Nephron
Original Paper
Renal Handling of Citrate in Chronic Renal InsufficiencyMarangella M. · Vitale C. · Manganaro M. · Cosseddu D. · Martini C. · Petrarulo M. · Linari F.Nephrology Division and Renal Stone Laboratory, Ospedale Mauriziano Umberto I, Turin, Italy
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Article / Publication Details
Accepted: June 05, 1990
Published online: December 11, 2008
Issue release date: 1991
Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 0
ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)
For additional information: https://www.karger.com/NEF
Abstract
Citrate is a relevant component of the inhibitory potential of the urine environment. Its excretion and renal handling have been widely studied in subjects with normal renal function, but little is known about changes induced by chronic renal insufficiency. We have investigated renal handling of citrate in 50 patients with different degrees of renal insufficiency as compared to 30 healthy subjects with normal renal function. Among patients 34 were defined as having mild renal insufficiency based on a GFR of 80 through 40 ml/min/1.73 m2 BSA, while 16 had moderate-to-severe renal failure, defined by a GFR ranging from 40 to 20 ml/min/1.73 m2 BSA. Serum citrate increased in mild renal insufficiency, while it tended to be restored to normal values at more advanced renal failure. There was a stepwise decrease in the filtered load of citrate as GFR decreased, while its renal clearance was significantly reduced only at higher degrees of renal failure. This behavior was due to an increase in the fractional excretion of citrate which was inversely related to the decrease in GFR (p = 0.015). These data suggest that serum citrate levels and excretion are governed by renal mechanisms at mild degrees of renal insufficiency; in these conditions citrate is shown to behave conformly to other poorly reabsorbable anions such as sulfate. At more advanced renal failure the ensuing metabolic acidosis plays a crucial role as a regulatory factor of both serum concentration and renal handling of citrate, by increasing cellular uptake and metabolism as well as tubular reabsorption of this anion. Thus, even the severely diseased kidney seems to respond to acid-base imbalance as efficiently as the normal kidney does.
© 1991 S. Karger AG, Basel
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Article / Publication Details
Accepted: June 05, 1990
Published online: December 11, 2008
Issue release date: 1991
Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 0
ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)
For additional information: https://www.karger.com/NEF
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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.
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