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      Hypertension and Dialysis

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          Abstract

          The high mortality rate seen in dialysis patients is related to long-standing high blood pressure and the presence of other traditional as well as non-traditional risk factors for cardiovascular disease. Hypertension is associated with increased risk for left ventricular hypertrophy, coronary artery disease, congestive heart failure and cerebrovascular complications. High blood pressure is frequent and difficult to control in the dialysis population. Available therapeutic options to normalize blood pressure in these patients include dietary salt and fluid restriction in combination with reduction of dialysate sodium concentration. A possible treatment option for these patients may be long, slow hemodialysis (3 × 8 h per week); short daily hemodialysis (2–3 h 7 times per week); nocturnal hemodialysis (6–7 times overnight per week). Reduction of residual renal function is a major cause of blood pressure increase in the peritoneal dialysis patient population. Therefore, hyperhydration should be avoided. If antihypertensive medication is needed, ACE inhibitors, β-blockers and/or calcium channel blockers are recommended. Optimal blood pressure in dialysis patients is not different from recommendations for the general population.

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          Most cited references 15

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          Blood pressure and long-term mortality in United States hemodialysis patients: USRDS Waves 3 and 4 Study.

           ,  C Herzog,  Sarah Collins (2002)
          The long-term prognostic associations of pre- and post-dialysis blood pressures, interdialytic weight gain, and antihypertensive use in hemodialysis patients are unclear. The United States Renal Data System (USRDS) Dialysis Morbidity and Mortality Waves 3 and 4 Study, a randomly generated sample of 11,142 subjects receiving hemodialysis on December 31, 1993, was examined, with vital status followed until May 2000. Pre- and post-dialysis blood pressure values, interdialytic weight gain and number of antihypertensives averaged 151.8/79.7, 137.0/74, 3.6% and 0.76, respectively. Prognostic discrimination was maximized by considering pre- and post-systolic and diastolic blood pressure values simultaneously, in a pattern suggesting that wide pulse pressures were associated with mortality (P < 0.0001). Comorbidity adjustment markedly affected associations, with low pre-dialysis diastolic (P < 0.05), low post-dialysis dialysis diastolic pressure (P < 0.05), high post-dialysis dialysis systolic pressure (P < 0.05), and high interdialytic weight gains (P = 0.005) associated with mortality. Each class of antihypertensive drug, except angiotensin-converting enzyme (ACE)-inhibitors, was associated with lower mortality in unadjusted models, an effect most pronounced for beta-blockers (hazards ratio 0.72, 95% CI 0.66 to 0.79, P < 0.0001). Comorbidity adjustment eliminated survival associations for each antihypertensive class except beta-blockers. Pre- and post-dialysis blood pressure values have independent associations with mortality, in a way that implicates wide pulse pressures. Much of the adverse prognosis of wide pulse pressures probably reflects older age and cardiovascular comorbidity. Large interdialytic weight gains are associated with shorter survival when comorbidity is taken into account. Beta-blocker use shows a robust association with survival, and may be protective.
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            Nuclear factor kappa-B and the heart.

            Nuclear factor kappa-B (NFkappaB), a redox-sensitive transcription factor regulating a battery of inflammatory genes, has been indicated to play a role in the development of numerous pathological states. Activation of NFkappaB induces gene programs leading to transcription of factors that promote inflammation, such as leukocyte adhesion molecules, cytokines, and chemokines, although some few substances with possible anti-inflammatory effects are also NFkappaB regulated. The present article reviews basic regulation of NFkappaB and its activation, cell biological effects of NFkappaB activation and the role of NFkappaB in apoptosis. Evidence involving NFkappaB as a key factor in the pathophysiology of ischemia-reperfusion injury and heart failure is discussed. Although activation of NFkappaB induces pro-inflammatory genes, it has lately been indicated that the transcription factor is involved in the signaling of endogenous myocardial protection evoked by ischemic preconditioning. A possible role of NFkappaB in the development of atherosclerosis and unstable coronary syndromes is discussed. Nuclear factor kappa-B may be a new therapeutic target for myocardial protection.
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              ACE inhibitors and survival of hemodialysis patients.

              Cardiovascular disease is a leading cause of death in patients with end-stage renal disease (ESRD). Hypertension is a major risk factor for cardiovascular complications in these patients. Angiotensin-converting enzyme (ACE) inhibitors are an effective treatment for hypertension in patients with ESRD and are known to improve prognosis in patients with chronic renal failure. We investigated their effect on mortality in patients undergoing long-term hemodialysis therapy. Clinical data for patients on hemodialysis therapy between 1994 and 2000 were reviewed. Patients were grouped according to whether they had been treated with ACE inhibitors. Sixty patients had been treated with ACE inhibitors (treated group) and 66 patients had not (untreated group). Blood pressure reduction was not significantly different between the treated and untreated groups. Nevertheless, comparing the treated group with the untreated group, mortality was decreased significantly in the treated group, with a risk reduction of 52% (rate ratio [RR], 0.482; confidence interval [CI], 0.25 to 0.91; P < 0.0019). In treated patients 65 years or younger, the absolute risk reduction of mortality was 79% (RR, 0.211; CI, 0.08 to 0.58; P < 0.0006). Although further research is needed, these preliminary findings suggest that ACE inhibitors, independently of their antihypertensive effect, may dramatically reduce mortality among chronic hemodialysis patients 65 years or younger. Copyright 2002 by the National Kidney Foundation, Inc.
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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
                978-3-8055-7600-0
                978-3-318-00991-0
                1420-4096
                1423-0143
                2003
                2003
                05 June 2003
                : 26
                : 2
                : 76-81
                Affiliations
                aDiabetes Research Institute, University of Düsseldorf, Germany and bDivision of Nephrology and Dialysis, Department of Medicine III, University of Vienna, Austria
                Article
                70987 Kidney Blood Press Res 2003;26:76–81
                10.1159/000070987
                12771530
                © 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: 1, References: 77, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/70987
                Categories
                Paper

                Cardiovascular Medicine, Nephrology

                Hypertension, Dialysis, Left ventricular hypertrophy

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