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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      Serum Oxidized LDL Is Inversely Associated with HDL2-Cholesterol Subclass in Renal Failure Patients on Hemodialysis

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          Abstract

          Background:Dyslipoproteinemia and oxidative modification of LDL (oxLDL) are common symptoms in patients suffering from chronic renal failure on hemodialysis (HD), and contribute to the development of oxidative stress. High-density lipoprotein cholesterol (HDL-C) protects against atherosclerosis by inhibiting the oxidation of lipoproteins and by supporting reverse cholesterol transport. This study intends to examine the association of oxLDL with HDL2 and HDL3 subclasses of HDL-C in HD patients, in order to elucidate whether oxidative stress influences HDL-C composition. Methods: Thirty-four patients on HD and 21 age- and sex-matched controls were studied. HDL2 and HDL3-C subclasses were isolated from serum according to a single-step precipitation method following a homogenous HDL-C assay. oxLDL was measured by ELISA. Results: In HD patients, oxLDL concentration was higher compared to the controls (1.40 ± 0.47 vs. 0.21 ± 0.05 mg/l, p = 0.017) and was significantly associated to total cholesterol (r = 0.480, p = 0.044), LDL-C (r = 0.544, p = 0.019), HDL-C (r = –0.589, p = 0.027) and C-reactive protein (r = 0.578, p = 0.024). Comparing HDL-C subclasses, only HDL2-C was negatively correlated to oxLDL levels (r = –0.565, p = 0.035). Conclusions: In HD patients, high serum levels of oxLDL are associated with low HDL2-C subclass levels. This might suggest that oxidative stress affects the HDL subclass more related to the protecting activity of HDL-C, contributing to atherosclerosis development.

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          The elephant in uremia: oxidant stress as a unifying concept of cardiovascular disease in uremia.

          Jonathan Himmelfarb, Peter Stenvinkel, T Alp Ikizler … (2002)
          Cardiovascular disease is the leading cause of mortality in uremic patients. In large cross-sectional studies of dialysis patients, traditional cardiovascular risk factors such as hypertension and hypercholesterolemia have been found to have low predictive power, while markers of inflammation and malnutrition are highly correlated with cardiovascular mortality. However, the pathophysiology of the disease process that links uremia, inflammation, and malnutrition with increased cardiovascular complications is not well understood. We hereby propose the hypothesis that increased oxidative stress and its sequalae is a major contributor to increased atherosclerosis and cardiovascular morbidity and mortality found in uremia. This hypothesis is based on studies that conclusively demonstrate an increased oxidative burden in uremic patients, before and particularly after renal replacement therapies, as evidenced by higher concentrations of multiple biomarkers of oxidative stress. This hypothesis also provides a framework to explain the link that activated phagocytes provide between oxidative stress and inflammation (from infectious and non-infections causes) and the synergistic role that malnutrition (as reflected by low concentrations of albumin and/or antioxidants) contributes to the increased burden of cardiovascular disease in uremia. We further propose that retained uremic solutes such as beta-2 microglobulin, advanced glycosylated end products (AGE), cysteine, and homocysteine, which are substrates for oxidative injury, further contribute to the pro-atherogenic milieu of uremia. Dialytic therapy, which acts to reduce the concentration of oxidized substrates, improves the redox balance. However, processes related to dialytic therapy, such as the prolonged use of catheters for vascular access and the use of bioincompatible dialysis membranes, can contribute to a pro-inflammatory and pro-oxidative state and thus to a pro-atherogenic state. Anti-oxidative therapeutic strategies for patients with uremia are in their very early stages; nonetheless, early studies demonstrate the potential for significant efficacy in reducing cardiovascular complications.
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            Monocyte recruitment and foam cell formation in atherosclerosis.

            A Bobryshev (2005)
            Atherosclerosis is a chronic immune-inflammatory disease in which the interactions of monocytes with activated endothelium are crucial events leading to atherosclerotic alteration of the arterial intima. In early atherosclerosis, monocytes migrate into the subendothelial layer of the intima where they differentiate into macrophages or dendritic cells. In the subendothelial space enriched with atherogenic lipoproteins, most macrophages transform into foam cells. Foam cells aggregate to form the atheromatous core and as this process progresses, the atheromatous centres of plaques become necrotic, consisting of lipids, cholesterol crystals and cell debris. This review highlights some aspects of monocyte recruitment and foam cell formation in atherosclerosis.
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              Endothelial dysfunction in chronic renal failure: roles of lipoprotein oxidation and pro-inflammatory cytokines.

              C Bolton, L. G. Downs, J G Victory … (2001)
              Chronic renal failure (CRF) is associated with an increased risk of ischaemic heart disease (IHD), but the mechanisms responsible are controversial. We investigated the relationship of two sets of candidate mechanisms-indices of LDL oxidation and markers of inflammatory activity-with vascular endothelial dysfunction (VED). We carried out cross-sectional analysis of 23 dialysed and 16 non-dialysed CRF patients, 28 healthy controls, and 20 patients with stable angina and normal renal function. The following were determined: (i) LDL oxidation by Cu(2+) and ultraviolet light, serum autoantibodies to oxidized LDL (oxLDL); (ii) forearm flow-mediated vasodilatation, plasma concentrations of adhesion molecules, and von Willebrand factor (vWF); and (iii) circulating levels of TNF-alpha and IL-6, C-reactive protein (CRP), and fibrinogen. Endothelium-dependent vasodilatation (EDV) was lower in angina, pre-dialysis, and dialysis CRF patients than in controls (all P<0.005). Compared with controls, vWf (P<0.005) and adhesion molecules (vCAM-1, P<0.005; iCAM-1, P=0.01; E-selectin, P=0.05) were raised in dialysis, and vCAM-1 (P=0.01) in pre-dialysis CRF patients. Dialysed patients had lower HDL cholesterol (P=0.01) and higher triglyceride (P=0.05) than controls, but LDL-oxidation was similar in all groups. Autoantibodies to oxLDL were raised in angina (P<0.005) and pre-dialysis (P=0.006), but were absent in most dialysed patients. Concentrations of IL-6, TNF-alpha, CRP and fibrinogen were elevated in CRF compared with control and angina patients (P<0.005). In the whole population, IL-6 and TNF-alpha correlated negatively with EDV, HDL cholesterol, and positively with triglyceride, blood pressure, vWf, iCAM-1, vCAM-1 and E-selectin (r=-0.43 to +0.70, all P<0.05). Endothelial dysfunction is unrelated to LDL oxidation, suggesting that LDL oxidation might not be a major cause of VED in CRF. In contrast VED was more severe in CRF than in angina patients and is associated with increased acute-phase proteins and plasma cytokines, demonstrating a chronic inflammatory state. These observations may explain the VED and increased IHD risk of patients with CRF.
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                Author and article information

                Journal
                Journal ID (publisher-id): NEC
                Journal ID (nlm-ta): Nephron Clin Pract
                Journal ID (doi): 10.1159/issn.1660-2110
                Title: Nephron Clinical Practice
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2110
                Publication date Subscription-year: 2010
                Publication date (Print): July 2010
                Publication date (Electronic): 28 April 2010
                Volume: 115
                Issue: 4
                Pages: c289-c294
                Affiliations
                aDepartment of Biochemistry, and bRenal Unit, Alexandra Hospital, and cRenal Unit, Aretaeio Hospital, Athens, Greece
                Article
                Publisher ID: 313488 Other ID: Nephron Clin Pract 2010;115:c289–c294
                DOI: 10.1159/000313488
                PubMed ID: 20424480
                SO-VID: b375e8f3-4adb-4551-bcd4-4dd6fc067252
                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.

                History
                Date received : 25 October 2009
                Date accepted : 10 January 2010
                Page count
                Figures: 1, Tables: 4, References: 39, Pages: 1
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Hemodialysis,Oxidized LDL,C-reactive protein,HDL-C subclasses
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Hemodialysis, Oxidized LDL, C-reactive protein, HDL-C subclasses

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