model, serum CRP greater than 0.8mg/dl was confirmed to be an independent predictor of VAT with a relative risk of 16.6 times (95% CI, 7.85–35.1). The area under the receiver operator characteristic (ROC) curve of CRP >0.8 mg/dl in predicting VAT events is 0.785 (95% CI, 0.712–0.858; p < 0.001). Sensitivity and specificity of CRP (>0.8 mg/dl) in predicting VAT were 80.4 and 72.7%. Conclusions: The serum CRP levels not only predict cardiovascular disease and mortality in hemodialysis patients but also predict the development of vascular access thrombosis in chronic hemodialysis patients.

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          Most cited references 12

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          Type of vascular access and mortality in U.S. hemodialysis patients.

          Vascular access (VA) complications account for 16 to 25% of hospital admissions. This study tested the hypothesis that the type of VA in use is correlated with overall mortality and cause-specific mortality. Data were analyzed from the U.S. Renal Data System Dialysis Morbidity and Mortality Study Wave 1, a random sample of 5507 patients, prevalent on hemodialysis as of December 31, 1993. The relative mortality risk during a two-year observation was analyzed by Cox-regression methods with adjustments for demographic and comorbid conditions. Using similar methods, cause-specific analyses also were performed for death caused by infection and cardiac causes. In diabetic mellitus (DM) patients with end-stage renal disease, the associated relative mortality risk was higher for those with arteriovenous graft (AVG; RR = 1.41, P < 0.003) and central venous catheter (CVC; RR = 1.54, P < 0.002) as compared with arteriovenous fistula (AVF). In non-DM patients, those with CVC had a higher associated mortality (RR = 1.70, P < 0.001), as did to a lesser degree those with AVG (RR = 1.08, P = 0.35) when compared with AVF. Cause-specific analyses found higher infection-related deaths for CVC (RR = 2.30, P < 0.06) and AVG (RR = 2.47, P < 0.02) compared with AVF in DM; in non-DM, risk was higher also for CVC (RR = 1.83, P < 0.04) and AVG (RR = 1.27, P < 0.33). In contrast to our hypothesis that AV shunting increases cardiac risk, deaths caused by cardiac causes were higher in CVC than AVF for both DM (RR = 1.47, P < 0.05) and non-DM (RR = 1.34, P < 0.05) patients. This case-mix adjusted analysis suggests that CVC and AVG are correlated with increased mortality risk when compared with AVF, both overall and by major causes of death.
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            Oxidative stress and increased expression of growth factors in lesions of failed hemodialysis access.

            The pathological role of oxidative stress in patients treated by hemodialysis has gained increasing recognition in recent years. Because complications related to vascular access are a major source of morbidity, immunohistochemical evidence of oxidative stress and activation of growth factors were examined in native arteriovenous (AV) fistulae (n = 11) and expanded polytetrafluoroethylene (ePTFE) grafts (n = 15) recovered from hemodialysis patients at the time of surgical revision or resection. To show the presence of oxidative stress in tissues, three markers were chosen: N(epsilon)(carboxymethyl)lysine, a structurally identified advanced glycation end product; 4-hydroxy-2,3-nonenol, a lipid peroxidation product; and redox-active transition metals bound to proteins, a source of Fenton chemistry-generated free radicals. Markers of cell growth and proliferation were endothelin-1 (ET-1), a potent mitogenic peptide implicated in the formation of intimal hyperplasia; transforming growth factor-beta (TGF-beta), a stimulus to vascular cell growth and matrix production; and platelet-derived growth factor (PDGF), a mediator of intimal hyperplasia. All specimens studied showed significant intimal hyperplasia. In general, the neointima close to the vascular lumen of the AV fistula and the pseudointima close to the lumen of the ePTFE graft were positive for oxidative stress markers. At sites of injury, especially in the presence of histological evidence of inflammation and healing, expression of oxidative markers was particularly intense. Prominent staining of PDGF was shown at sites of anastomotic hyperplasia and in neovasculature. TGF-beta was associated with proliferation or repair in both AV fistulae and ePTFE grafts. ET-1 staining was most intense in the neointima and pseudointima. This study showed histochemical colocalization of markers of oxidative stress with growth factors known to contribute to intimal hyperplasia.
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              Local generation of C-reactive protein in diseased coronary artery venous bypass grafts and normal vascular tissue.

              Venous coronary artery bypass grafts (CABGs) are prone to accelerated atherosclerosis. In atherosclerotic diseases, serum C-reactive protein (CRP) levels have become an important diagnostic and prognostic marker. The origin of CRP in this setting remains to be elucidated. Monoclonal anti-CRP identified CRP expression in medial and intimal alpha-actin-positive smooth muscle cells (SMCs) of diseased CABGs with type V and VI lesions and also of native saphenous veins of atherosclerotic individuals. In addition, patent coronary arteries with type IV and V but not with type I through III lesions exhibited intense SMC staining for CRP. Calcified desobliterates of occluded coronary arteries with end-stage disease did not show SMC staining for CRP and were consistently negative for CRP mRNA, as detected by means of real-time polymerase chain reaction. However, CRP mRNA was expressed in 11 of 15 diseased CABGs and also in 10 of 15 native veins. By contrast, only 3 of 18 internal mammary and 4 of 12 radial arteries with virtually no atherosclerosis were positive for CRP mRNA. CRP is produced by SMCs of atherosclerotic lesions with active disease but not in end-stage plaques. The role of CRP constitutively expressed by normal vascular tissue in vein graft disease has yet to be elucidated.
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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                0253-5068
                1421-9735
                2006
                August 2006
                14 August 2006
                : 24
                : 4
                : 342-346
                Affiliations
                Division of Nephrology, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan, ROC
                Article
                92558 Blood Purif 2006;24:342–346
                10.1159/000092558
                16601326
                © 2006 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: 2, Tables: 3, References: 16, Pages: 5
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/92558
                Categories
                Original Paper

                Cardiovascular Medicine, Nephrology

                Stenosis, Thrombosis, Vascular access, C-reactive protein, Hemodialysis

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