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      Pulmonary Hypertension in Chronic Renal Failure Patients

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          Abstract

          Pulmonary hypertension (PHT) has been reported to be high among end-stage renal disease (ESRD) patients. This study evaluated PHT in ESRD patients and the role of arteriovenous fistula (AVF), thromboxane B(2) (TXB(2)) and pro-BNP in this complication. 45 ESRD patients on regular hemodialysis (HD) (group 1) and 31 ESRD patients on conservative treatment (group 2) underwent clinical and biochemical testing. Pulmonary artery pressure (PAP) was evaluated using Doppler echocardiography. Cardiac assessment by echocardiography and AVF flow measurement by Doppler ultrasound were done. Levels of TXB(2) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in plasma were determined. PHT was found in 44.4% in group 1 and in 32.3% in group 2. Comparing the two groups shows a significant difference with regard to PAP, proBNP, and TXB(2). Patients with PHT have a significantly higher AVF blood flow, proBNP, and TXB(2). In patients with PHT, 76.7% have left ventricular diastolic dysfunction (LVDD). PAP correlates with AVF flow, proBNP, and TXB(2). Results show a high prevalence of PHT among patients with ESRD on chronic HD or on conservative treatment. PHT in such patients is related to AVF flow, TXB(2) and NT-proBNP level and LVDD. AVF flow is an important correctable cause of PHT. Copyright 2008 S. Karger AG, Basel.

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          Diagnosis and differential assessment of pulmonary arterial hypertension.

          Pulmonary arterial hypertension (PAH) is diagnosed by various investigations that are essential for making the diagnosis, and by additional tests to clarify the category of pulmonary hypertension (PH). A diagnostic algorithm can guide the evaluation of PH, but like all guidelines the algorithm can be modified according to specific clinical circumstances. Most patients are diagnosed as the result of an evaluation of symptoms, whereas others are diagnosed during screening of asymptomatic populations at risk. Right heart catheterization (RHC) must be performed in patients with suspected PH to establish the diagnosis and document pulmonary hemodynamics. Before initiation of medical therapy, assessment of acute vasoreactivity (during catheterization) is necessary to determine the appropriate therapy for an individual patient. An acute response is generally defined as a decrease in mean pulmonary arterial pressure of at least 10 mm Hg with the mean pulmonary arterial pressure decreasing to 40 mm Hg or below, accompanied by a normal or high cardiac output. After PAH is diagnosed, disease severity should be assessed in order to accurately determine risk:benefit profiles for various therapeutic options. Useful tools to predict outcome include functional class, exercise capacity, pulmonary hemodynamics, acute vasoreactivity, right ventricular function, as well as brain natriuretic peptide, endothelin-1, uric acid, and troponin levels. Repeating these tests serially on treatment is useful for monitoring the response to a given therapy. Close follow-up at a center specializing in management of PH is recommended, with careful periodic reassessment and adjustment of therapy.
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            Pulmonary hypertension in patients with end-stage renal disease.

            The aims of this study were to evaluate the incidence of unexplained pulmonary hypertension (PH) among patients with end-stage renal disease (ESRD) and to suggest possible etiologic factors. The incidence of PH was prospectively estimated by Doppler echocardiography in 58 patients with ESRD receiving long-term hemodialysis via arteriovenous access, and in control groups of 5 patients receiving peritoneal dialysis (PD) and 12 predialysis patients without a known other cause to suggest the presence of PH. Clinical variables were compared between patients with and without PH receiving hemodialysis. Changes in pulmonary artery pressure (PAP) values before and after onset of hemodialysis via arteriovenous access, arteriovenous access compression, and successful kidney transplantation were recorded. PH > 35 mm Hg was found in 39.7% of patients receiving hemodialysis (mean +/- SD, 44 +/- 7 mm Hg; range, 37 to 65 mm Hg), in none of the patients receiving PD, and in 1 of 12 predialysis patients. Patients with PH receiving hemodialysis had a significantly higher cardiac output (6.9 L/min vs 5.5 L/min, p = 0.017). PH developed in four of six patients with normal PAP after onset of hemodialysis therapy via arteriovenous access. One-minute arteriovenous access compression in four patients decreased the mean systolic PAP from 52 +/- 7 to 41 +/- 4 mm Hg (p = 0.024). PH normalized in four of five patients receiving hemodialysis following kidney transplantation. Kaplan-Meier survival analysis according to PAP values revealed significant survival differences (p < 0.024). This study demonstrates a surprisingly high incidence of PH among patients with ESRD receiving long-term hemodialysis with surgical arteriovenous access. Both ESRD and long-term hemodialysis via arteriovenous access may be involved in the pathogenesis of PH by affecting pulmonary vascular resistance and cardiac output.
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              The relationship between the flow of arteriovenous fistula and cardiac output in haemodialysis patients.

              Satisfactory haemodialysis (HD) vascular access flow (Qa) is necessary for dialysis adequacy. High Qa is postulated to increase cardiac output (CO) and cause high-output cardiac failure. Aim of the present prospective study was to evaluate the relationship between Qa of arteriovenous fistulas (AVFs) and CO in order to have a closer insight into this scarcely explored aspect of HD pathophysiology. Ninety-six patients bearing an AVF entered the study. All were evaluated a priori for the existence of cardiac failure according to the functional classification of the American College of Cardiology/American Heart Association task force. Qa and CO were measured by means of the ultrasound dilution Transonic Hemodialysis Monitor HD02. The mean Qa of the 65 lower arm AVFs was 0.948+/-0.428 SD l/min, whereas that of the 31 upper arm AVFs was 1.58+/-0.553 l/min. The difference was statistically significant (P or= 2.0 l/min predicted the occurrence of high-output cardiac failure more accurately than two other Qa values (sensitivity 89%, specificity 100%, curve area 0.99) and three Qa/CO ratio values (cardio-pulmonary recirculation-CPR). The better performance among the latter was that of CPR values >or= 20% (sensitivity 100%, specificity 74.7%, curve area 0.92). Our prospective study shows that the relationship between Qa of AVFs and CO is complex and a third-order polynomial regression model best fits this relationship. Furthermore, it is the first study to clearly show the high predictive power for high-output cardiac failure occurrence of Qa cut-off values >or= 2.0 l/min.
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                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                S. Karger AG
                0250-8095
                1421-9670
                2008
                October 2008
                17 July 2008
                : 28
                : 6
                : 990-997
                Affiliations
                aFaculty of Medicine, Ain Shams University, and bAl Minufiyah University, Cairo, Egypt
                Article
                146076 Am J Nephrol 2008;28:990–997
                10.1159/000146076
                18635926
                91d6acc0-42ba-4469-ba56-7400b7da3e56
                © 2008 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
                : 04 April 2008
                : 10 April 2008
                Page count
                Pages: 8
                Categories
                Original Report: Patient-Oriented, Translational Research

                Cardiovascular Medicine,Nephrology
                Pulmonary hypertension,Hemodialysis complications,Thromboxane,Chronic renal failure complications,Brain natriuretic peptide

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