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      Effect of Trimethoprim-Sulfamethoxazole on Na + and K + Transport Properties in the Rabbit Cortical Collecting Duct Perfused in vitro


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          Background: In this study, the membrane mechanisms of hyperkalemia caused by trimethoprim-sulfamethoxazole (TMP-SMX) combination antibiotics were assessed in the cortical collecting duct (CCD). Methods: We used the microelectrode technique and flux measurements, and examined the effects of TMP and SMX on electrical properties of the apical and basolateral membranes in the rabbit CCD perfused in vitro. Results: TMP in the lumen caused increases in apical membrane voltage, fractional apical membrane resistance (fR<sub>A</sub>), and transepithelial resistance (R<sub>T</sub>), all effects which were completely inhibited by luminal amiloride, but not by luminal Ba<sup>2+</sup>. The luminal TMP inhibited both net Na<sup>+</sup> reabsorption and K<sup>+</sup> secretion in the CCD. TMP in the bath slightly but significantly depolarized transepithelial voltage and basolateral membrane voltage without influencing fR<sub>A</sub> or R<sub>T</sub>. SMX in the lumen or bath had no effect on barrier voltages or resistances. Conclusion: TMP mainly acts on the apical membrane of the CCD, inhibits the amiloride-sensitive macroscopic Na<sup>+</sup> conductance in this membrane, and thereby decreases the net driving force for K<sup>+</sup> exit across the membrane, resulting in an inhibition of K<sup>+</sup> secretion. SMX in the lumen or bath had no effect on the CCD.

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          Brief report: trimethoprim-induced hyperkalemia in a patient with AIDS.

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            Electrophysiological identification of alpha- and beta-intercalated cells and their distribution along the rabbit distal nephron segments.

            By cable analysis and intracellular microelectrode impalement in the in vitro perfused renal tubule, we identified alpha- and beta-intercalated (IC) cells along the rabbit distal nephron segments, including the connecting tubule (CNT), the cortical collecting duct (CCD), and the outer medullary collecting duct in the inner stripe (OMCDi). IC cells were distinguished from collecting duct (CD) cells by a relatively low basolateral membrane potential (VB), a higher fractional apical membrane resistance, and apparent high Cl- conductances of the basolateral membrane. Two functionally different subtypes of IC cells in the CCD were identified based on different responses of VB upon reduction of the perfusate Cl- from 120 to 12 mM: the basolateral membrane of beta-IC cells was hyperpolarized, whereas that of alpha-IC cells was unchanged. This is in accord with the hypothesis that the apical membrane of beta-IC cells contains some Cl(-)-dependent entry processes, possibly a Cl-/HCO3- exchanger. Further characterization of electrical properties of both subtypes of IC cells were performed upon lowering bath or perfusate Cl- from 120 to 12 mM, and raising bath or perfusate K+ from 5 to 50 mM. A 10-fold increase in the perfusate K+ had no effect on VB in both subtypes of IC cells. Upon abrupt changes in Cl- or K+ concentration in the bath, a large or a small depolarization of the basolateral membrane, respectively, was observed in both subtypes of IC cells. The electrical properties of alpha- and beta-IC cells were similar among the distal nephron segments, but their distribution was different: in the CNT, which consists of IC cells and CNT cells, 97.3% (36/37) of IC cells were of the beta type. In the CCD, which consists of IC cells and CD cells, 79.8% (79/99) of IC cells were of the beta-type, whereas in the OMCDi 100% (19/19) were of the alpha type, suggesting that the beta type predominates in the earlier and the alpha type in the later segment.
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              Hyporeninemic hypoaldosteronism associated with acquired immune deficiency syndrome.

              Four patients with the acquired immune deficiency syndrome (AIDS) and persistent unexplained hyperkalemia were studied. Testing with cosyntropin (0.25 mg intravenously) revealed normal baseline and stimulated cortisol levels and adequate aldosterone stimulation. The baseline aldosterone level was low for the degree of hyperkalemia. Renin/aldosterone stimulation testing was performed by intravenous injection of 80 mg of furosemide followed by four hours of upright posture. This study showed low baseline renin and aldosterone levels and inadequate renin and aldosterone stimulation. Three patients were subsequently treated with fludrocortisone (0.1 to 0.2 mg per day), with normalization of serum potassium levels. It is concluded that hyporeninemic hypoaldosteronism is responsible for hyperkalemia in some patients with AIDS and that treatment with fludrocortisone is effective in these cases.

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                February 2006
                23 February 2006
                : 102
                : 3-4
                : p51-p60
                Departments of Nephrologyand Clinical Pharmacology, Jichi Medical School, Minamikawachi, Kawachi, Tochigi, Japan
                89682 Nephron Physiol 2006;102:p51–p60
                © 2006 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.

                : 10 March 2005
                : 20 July 2005
                Page count
                Figures: 7, Tables: 5, References: 22, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/89682
                Self URI (text/html): https://www.karger.com/Article/FullText/89682
                Self URI (journal page): https://www.karger.com/SubjectArea/Nephrology
                Original Paper

                Cardiovascular Medicine,Nephrology
                Hyperkalemia,Rabbit cortical collecting duct,Trimethoprim,Sulfamethoxazole


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