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      Left Ventricular Hypertrophy and Chronic Renal Insufficiency in the Elderly

      review-article
      *
      Cardiorenal Medicine
      S. Karger AG
      Renal insufficiency, Elderly, Left ventricular hypertrophy

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          Abstract

          Background: The global population is aging. Cardiovascular disease is the leading cause of death in both men and women older than 65 years. In particular, elderly patients have an increased prevalence of left ventricular hypertrophy (LVH) and chronic kidney disease (CKD), both of which predict increased cardiovascular morbidity and mortality. LVH and CKD frequently coexist in the elderly, and LVH is a powerful predictor of mortality in patients with end-stage renal disease. Key Messages: Several hemodynamic factors contribute to LVH and CKD in the elderly. Increased arterial stiffness in the elderly is associated with LVH and CKD. Studies using noninvasive measures of arterial stiffening have shown a correlation between these measures and LVH in patients with CKD. Hypertensive patients with an altered circadian blood pressure pattern such as nondippers have an increased incidence of LVH and CKD. Anemia is a risk factor for LVH in patients in all stages of CKD, and studies have shown correlations between age, anemia and LV mass. Nonhemodynamic factors include chronic inflammation, increased oxidative stress, and reduced autophagy, all of which are present in the elderly. Disordered mineral metabolism in the elderly with reduced levels of vitamin D and elevated levels of parathyroid hormone and phosphorus is associated with LVH and CKD. Conclusions: Multiple pathophysiologic mechanisms contribute to the development of LVH and CKD in the elderly. Future research should be directed at interfering with this development and reducing the burden of cardiovascular and renal diseases in this growing population. i 2014 S. Karger AG, Basel

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          Most cited references46

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          Inflammatory markers and onset of cardiovascular events: results from the Health ABC study.

          Inflammation plays an important role in cardiovascular disease. The aim of this study is to investigate the predictive value of several inflammatory markers on the incidence of cardiovascular events in well-functioning older persons. The subjects were 2225 participants 70 to 79 years old, without baseline cardiovascular disease, who were enrolled in the Health, Aging, and Body Composition study. Incident coronary heart disease (CHD), stroke, and congestive heart failure (CHF) events were detected during an average follow-up of 3.6 years. Blood levels of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-alpha) were assessed. After adjustment for potential confounders, IL-6 was significantly associated with all outcomes (CHD events, per IL-6 SD increase: RR, 1.27; 95% CI, 1.10 to 1.48; stroke events, per IL-6 SD increase: RR, 1.45; 95% CI, 1.12 to 1.86; CHF events, per IL-6 SD increase: RR, 1.72; 95% CI, 1.40 to 2.12). TNF-alpha showed significant associations with CHD (per TNF-alpha SD increase: RR, 1.22; 95% CI, 1.04 to 1.43) and CHF (per TNF-alpha SD increase: RR, 1.59; 95% CI, 1.30 to 1.95) events. CRP was significantly associated with CHF events (per CRP SD increase: RR, 1.48; 95% CI, 1.23 to 1.78). A composite summary indicator of inflammation showed a strong association with incident cardiovascular events, with an especially high risk if all 3 inflammatory markers were in the highest tertile. Findings suggest that inflammatory markers are independent predictors of cardiovascular events in older persons.
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            Fibroblast growth factor-23 and death, heart failure, and cardiovascular events in community-living individuals: CHS (Cardiovascular Health Study).

            This study sought to determine the association of fibroblast growth factor (FGF)-23 with death, heart failure (HF), and cardiovascular disease (CVD) in the general population, as well as the influence of chronic kidney disease (CKD) in this setting. FGF-23 increases renal phosphorus excretion and inhibits vitamin D activation. In end-stage renal disease, high FGF-23 levels are associated with mortality. The association of FGF-23 with death, HF, and CVD in the general population, and the influence of CKD in this setting, are unknown. Plasma FGF-23 was measured in 3,107 community-living persons ≥ 65 years of age in 1996 and 1997, and participants were followed through 2008. HF and CVD events were adjudicated by a panel of experts. Associations of FGF-23 with each outcome were evaluated using Cox proportional hazards models, and we tested whether associations differed by CKD status. Both lower estimated glomerular filtration rate and higher urine albumin to creatinine ratios were associated with high FGF-23 at baseline. During 10.5 years (median) follow-up, there were 1,730 deaths, 697 incident HF events, and 797 incident CVD events. Although high FGF-23 concentrations were associated with each outcome in combined analyses, the associations were consistently stronger for those with CKD (p interactions all <0.006). In the CKD group (n = 1,128), the highest FGF-23 quartile had adjusted hazards ratios (HR) of 1.87 (95% confidence interval [CI]: 1.47 to 2.38) for all-cause death, 1.94 (95% CI: 1.32 to 2.83) for incident HF, and 1.49 (95% CI: 1.02 to 2.18) for incident CVD events compared with the lowest quartile. Corresponding HRs in those without CKD (n = 1,979) were 1.29 (95% CI: 1.05 to 1.59), 1.37 (95% CI: 0.99 to 1.89), and 1.07 (95% CI: 0.79 to 1.45). FGF-23, a hormone involved in phosphorous and vitamin D homeostasis, is independently associated with all-cause death and incident HF in community-living older persons. These associations appear stronger in persons with CKD. Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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              Cardiac hypertrophy in vitamin D receptor knockout mice: role of the systemic and cardiac renin-angiotensin systems.

              Our recent studies suggest that 1,25-dihydroxyvitamin D3 functions as an endocrine suppressor of renin biosynthesis. Genetic disruption of the vitamin D receptor (VDR) results in overstimulation of the renin-angiotensin system (RAS), leading to high blood pressure and cardiac hypertrophy. Consistent with the higher heart-to-body weight ratio, the size of left ventricular cardiomyocytes in VDR knockout (KO) mice was markedly increased compared with wild-type (WT) mice. As expected, levels of atrial natriuretic peptide (ANP) mRNA and circulating ANP were also increased in VDRKO mice. Treatment of VDRKO mice with captopril reduced cardiac hypertrophy and normalized ANP expression. To investigate the role of the cardiac RAS in the development of cardiac hypertrophy, the expression of renin, angiotensinogen, and AT-1a receptor in the heart was examined by real-time RT-PCR and immunostaining. In VDRKO mice, the cardiac renin mRNA level was significantly increased, and this increase was further amplified by captopril treatment. Consistently, intense immunostaining was detected in the left ventricle of captopril-treated WT and VDRKO mice by use of an anti-renin antibody. Levels of cardiac angiotensinogen and AT-1a receptor mRNAs were unchanged in the mutant mice. These data suggest that the cardiac hypertrophy seen in VDRKO mice is a consequence of activation of both the systemic and cardiac RAS and support the notion that 1,25-dihydroxyvitamin D(3) regulates cardiac functions, at least in part, through the RAS.
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                Author and article information

                Journal
                CRM
                Cardiorenal Med
                10.1159/issn.1664-5502
                Cardiorenal Medicine
                S. Karger AG
                1664-3828
                1664-5502
                2014
                December 2014
                17 September 2014
                : 4
                : 3-4
                : 168-175
                Affiliations
                Coronary Care Unit, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
                Author notes
                *David Leibowitz, MD, Coronary Care Unit, Hadassah-Hebrew University Medical Center, Mount-Scopus, Jerusalem 91240 (Israel), E-Mail oleibo@hadassah.org.il
                Article
                366455 PMC4299265 Cardiorenal Med 2014;4:168-175
                10.1159/000366455
                PMC4299265
                25737681
                d4950963-2626-4d8d-9447-33bfcbea782a
                © 2014 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.

                History
                : 26 May 2014
                : 30 July 2014
                Page count
                Pages: 8
                Categories
                Review

                Cardiovascular Medicine,Nephrology
                Renal insufficiency,Elderly,Left ventricular hypertrophy
                Cardiovascular Medicine, Nephrology
                Renal insufficiency, Elderly, Left ventricular hypertrophy

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