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      Renal Lesions of Hyperlipidemic Imai Rats: A Spontaneous Animal Model of Focal Glomerulosclerosis

      research-article
      a , b
      Nephron
      S. Karger AG
      Focal glomerulosclerosis, Nephrotic syndrome, Hyperlipidemia, Animal model

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          Abstract

          The hyperlipidemic Imai rat was originally developed as an animal model of spontaneous hyperlipidemia. We report the natural course of the Imai rat up to 32 weeks of age focusing on renal pathology. The degree of proteinuria, which first appeared at 8 weeks, increased with age, and all Imai rats developed heavy proteinuria (mean, 228 mg/24 h) with impaired renal function (mean BUN, 78.7 mg/dl) at 32 weeks. Histologic changes of the glomeruli were characterized by focal and segmental sclerosis and hyalinosis. Both the percentage of affected glomeruli and the severity of each affected glomerulus were progressively increased with age. The immunofluorescence and electron-microscopic findings were also comparable to those of focal glomerulosclerosis (FGS) in humans. The serum levels of total cholesterol, triglyceride, and phospholipid in Imai rats were significantly higher than those in normal Sprague-Dawley rats at 8 weeks of age, and progressively increased thereafter. The proteinuria, glomerular involvements, and hyperlipidemia were generally less severe in the females than in the males. We conclude that the hyperlipidemic Imai rat, a naturally occurring animal model of FGS, is useful in studying the pathogenesis of FGS and the renal effects of hyperlipidemia in humans.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1991
          1991
          11 December 2008
          : 59
          : 3
          : 471-476
          Affiliations
          aDepartment of Pathology, Saga Medical School, Japan; bThe Chemical Inspection and Testing Center, Hita, Japan
          Article
          186611 Nephron 1991;59:471–476
          10.1159/000186611
          1758540
          41f045dc-ce83-4ca8-adc9-612ab29122b5
          © 1991 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
          : 04 January 1991
          Page count
          Pages: 6
          Categories
          Original Paper

          Cardiovascular Medicine,Nephrology
          Focal glomerulosclerosis,Nephrotic syndrome,Hyperlipidemia,Animal model

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