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      Effects of LDL Apheresis and Vitamin E-Modified Membrane on Carotid Atherosclerosis in Hemodialyzed Patients with Arteriosclerosis obliterans

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          Abstract

          Background: Hemodialysis patients manifest accelerated atherosclerosis. Hemodialysis is associated with oxidative stress, which can be partially prevented with the use of a vitamin E-coated dialyzer. Adsorption of low-density lipoprotein (LDL) has been applied in the treatment of arteriosclerosis obliterans (ASO). The aim of the present study was to determine whether the vitamin E-coated dialyzer and/or LDL apheresis affects carotid atherosclerosis in hemodialysis patients with ASO. Methods: Thirty hemodialysis patients with ASO were divided into four treatment groups: treatment with conventional cellulose or synthetic membranes (group A, n = 12), treatment with vitamin E-coated membrane (group B, n = 7), treatment with conventional membrane and LDL apheresis (group C, n = 6), and treatment with vitamin E-coated membrane and LDL apheresis (group D, n = 5). Carotid artery intima-media thickness (IMT) and arterial stiffness assessed by pulse wave velocity (PWV), plasma C-reactive protein (CRP) and interleukin (IL)-6 were measured before and 10 weeks after treatment and compared between groups. All values were referred to measurements after LDL apheresis. Results: IMT and PWV, plasma CRP and IL-6 showed little change in group A throughout the experimental period. These decreased slightly from the baseline value in group B, but the change was not significant. In group C, IMT decreased from 1.12 ± 0.24 to 1.02 ± 0.18 mm (p < 0.05), and PWV decreased from 2,266 ± 380 to 1,968 ± 342 cm/s (p < 0.05). Plasma CRP and IL-6 concentrations also decreased significantly compared with baseline (p < 0.05). In group D, IMT decreased from 1.18 ± 0.26 to 0.92 ± 0.18 mm (p < 0.01), and PWV decreased from 2,284 ± 390 to 1,786 ± 284 cm/s (p < 0.01). Plasma CRP and IL-6 levels also decreased significantly compared with baseline (p < 0.01). Conclusion: These data suggest that LDL apheresis and the vitamin E-coated membrane dialysis in combination may prevent further progression of atherosclerosis in hemodialysis patients with ASO.

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          Most cited references 10

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          Validity, reproducibility, and clinical significance of noninvasive brachial-ankle pulse wave velocity measurement.

          The present study was conducted to evaluate the validity and reproducibility of noninvasive brachial-ankle pulse wave velocity (baPWV) measurements and to examine the alteration of baPWV in patients with coronary artery disease (CAD). Simultaneous recordings of baPWV by a simple, noninvasive method and aortic pulse wave velosity (PWV) using a catheter tip with pressure manometer were performed in 41 patients with CAD, vasospastic angina, or cardiomyopathy. In 32 subjects (15 controls and 17 patients with CAD), baPWV was recorded independently by two observers in a random manner. In 55 subjects (14 controls and 41 patients with CAD), baPWV was recorded twice by a single observer on different days. baPWV were compared among 172 patients with CAD (aged 62 +/- 8 years); 655 age-matched patients without CAD but with hypertension, diabetes mellitus, or dyslipidemia; and 595 age-matched healthy subjects without these risk factors. baPWV correlated well with aortic PWV (r=0.87, p<0.01). Pearson's correlation coefficients of interobserver and intraobserver reproducibility were r=0.98 and r=0.87, respectively. The corresponding coefficients of variation were 8.4% and 10.0%. baPWV were significantly higher in CAD patients than in non-CAD patients with risk factors, for both genders (p<0.01). In addition, baPWV were higher in non-CAD patients with risk factors than in healthy subjects without risk factors. Thus, the validity and reproducibility of baPWV measurements are considerably high, and this method seems to be an acceptable marker reflecting vascular damages. baPWV measured by this simple, noninvasive method is suitable for screening vascular damages in a large population.
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            Iron therapy, advanced oxidation protein products, and carotid artery intima-media thickness in end-stage renal disease.

            Increased common carotid artery intima-media thickness (CCA-IMT) is a marker of early atherosclerosis. Low-grade inflammation is associated with the pathogenesis of atherosclerosis. Low-grade inflammation and increased CCA-IMT are observed in end-stage renal disease (ESRD). Oxidative stress is involved in uremia-related inflammation. Advanced oxidation protein products (AOPP) are markers of oxidant-mediated protein damage in ESRD. Intravenous iron given to patients on hemodialysis (HD) might induce oxidative stress. We investigated the relationships between AOPP, iron therapy, and CCA-IMT in stable HD patients. Plasma AOPP and blood chemistry, including iron status, were analyzed in a cohort of 79 ESRD patients on HD. Measurements of CCA-IMT and CCA diameter, as assessed by B-mode ultrasonography, were obtained in 60 patients. AOPP levels were elevated in ESRD patients, and in univariate (r=0.42, P<0.0001) and multivariate analyses (r=0.38, P<0.001), they correlated with serum ferritin and with the intravenous iron dose received during the 12 months preceding the study (ferritin, P<0001; AOPP, P<0.01). Univariate and multivariate analyses identified the AOPP concentration as being significantly associated with CCA-IMT (P=0.0197) and CCA wall-to-lumen ratio (r=0.560, P<0.0001). Independently of AOPP concentration, cumulative iron dose was positively related to CCA-IMT (P=0.015) in patients <60 years. In ESRD patients, CCA-IMT and CCA wall-to-lumen ratio were associated with plasma AOPP, serum ferritin, and the annual intravenous iron dose administered. These findings support the concept of a role of oxidative stress in the early atherosclerosis of ESRD patients, which may be increased by the usually recommended doses of intravenous iron.
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              Advanced atherosclerosis in predialysis patients with chronic renal failure.

              Atherosclerosis is advanced in hemodialysis patients as shown by increased intima-media thickness of carotid arteries (CA-IMT), although it is not established whether the advanced atherosclerosis results from hemodialysis treatment or from chronic renal failure. The purpose of this study was to evaluate the effects of hemodialysis and renal failure on CA-IMT in patients with chronic renal failure. CA-IMT was measured by high-resolution B-mode ultrasonography in 110 patients with chronic renal failure before starting dialysis (CRF group), and compared with CA-IMT of 345 hemodialysis patients (HD group) and 302 healthy control subjects. They were all nondiabetic and the three groups were comparable in age and gender. As compared with the healthy control subjects, the CRF and HD groups had greater CA-IMTs, whereas CA-IMTs of the CRF and HD groups were not statistically different. There was no significant correlation between duration of hemodialysis and CA-IMT in the HD group. Multiple regression analysis in the total subjects indicated that presence of renal failure, but not being treated with hemodialysis, was a significant factor associated with increased CA-IMT independent of age, gender, blood pressure, smoking, high-density lipoprotein (HDL) and non-HDL cholesterol levels. These results demonstrate that thickening of arterial wall is present in patients with chronic renal failure before starting hemodialysis treatment, and support the concept that advanced atherosclerosis in hemodialysis patients is due not to hemodialysis treatment, but to renal failure and/or metabolic abnormalities secondary to renal failure.
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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
                2003
                2003
                29 July 2003
                : 26
                : 3
                : 185-191
                Affiliations
                aDepartment of Medicine, Shinmatsudo Central General Hospital, Chiba; bDepartment of Medicine, Mizue Dialysis Center, Tokyo, and cDepartment of Medicine, Koto Hospital, Tokyo, Japan
                Article
                71884 Kidney Blood Press Res 2003;26:185–191
                10.1159/000071884
                12886046
                © 2003 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
                Tables: 6, References: 21, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/71884
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