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      Renal Handling of Calcium

      Nephron

      S. Karger AG

      Diuretics, Amiloride, Thiazide, Furosemide, Calcium

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          Abstract

          Ca absorption is mediated by both active and passive processes. Absorption in both proximal tubule and thick ascending limb is mainly coupled indirectly to Na absorption and is a passive process through the paracellular pathway. In the distal convoluted tubule, Ca absorption is regulated independently of Na absorption; this is the principal site of action of parathyroid hormone, calcitonin, and 1,25-(OH)<sub>2</sub>D<sub>3</sub>. Models for transport in proximal tubule, thick ascending limb, and distal convoluted tubule afford attractive explanations for the influence on Ca transport of effective arterial blood volume, parathyroid hormone, acid-base balance, genetic disturbances such as Bartter’s and Gitelman’s syndromes, and diuretic action.

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          Most cited references 2

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          Bartter's syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na-K-2Cl cotransporter NKCC2.

          Inherited hypokalaemic alkalosis with low blood pressure can be divided into two groups-Gitelman's syndrome, featuring hypocalciuria, hypomagnesaemia and milder clinical manifestations, and Bartter's syndrome, featuring hypercalciuria and early presentation with severe volume depletion. Mutations in the renal Na-Cl cotransporter have been shown to cause Gitelman's syndrome. We demonstrate linkage of Bartter's syndrome to the renal Na-K-2Cl cotransporter gene NKCC2, and identify frameshift or non-conservative missense mutations for this gene that co-segregate with the disease. These findings demonstrate the molecular basis of Bartter's syndrome, provide the basis for molecular classification of patients with inherited hypokalaemic alkalosis, and suggest potential phenotypes in heterozygous carriers of NKCC2 mutations.
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            Genetic heterogeneity of Bartter's syndrome revealed by mutations in the K+ channel, ROMK.

            Mutations in the Na-K-2Cl cotransporter (NKCC2), a mediator of renal salt reabsorption, cause Bartter's syndrome, featuring salt wasting, hypokalaemic alkalosis, hypercalciuria and low blood pressure. NKCC2 mutations can be excluded in some Bartter's kindreds, prompting examination of regulators of cotransporter activity. One regulator is believed to be ROMK, an ATP-sensitive K+ channel that 'recycles' reabsorbed K+ back to the tubule lumen. Examination of the ROMK gene reveals mutations that co-segregate with the disease and disrupt ROMK function in four Bartter's kindreds. Our findings establish the genetic heterogeneity of Bartter's syndrome, and demonstrate the physiologic role of ROMK in vivo.
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              Author and article information

              Journal
              NEF
              Nephron
              10.1159/issn.1660-8151
              Nephron
              S. Karger AG
              978-3-8055-6818-0
              978-3-318-00390-1
              1660-8151
              2235-3186
              1999
              December 1998
              24 December 1998
              : 81
              : Suppl 1
              : 2-7
              Affiliations
              Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Tex., USA
              Article
              46292 Nephron 1999;81(suppl 1):2–7
              10.1159/000046292
              9873208
              © 1998 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
              Figures: 7, References: 11, Pages: 6
              Product
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/46292
              Categories
              Paper

              Cardiovascular Medicine, Nephrology

              Calcium, Furosemide, Amiloride, Diuretics, Thiazide

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