+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Pulse Pressure Is an Independent Predictor of Aortic Stiffness in Patients with Mild to Moderate Chronic Kidney Disease

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Background: In patients with end-stage renal disease pulse wave velocity (PWV) has been widely assessed, but its behavior in mild to moderate chronic kidney disease (CKD) has been less investigated. We evaluated PWV in mild to moderate CKD. Methods: We studied 31 patients with grade II–IV CKD. Aortic PWV (aPWV), aortic and upper limb augmentation index, creatinine clearance, C-reactive protein, serum fibrinogen, interleukin-1, interleukin-6, tumor necrosis factor, albumin, total and high-density lipoprotein cholesterol and blood pressure were evaluated. Results: aPWV (7.95 ± 0.64 m/s), but not augmentation index was significantly higher (p = 0.03) in CKD patients than age-matched healthy subjects (aPWV: 6.24 ± 0.43 m/s; upper limb: 32.8 ± 1.9; aortic: 27.7 ± 1.9). At univariate regression analysis, aPWV was significantly correlated with age (r = 0.44; p = 0.013), interleukin-6 (r = 0.43; p = 0.027), pulse (r = 0.39; p = 0.029), systolic blood pressure (r = 0.37; p = 0.038) and tumor necrosis factor (r = 0.39; p = 0.029). At multivariate analysis, pulse pressure was the only significant independent determinant (β = 0.37; p = 0.05) of aPWV. Conclusion: The results of this study confirm an aPWV increase in mild to moderate CKD and emphasize association between pulse pressure and PWV, independently of renal failure.

          Related collections

          Most cited references 27

          • Record: found
          • Abstract: not found
          • Article: not found

          Accelerated atherosclerosis in prolonged maintenance hemodialysis.

            • Record: found
            • Abstract: found
            • Article: not found

            Arterial stiffening and vascular calcifications in end-stage renal disease.

            Epidemiological studies have identified aortic stiffness as an independent predictor of cardiovascular mortality in end-stage renal disease (ESRD) patients. In these patients, aortic pulse wave velocity (PWV) was associated with mediacalcosis, but the influence of arterial calcifications on the viscoelastic properties of large arteries was not well characterized. The purpose of the present study was to analyse the influence of arterial calcifications on arterial stiffness in stable haemodialysed patients. We studied 120 stable ESRD patients on haemodialysis. All patients underwent B-mode ultrasonography of common carotid artery (CCA), aorta, and femoral arteries to determine CCA distensibility, the elastic incremental modulus (Einc), and the presence of vascular calcifications. All patients underwent measurement of aortic PWV and echocardiogram. The presence of calcifications was analysed semiquantitatively as a score (0 to 4) according to the number of arterial sites with calcifications. Our observations indicate that arterial and aortic stiffness is significantly influenced by the presence and extent of arterial calcifications. The extent of arterial calcifications is in part responsible for increased left ventricular afterload, and is inversely correlated with stroke volume. The influence of calcifications is independent of the role of ageing and blood pressure. Arterial calcifications density increases with age, duration of haemodialysis, the fibrinogen level, and the prescribed dose of calcium-based phosphate binders. The results of this study showed that the presence of vascular calcifications in ESRD patients was associated with increased stiffness of large capacity, elastic-type arteries, like the aorta and CCA. The extent of arterial calcifications increased with the use of calcium-based phosphate-binders.
              • Record: found
              • Abstract: found
              • Article: not found

              Renal function, neurohormonal activation, and survival in patients with chronic heart failure.

              Because renal function is affected by chronic heart failure (CHF) and it relates to both cardiovascular and hemodynamic properties, it should have additional prognostic value. We studied whether renal function is a predictor for mortality in advanced CHF, and we assessed its relative contribution compared with other established risk factors. In addition, we studied the relation between renal function and neurohormonal activation. The study population consisted of 1906 patients with CHF who were enrolled in a recent survival trial (Second Prospective Randomized study of Ibopamine on Mortality and Efficacy). In a subgroup of 372 patients, plasma neurohormones were determined. The baseline glomerular filtration rate (GFR(c)) was calculated using the Cockroft Gault equation. GFR(c) was the most powerful predictor of mortality; it was followed by New York Heart Association functional class and the use of angiotensin-converting enzyme inhibitors. Patients in the lowest quartile of GFR(c) values ( 76 mL/min). Impaired left ventricular ejection fraction (LVEF) was only modestly predictive (P=0.053). GFR(c) was inversely related with N-terminal atrial natriuretic peptide (ANP; r=-0.53) and, to a lesser extent, with ANP itself (r=-0.35; both P<0.001). Impaired renal function (GFR(c)) is a stronger predictor of mortality than impaired cardiac function (LVEF and New York Heart Association class) in advanced CHF, and it is associated with increased levels of N-terminal ANP. Moreover, impaired renal function was not related to LVEF, which suggests that factors other than reduced cardiac output are causally involved.

                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                September 2007
                06 July 2007
                : 30
                : 5
                : 283-288
                Departments of aMedicine and Systemic Diseases, and bBiomedical Sciences, University of Catania, Catania, Italy
                105264 Kidney Blood Press Res 2007;30:283–288
                © 2007 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: 1, Tables: 3, References: 48, Pages: 6
                Original Paper


                Comment on this article