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      Role of Sodium and Volume in the Pathogenesis of Hypertension in Dialysis Patients

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          Abstract

          Volume and sodium excess is the predominant factor in the pathogenesis of hypertension in dialysis patients. However, except for anephric patients, the relationship between volume status, blood pressure, and hemodynamics is not straightforward, but may vary between subgroups of patients. In general, the sensitivity of blood pressure to changes in the volume/sodium status appears to be increased in patients with end-stage renal disease. The blood pressure response to changes in the sodium/volume status may be influenced by disturbances in the activity of and response to various neurohumoral mechanisms, such as the renin-angiotensin and sympathetic nervous systems, Na-K-ATP-ase inhibitors, and the nitric oxide system. Regarding these aspects, there might be a parallel with salt-sensitive (essential) hypertension. Preliminary data showed a beneficial effect of sodium removal beyond changes in the volume status. Also of interest is the fact that prolonging dialysis time may improve blood pressure control without clear changes in the fluid status. It is hypothesized that a reduction in exchangeable sodium, by increased diffusive transport of sodium, in combination with increased removal of vasopressor substances, might be partly responsible for the observed blood pressure changes during long dialysis times. In conclusion, sodium and volume overload and neurohumoral factors coincide in the pathogenesis of hypertension in dialysis patients. Nevertheless, their exact relationship has not yet been elucidated and deserves further study.

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          Most cited references 10

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          Oxidative stress in Dahl salt-sensitive hypertension.

          The role of oxidative stress in the long-term regulation of arterial pressure, renal hemodynamics, and renal damage was studied in Dahl salt-sensitive rats. Twenty-eight Dahl S/Rapp strain rats, equipped with indwelling arterial and venous catheters, were subjected to a 3-week intravenous infusion of either low Na (0.9 mmol/d) or high Na (20.6 mmol/d) or the superoxide dismutase mimetic, 4-hydroxyl-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol), at 125 micromol x kg(-1) x h(-1) plus low Na or high Na. After 21 days, mean arterial pressure was 140+/-3 mm Hg in the high-Na group, 118+/-1 mm Hg (P<0.05) in the high-Na/Tempol group, and unchanged in the low-Na/Tempol and low-Na groups. Tempol did not change renal blood flow, glomerular filtration rate, or glomerular cross-sectional area in rats subjected to the high-Na intake but did decrease urinary protein excretion, the percentage of sclerotic glomeruli, and the kidney weight to body weight ratio. In 15 additional Dahl S rats subjected to high or low Na intake for 3 weeks, renal cortical and medullary O2*- release increased significantly in the high-Na group when compared with the low-Na group. Tempol decreased both renal cortical and medullary O2*- release in the high- and low-Na rats, but the decrease in O2*- release was greater in high-Na rats. The data suggest that oxidative stress contributes to Dahl salt-sensitive hypertension and the accompanying renal damage.
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            Adjusting Dry Weight by Extracellular Volume and Body Composition in Hemodialysis Patients

            Background: At present, the determination of dry weight in patients on hemodialysis is largely made empirically by trial and error. Extracellular volume (ECV) assessment by bioimpedance analysis (BIA) is a preferable technique for determining dry weight, and it also provides useful data on body composition. Methods: We measured the ECV of 74 normal subjects and 121 stable chronic hemodialysis patients postdialysis. In addition, for the dialysis patients, we measured intracellular volume (ICV) and lean body mass (LBM) by BIA, and analyzed the ECV, blood pressure and complications of dialysis. We adjusted dry weight according to the ECV and repeated a BIA exam 4 months later to evaluate changes in body composition, blood pressure and dialysis status of these patients. Results: The ECV as a percentage of weight (ECV%) of hypertensive patients was significantly higher than that of normotensive patients (24.29 ± 3.56% vs. 21.50 ± 2.38%, p < 0.001). All patients with excessive ECV% had hypertension, but not all hypertensive patients had excessive ECV%. None of the normotensive patients had ECV excess. Some hypertensive patients with symptoms of dialysis complications still had excessive ECV%. Eight hypertensive patients with excessive ECV had decreased dry weight. ECV% (29.80 ± 2.03% vs. 27.10 ± 2.99%, p < 0.001) and blood pressure (159 ± 7 / 97 ± 4 vs. 137 ± 10 / 86 ± 8 mm Hg, p = 0.006 for systolic and p = 0.004 for diastolic) decreased. ECV was the only portion of body composition that decreased (p < 0.001) after decreasing dry weight, the other parameters remaining unchanged. Twenty symptomatic normotensive patients improved with elevation of the dry weight. The ECV (p = 0.007), ICV (p = 0.009) and LBM (p < 0.001) were significantly increased after increasing dry weight, while the ECV% (p = 0.39) and fat (p = 0.46) remained unchanged. Conclusions: (1) For hypertensive patients, ECV must be evaluated in order to adjust dry weight and correct hypertension. (2) For normotensive patients, if dialysis complications occur, dry weight should be increased until symptoms disappear or the blood pressure begins to rise.
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              Salt and Hypertension in End-Stage Renal Disease

              Salt and fluid overload play an important role in the pathogenesis of hypertension in patients with end-stage renal disease. However, in the individual patient, the relation between salt loading and blood pressure response is variable and appears to be influenced by various neurohumoral regulatory mechanisms. This may also have implications for the pathogenesis of structural cardiovascular abnormalities in patients with end-stage renal disease.
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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                978-3-8055-7683-3
                978-3-318-01049-7
                0253-5068
                1421-9735
                2004
                July 2004
                20 January 2004
                : 22
                : 1
                : 55-59
                Affiliations
                Department of Internal Medicine, University Hospital of Maastricht, Maastricht, The Netherlands
                Article
                74924 Blood Purif 2004;22:55–59
                10.1159/000074924
                14732812
                © 2004 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
                References: 47, Pages: 5
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/74924
                Categories
                Paper

                Cardiovascular Medicine, Nephrology

                Volume overload, Dialysis time, Hypertension, Sodium, Sensitivity, salt

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