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      Effects of Metabolic Acidosis on Renal Na and H 2O Handling in Humans

      , , ,

      Nephron

      S. Karger AG

      Metabolic acidosis, Proximal sodium reabsorption, Renal fuels

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          Abstract

          An acidotic state has been shown to inhibit sodium (Na) transport both in vitro in toad and turtle bladders an in vivo in rat and dog proximal tubules. To determine if renal Na transport was altered in man by acidosis, we examined the effect of metabolic acidosis produced by ammonium chloride (NH<sub>4</sub>CI) ingestion on proximal and distal tubular Na reabsorption under conditions of maximal water diuresis in seven normal volunteers. During maximal water diuresis, urinary volume (V) can be used as an estimate of Na and H<sub>2</sub>O delivered out of proximal tubule, the clearances of free water and sodium (CH<sub>2</sub>O + CNa) as an estimate of distal Na delivery, and the clearance of free water (CH<sub>2</sub>O) as a measure of Na reabsorption in the diluting segment. The urinary volume, the distal Na delivery, and the clearance of free water were not significantly different in the control (HCO<sub>3</sub> – 24.6 mEq/l, venous pH 7.34) and experimental (HCO<sub>3</sub> – 15.9 mEq/l, venous pH 7.25) states. However, the proportion of Na load reabsorbed by the diluting segment CH<sub>2</sub>OCH<sub>2</sub>O±CNa×100 Can was higher in the acidotic state (p < 0.01). It is concluded that moderate metabolic acidosis does not affect proximal Na reabsorption in man. An increased fractional reabsorption of Na distally is seen in acidosis and may reflect a direct effect of metabolic acidosis on the diluting segment or be secondary to the greater chloride and lesser bicarbonate presented to the diluting segment during acidosis.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1977
          1977
          02 December 2008
          : 19
          : 5
          : 278-283
          Affiliations
          Nephrology Division, Department of Medicine and Pathology, Georgetown University School of Medicine, Washington, D.C.
          Article
          180905 Nephron 1977;19:278–283
          10.1159/000180905
          917178
          © 1977 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: 6
          Categories
          Original Paper

          Cardiovascular Medicine, Nephrology

          Renal fuels, Proximal sodium reabsorption, Metabolic acidosis

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