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      Dialysis Patients and Cardiovascular Problems: Can Technology Help Solve the Complex Equation?

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          Abstract

          Patients with end-stage kidney disease undergoing chronic hemodialysis (HD) present higher mortality rates compared with the general population. Once patients are on HD, the risk of cardiovascular death is approximately 30 times higher than in the general population and remains 10–20 times higher after stratification for age, gender, and the presence of diabetes. About half the deaths of patients on dialysis are attributed to cardiovascular causes including coronary heart disease, cerebrovascular disease, peripheral vascular disease, and heart failure. The cardiovascular burden of the HD patient arises from three different sources: risks inherent to the patient and the uremic syndrome, traditional risk factors, and risk factors related to the dialysis therapy. Based on these considerations and the fact that several aspects of the dialysis procedure can either add to the cardiovascular burden or modify the existing burden, new technologies should be directed towards the approach of a potential ‘cardioprotective dialysis therapy’; such an approach may be facilitated by the application of new techniques and advanced dialysis machines. Created to make dialysis easy and safe, new machines feature several options that make patient monitoring and online hemodiafiltration therapy routine procedures. These and other features will possibly make dialysis better tolerated and more efficient in protecting patients from undesirable or potentially fatal cardiovascular events.

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          Most cited references 32

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          Cardiovascular disease and chronic renal disease: a new paradigm.

          Cardiovascular disease (CVD) is a major cause of morbidity and mortality among patients with chronic renal disease (CRD). Despite Improvement in treatment for CVD over the past 30 years, CVD mortality is approximately 15 times higher in dialysis patients than in the general population. The high prevalence of CVD among Incident dialysis patients suggests that CVD begins in earlier stages of CRD, and that implementation of risk factor reduction strategies earlier in the course of CRD may provide an opportunity to prevent CVD in CRD. Based on parallels between CVD and renal disease progression, we have proposed a paradigm that CVD and CRD are outcomes of the same underlying disorders. We propose that risk factor reduction strategies used to prevent CVD in the general population also be applied to patients with CRD, with the hope of preventing progression of renal disease, as well as preventing CVD.
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            Cardiovascular complications in chronic kidney disease.

            The risk for cardiovascular disease (CVD) morbidity and mortality remains alarmingly high in all stages of chronic kidney disease (CKD). CVD often begins before end-stage renal disease (ESRD), and patients with reduced kidney function are more likely to die of CVD than to develop ESRD. Three pathological forms of CVD should be considered in patients with CKD: alterations in cardiac geometry, including left ventricular hypertrophy, atherosclerosis, and arteriosclerosis. All are highly prevalent in patients with CKD. Although patients with CKD share many of the same risk factors for CVD as the general population, there are a number of uremia-related risk factors, such as anemia and alterations in calcium/phosphorus metabolism, that also play a role in promoting CVD. Treatment of both traditional and uremia-related risk factors should be initiated in the earlier stages of CKD. Additional clinical trials with a goal to reduce CVD are urgently needed in CKD.
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              Interleukin-6 predicts hypoalbuminemia, hypocholesterolemia, and mortality in hemodialysis patients.

              Low serum albumin and low serum cholesterol levels are among the most consistent predictors of mortality in patients with end-stage renal disease (ESRD) undergoing hemodialysis. Hypoalbuminemia is often interpreted as a marker of poor nutrition, but serum albumin and cholesterol levels can also be low as part of a cytokine-mediated acute-phase reaction to acute or chronic inflammation. Here we report the results from a 900-day prospective study designed to determine whether tumor necrosis factor-alfa (TNF-alpha) and interleukin-6 (IL-6) predict serum albumin and cholesterol levels and mortality in a group of 90 ambulatory, adult hemodialysis patients with no acute infection, hospitalization or surgery, and no known acquired immunodeficiency syndrome (AIDS), malignancy, or liver disease. Measurable levels of TNF-alpha and/or IL-6 were found in 89 of 90 patients. Significant relationships were found between TNF-alpha and IL-6 and the degree of hypoalbuminemia and dyslipoproteinemia. IL-6 was the strongest predictor of mortality in univariate and multivariate analysis, followed by age, albumin level, and body mass index (BMI). Although the cause of hypercytokinemia was not addressed in this study, the data support the view that hypoalbuminemia and hypocholesterolemia are negative acute-phase responses to inflammatory stimuli. These results suggest that efforts to identify the nature of the stimuli for cytokine production and to lower cytokine levels in hemodialysis patients might be effective in improving the survival of patients undergoing hemodialysis.
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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                978-3-8055-8052-6
                978-3-318-01301-6
                0253-5068
                1421-9735
                2006
                December 2005
                23 December 2005
                : 24
                : 1
                : 39-45
                Affiliations
                aDepartment of Nephrology, St. Bortolo Hospital, Vicenza, Italy; bFresenius Medical Care GmbH, Bad Homburg, Germany
                Article
                89435 Blood Purif 2006;24:39–45
                10.1159/000089435
                16361839
                © 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: 3, References: 61, Pages: 7
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/89435
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