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      Ultrafiltration Therapy for Cardiorenal Syndrome: Physiologic Basis and Contemporary Options

      review-article
      ,
      Blood Purification
      S. Karger AG
      Heart failure, Extracorporeal therapies, Ultrafiltration, Peritoneal dialysis

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          Abstract

          Background: Heart failure (HF) has a high readmission rate in part due to conventional and recently developed therapeutic options having suboptimal results. Extracorporeal and peritoneal ultrafiltration have been advocated as more beneficial methods for fluid removal in decompensated or refractory HF, respectively. Methods: Traditional and emerging concepts explaining the pathophysiology of HF and the cardiorenal syndrome are reviewed. Extracorporeal and peritoneal ultrafiltration clinical trials are then discussed in terms of potential physiologic benefits, feasibility and their effects on both cardiac and renal function. Results: Ultrafiltration therapy can efficiently correct volume overload in the acute setting, improve cardiac functional and quality of life parameters, and is associated with long-lasting benefits such as reduced HF-related readmissions. Although excessive fluid removal can adversely affect the kidneys, there is evidence that careful protocols can restore diuretic sensitivity and maintain stable renal function; crafting safe parameters has yet to be studied. Conclusion: While extracorporeal ultrafiltration is an appealing therapeutic option for patients with acute decompensated HF, determining the optimal fluid removal rate and the impact on renal function need further investigation. Peritoneal dialysis may be an appropriate alternative in the setting of chronic refractory HF, but controlled studies are needed. Further trials are warranted to determine the long-term outcomes from both ultrafiltration modalities in HF.

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          Most cited references43

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          Importance of venous congestion for worsening of renal function in advanced decompensated heart failure.

          To determine whether venous congestion, rather than impairment of cardiac output, is primarily associated with the development of worsening renal function (WRF) in patients with advanced decompensated heart failure (ADHF). Reduced cardiac output is traditionally believed to be the main determinant of WRF in patients with ADHF. A total of 145 consecutive patients admitted with ADHF treated with intensive medical therapy guided by pulmonary artery catheter were studied. We defined WRF as an increase of serum creatinine >/=0.3 mg/dl during hospitalization. In the study cohort (age 57 +/- 14 years, cardiac index 1.9 +/- 0.6 l/min/m(2), left ventricular ejection fraction 20 +/- 8%, serum creatinine 1.7 +/- 0.9 mg/dl), 58 patients (40%) developed WRF. Patients who developed WRF had a greater central venous pressure (CVP) on admission (18 +/- 7 mm Hg vs. 12 +/- 6 mm Hg, p < 0.001) and after intensive medical therapy (11 +/- 8 mm Hg vs. 8 +/- 5 mm Hg, p = 0.04). The development of WRF occurred less frequently in patients who achieved a CVP <8 mm Hg (p = 0.01). Furthermore, the ability of CVP to stratify risk for development of WRF was apparent across the spectrum of systemic blood pressure, pulmonary capillary wedge pressure, cardiac index, and estimated glomerular filtration rates. Venous congestion is the most important hemodynamic factor driving WRF in decompensated patients with advanced heart failure.
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            Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial.

            Vasopressin mediates fluid retention in heart failure. Tolvaptan, a vasopressin V2 receptor blocker, shows promise for management of heart failure. To investigate the effects of tolvaptan initiated in patients hospitalized with heart failure. The Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study With Tolvaptan (EVEREST), an event-driven, randomized, double-blind, placebo-controlled study. The outcome trial comprised 4133 patients within 2 short-term clinical status studies, who were hospitalized with heart failure, randomized at 359 North American, South American, and European sites between October 7, 2003, and February 3, 2006, and followed up during long-term treatment. Within 48 hours of admission, patients were randomly assigned to receive oral tolvaptan, 30 mg once per day (n = 2072), or placebo (n = 2061) for a minimum of 60 days, in addition to standard therapy. Dual primary end points were all-cause mortality (superiority and noninferiority) and cardiovascular death or hospitalization for heart failure (superiority only). Secondary end points included changes in dyspnea, body weight, and edema. During a median follow-up of 9.9 months, 537 patients (25.9%) in the tolvaptan group and 543 (26.3%) in the placebo group died (hazard ratio, 0.98; 95% confidence interval [CI], 0.87-1.11; P = .68). The upper confidence limit for the mortality difference was within the prespecified noninferiority margin of 1.25 (P<.001). The composite of cardiovascular death or hospitalization for heart failure occurred in 871 tolvaptan group patients (42.0%) and 829 placebo group patients (40.2%; hazard ratio, 1.04; 95% CI, 0.95-1.14; P = .55). Secondary end points of cardiovascular mortality, cardiovascular death or hospitalization, and worsening heart failure were also not different. Tolvaptan significantly improved secondary end points of day 1 patient-assessed dyspnea, day 1 body weight, and day 7 edema. In patients with hyponatremia, serum sodium levels significantly increased. The Kansas City Cardiomyopathy Questionnaire overall summary score was not improved at outpatient week 1, but body weight and serum sodium effects persisted long after discharge. Tolvaptan caused increased thirst and dry mouth, but frequencies of major adverse events were similar in the 2 groups. Tolvaptan initiated for acute treatment of patients hospitalized with heart failure had no effect on long-term mortality or heart failure-related morbidity. clinicaltrials.gov Identifier: NCT00071331
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              Increased central venous pressure is associated with impaired renal function and mortality in a broad spectrum of patients with cardiovascular disease.

              We sought to investigate the relationship between increased central venous pressure (CVP), renal function, and mortality in a broad spectrum of cardiovascular patients. The pathophysiology of impaired renal function in cardiovascular disease is multifactorial. The relative importance of increased CVP has not been addressed previously. A total of 2,557 patients who underwent right heart catheterization in the University Medical Center Groningen, the Netherlands, between January 1, 1989, and December 31, 2006, were identified, and their data were extracted from electronic databases. Estimated glomerular filtration rate (eGFR) was assessed with the simplified modification of diet in renal disease formula. Mean age was 59 +/- 15 years, and 57% were men. Mean eGFR was 65 +/- 24 ml/min/1.73 m(2), with a cardiac index of 2.9 +/- 0.8 l/min/m(2) and CVP of 5.9 +/- 4.3 mm Hg. We found that CVP was associated with cardiac index (r = -0.259, p < 0.0001) and eGFR (r = -0.147, p < 0.0001). Also, cardiac index was associated with eGFR (r = 0.123, p < 0.0001). In multivariate analysis CVP remained associated with eGFR (r = -0.108, p < 0.0001). In a median follow-up time of 10.7 years, 741 (29%) patients died. We found that CVP was an independent predictor of reduced survival (hazard ratio: 1.03 per mm Hg increase, 95% confidence interval: 1.01 to 1.05, p = 0.0032). Increased CVP is associated with impaired renal function and independently related to all-cause mortality in a broad spectrum of patients with cardiovascular disease.
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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                978-3-318-02240-7
                978-3-318-02241-4
                0253-5068
                1421-9735
                2012
                October 2012
                24 October 2012
                : 34
                : 2
                : 149-157
                Affiliations
                Division of Nephrology, Hypertension, and Renal Transplantation, University of Florida, Gainesville, Fla., USA
                Author notes
                *Edward A. Ross, MD, Division of Nephrology, Hypertension and Renal Transplantation, University of Florida, Box 100224, 1600 SW Archer Road, Gainesville, FL 32610-0224 (USA), Tel. +1 352 273 8821, E-Mail Rossea@medicine.ufl.edu
                Article
                342080 Blood Purif 2012;34:149–157
                10.1159/000342080
                23095414
                fe3f3cae-2668-4ff8-9a8a-c509b09f8635
                © 2012 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
                Page count
                Figures: 1, Pages: 9
                Categories
                Special Situations

                Cardiovascular Medicine,Nephrology
                Heart failure,Extracorporeal therapies,Ultrafiltration,Peritoneal dialysis

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