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      Reduction in Platelet Activation by Citrate Anticoagulation Does Not Prevent Intradialytic Hemodynamic Instability

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          Abstract

          Background: The etiology of intradialytic hemodynamic instability is multifactorial. Of the various factors involved, a rise in core temperature seems to be crucial. In this respect, the bioincompatibility of hemodialysis (HD) treatment might play an important role. The application of cool dialysate reduces the number of periods of intradialytic hypotension (IDH) considerably. In rats, roller pump perfusion caused hypotension by shear stress induced platelet aggregation and subsequent serotonin release. During clinical HD, citrate anticoagulation abolished platelet activation almost completely. Hence, citrate anticoagulation might reduce IDH, whereas the beneficial effect of cool dialysate might be partly explained by reduced platelet activation. Methods: In the present study, blood pressure, IDH episodes, platelet activation, platelet aggregation, and serotonin release were studied crossover in 10 patients during HD with dalteparin anticoagulation at normal and low dialysate temperatures and during HD with citrate. Results: Citrate strongly reduced platelet activation, but did not improve IDH. The blood pressure was best preserved during cool-temperature HD, despite manifest platelet activation. Platelet activation was not accompanied by a rise in the plasma serotonin concentration. Conclusions: Three major conclusions can be drawn: (1) it is unlikely that platelet activation and subsequent serotonin release underlie IDH in the clinical situation; (2) the protective effects of cool dialysate on IDH appear to be independent of HD-induced platelet activation, and (3) extrapolating results from rat experiments to the human situation requires uppermost prudence.

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          Hemodialysis-associated hypotension as an independent risk factor for two-year mortality in hemodialysis patients.

          Tatsuya Shoji, M Fujii, Yoshiharu Tsubakihara … (2004)
          The relationship between blood pressure (BP) and mortality in hemodialysis patients has remained controversial. Some studies suggested that a lower pre- or postdialysis BP was associated with excess mortality, while others showed poorer outcome in patients with uncontrolled hypertension. We conducted a multicenter prospective cohort study to evaluate the impact of hemodialysis-associated hypotension on mortality. We recruited 1244 patients (685 males; mean age, 60 +/- 13 years) who underwent hemodialysis in 28 units during the two-year study period beginning in December 1999. Pre-, intra-, and postdialysis BP, and BP upon standing soon after hemodialysis, were measured in all patients at entry. Logistic regression analysis was used to assess the effect on mortality of pre-, intra-, and postdialysis BP, a fall in BP during hemodialysis, and a fall in BP upon standing soon after hemodialysis. During the study period, 149 patients died. Logistic models identified the lowest intradialysis systolic blood pressure (SBP) and degree of fall in SBP upon standing soon after hemodialysis as significant factors affecting mortality, but not pre- or postdialysis SBP and diastolic BP. The adjusted odds ratio for death was 0.79 (95% CI 0.64-0.98) when the lowest intradialysis SBP was analyzed in increments of 20 mm Hg, and was 0.82 (95% CI 0.67-0.98) when the fall in SBP upon standing soon after hemodialysis was analyzed in increments of 10 mm Hg. These results suggest that intradialysis hypotension and orthostatic hypotension after hemodialysis are significant and independent factors affecting mortality in hemodialysis patients.
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            Pathophysiology of dialysis hypotension: an update.

            J Daugirdas (2001)
            Dialysis hypotension occurs because a large volume of blood water and solutes are removed over a short period of time, overwhelming normal compensatory mechanisms, including plasma refilling and reduction of venous capacity, due to reduction of pressure transmission to veins. In some patients, seemingly paradoxical and inappropriate reduction of sympathetic tone may occur, causing reduction of arteriolar resistance, increased transmission of pressure to veins, and corresponding increase in venous capacity. Increased sequestration of blood in veins under conditions of hypovolemia reduces cardiac filling, cardiac output, and, ultimately, blood pressure. Adenosine release due to tissue ischemia may participate in reducing norepinephrine release locally, and activation of the Bezold-Jarisch reflex, perhaps in patients with certain but as yet undefined cardiac pathology, may be responsible for sudden dialysis hypotension. Patients with diastolic dysfunction may be more sensitive to the effects of reduced cardiac filling. The ultimate solution is reducing the ultrafiltration rate by use of longer dialysis sessions, more frequent dialysis, or reduction in salt intake. Increasing dialysis solution sodium chloride levels helps maintain blood volume and refilling but ultimately increases thirst and interdialytic weight gain, with a possible adverse effect on hypertension. Blood volume monitoring with ultrafiltration or dialysis solution sodium feedback loops are promising new strategies. Maintaining tissue oxygenation via an adequate blood hemoglobin level seems to be important. Use of adenosine antagonists remains experimental. Given the importance of sympathetic withdrawal, the use of pharmacologic sympathetic agonists is theoretically an attractive therapeutic strategy.
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              Blood volume controlled hemodialysis in hypotension-prone patients: a randomized, multicenter controlled trial.

              Giuliano Colasanti, Roberto Bolzani, Fabio Chiodo Grandi … (2002)
              Recently we have devised and tested a biofeedback system for controlling blood volume (BV) changes during hemodialysis (HD) along an ideal trajectory (blood volume tracking, BVT), continuously modifying the weight loss rate and dialysate conductivity. This multicenter, prospective, randomized, crossover study aimed to clarify whether BVT (treatment B) can improve hypotension-prone patients' treatment tolerance, compared with conventional hemodialysis (treatment A). Thirty-six hypotension-prone patients enrolled from 10 hemodialysis (HD) centers were randomly assigned to either of the study sequences ABAB or BABA, each lasting four months. A 30% reduction in intradialytic hypotension (IDH) events was observed in treatment B as compared with A (23.5% vs. 33.5%, P = 0.004). The reduction was related to the number of IDH in treatment A (y = 0.54x + 5; r = 0.4; P < 0.001): the more IDH episodes in treatment A, the better the response in treatment B. The best responders to treatment B showed pre-dialysis systolic blood pressure values higher than the poor responders (P = 0.04). A 10% overall reduction in inter-dialysis symptoms was obtained also in treatment B compared to A (P < 0.001). Body weight gain, pre-dialysis blood pressure, intradialytic weight loss as well as Kt/V did not differ between the two treatments. An overall improvement in the treatment tolerance was observed with BVT, particularly intradialytic cardiovascular stability. Patients with the highest incidence of IDH during conventional HD and free from chronic pre-dialysis hypotension seem to respond better. Inter-dialysis symptoms also seem to improve with control of BV.
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                Author and article information

                Journal
                Journal ID (publisher-id): NEC
                Journal ID (nlm-ta): Nephron Clin Pract
                Journal ID (doi): 10.1159/issn.1660-2110
                Title: Nephron Clinical Practice
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2110
                Publication date Subscription-year: 2007
                Publication date (Print): May 2007
                Publication date (Electronic): 07 March 2007
                Volume: 106
                Issue: 1
                Pages: c9-c16
                Affiliations
                Departments of aNephrology and bClinical Chemistry, Medical Center Alkmaar, Alkmaar, cDepartment of Nephrology and dLaboratory for Physiology, VU University Medical Center, Amsterdam, The Netherlands
                Article
                Publisher ID: 100496 Other ID: Nephron Clin Pract 2007;106:c9–c16
                DOI: 10.1159/000100496
                PubMed ID: 17347579
                SO-VID: 071dc273-9782-4561-8450-770aa72e5e1a
                Copyright © © 2007 S. Karger AG, Basel
                License:

                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
                Date received : 16 May 2006
                Date accepted : 20 December 2006
                Page count
                Figures: 6, Tables: 1, References: 20, Pages: 1
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Degranulation,P-selectin,Hemodialysis,Intradialytic hypotension,Platelet activation,Bioincompatibility, hemodialysis,Anticoagulation,Citrate,Dalteparin,Platelet factor 4,Serotonin
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Degranulation, P-selectin, Hemodialysis, Intradialytic hypotension, Platelet activation, Bioincompatibility, hemodialysis, Anticoagulation, Citrate, Dalteparin, Platelet factor 4, Serotonin

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