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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      Lacidipine Protects against Cyclosporine-Induced Nephrotoxicity in Rats

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          Abstract

          The effect of lacidipine (LA), a new calcium channel blocker with an antioxidant effect, has been studied on cyclosporine (CsA)-induced nephrotoxicity in male Wistar rats. Lacidipine (1 mg/kg BW) was administered orally 3 days before and 14 days concurrently with CsA (50 mg/kg BW orally). Urine volume, Na<sup>+</sup>, K<sup>+</sup>, Li<sup>+</sup> and creatinine in urine, and blood urea, serum creatinine, lithium, plasma malondialdehyde (MDA) and CsA levels were estimated in blood after 14 days CsA treatment. Kidneys were examined using histological techniques. Blood urea and serum creatinine were increased by 305 and 211%, respectively, with CsA when compared to the saline-treated animals. Creatinine clearance (Ccr) and lithium clearance (Licr) were decreased and proximal tubule fractional reabsorption 1-(Licr/Ccr) was significantly increased with CsA. Lacidipine protected rats from CsA-induced nephrotoxicity. Changes in blood urea, serum creatinine, Ccr, Licr and proximal tubule fractional reabsorption induced by CsA were significantly prevented by LA. There was a 160% rise in MDA levels with CsA, which was significantly reduced equal to control with LA. Histomorphology showed microcalcification with CsA, while it was normal with LA. In rats treated with LA, CsA did not show any microcalcification. Our data suggest that supplementation of LA may be helpful to reduce CsA nephrotoxicity.

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          Decrease in kidney calbindin-d 28kda as a possible mechanism mediating cyclosporine A- and FK-506-induced calciuria and tubular mineralization

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            Calcium antagonists and renal protection. Current status and future perspectives.

            During the past decade, considerable attention has been focused on the effects of calcium antagonists on renal function. Direct in vivo and in vitro observations in diverse experimental models indicate that calcium antagonists antagonize preglomerular vasoconstriction. Furthermore, calcium antagonists are postulated to have additional properties that contribute to their ability to afford renal protection. These putative mechanisms include the ability to retard renal growth, and possibly to attenuate mesangial entrapment of macromolecules, and to attenuate the mitogenic effects of diverse growth factors. Although the clinical implications of the above-mentioned findings have not been fully delineated, the results of recent clinical trials indicate that calcium antagonists exert salutary effects on renal function in clinical settings characterized by impaired renal hemodynamics, including transplant-associated acute renal insufficiency and, possibly, cyclosporine nephrotoxicity. Evidence has accrued suggesting that calcium antagonists may also be protective against acute radiocontrast-induced nephrotoxicity. Finally, the renal hemodynamic and natriuretic effects of calcium antagonists commend their use as antihypertensive agents in the management of essential hypertension, renovascular hypertension, and transplant-associated hypertension.
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              Prevention of cyclosporin-induced vasoconstrictive effect in rat isolated glomeruli with pharmacological vasoactive agents

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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                1999
                1999
                13 January 1999
                : 81
                : 1
                : 60-66
                Affiliations
                aCentral Research Laboratory, Department of Clinical Pharmacology and Therapeutics, and bDepartment of Pathology, Nizam’s Institute of Medical Sciences, Punjagutta, Hyderabad, India
                Article
                45247 Nephron 1999;81:60–66
                10.1159/000045247
                9884421
                c882e2cf-cbfd-46c5-b8bd-84d561a59555
                © 1999 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.

                History
                Page count
                Figures: 2, Tables: 2, References: 42, Pages: 7
                Categories
                Original Paper

                Cardiovascular Medicine,Nephrology
                Calcium channel blocker,Antioxidant,Lacidipine,Nephrotoxicity,Cyclosporine

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