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

      The ‘Hepatorenal’ Syndrome and Refractory Ascites

      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.


          The charts of 30 consecutive patients who underwent implantation of a LeVeen type of peritoneal-venous (P-V) shunt were reviewed. 29 patients had Laennec’s cirrhosis and ascites refractory to medical therapy. Of these, 7 or 24% had hepatorenal syndrome (HRS), i.e. creatininemia and azotemia, a low urinary sodium (UNa), and no other apparent cause for renal failure. In these patients with plasma creatinine (pCr) > 1.6 mg/dl and BUN > 30 mg/dl and UNa < 10 mEq/1, the P-V shunt s ingificantly improved all 3 measures of renal function: pCr decreased from 4.3 to 2.7 mg/dl (p < 0.025) BUN decreased from 79 to 38 mg/dl (p < 0.025) and UNa increased to 70 mEq/1. 4 of these patients are still alive, a mean of 418 days after being shunted (preshunt BUN = 60 mg/dl). 3 patients died a mean of 81.7 days after shunt implantation (preshunt BUN = 83 mg/dl), none from renal failure. Of the 29 patients with refractory ascites, + / – HRS, the implantation of this shunt was associated with a significant increase in renal sodium clearance (CNa) and fraction of the filtered sodium being excreted CNa/Ccr. The CNa/Ccr increased after shunting in patients studied while off diuretics from 0.21 to 1.45% (p < 0.025). The avid renal salt adsorption characteristic of refractory ascites and HRS appears to have been reversed. The P-V shunt appears to be beneficial therapy, especially in preterminal HRS, and appears to function in a physiologic manner, by decreasing the renal reabsorption of sodium and water.

          Related collections

          Author and article information

          S. Karger AG
          02 December 2008
          : 23
          : 5
          : 228-232
          Veterans Administration Hospital and Downstate Medical Center, State University of New York, Brooklyn, N.Y., and Marshall University School of Medicine, HuntingtonW.Va.
          181640 Nephron 1979;23:228–232
          © 1979 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
          Pages: 5
          Original Paper

          Cardiovascular Medicine, Nephrology

          Renal failure cirrhosis, Renal sodium reabsorption


          Comment on this article