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      Urinary Levels of Macrophage Migration Inhibitory Factor in Patients with IgA Nephropathy

      ,

      Nephron

      S. Karger AG

      IgA nephropathy, Minimal-change nephrotic syndrome, Macrophage migration inhibitory factor

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          Abstract

          Background/Aim: The processes involved in development of IgA nephropathy (IgAN) are not yet well understood. Macrophage migration inhibitory factor (MIF) is a potent pro-inflammatory cytokine and is an essential component of immune and inflammatory responses. To examine further the possible role of MIF in IgAN, we measured MIF levels in the urine. The purpose of the present study was to evaluate the involvement of MIF in IgAN. Methods: Urine samples were obtained from 20 IgAN patients. The disease controls included 20 patients with minimal-change nephrotic syndrome (MCNS). A group of healthy subjects served as control. The samples were assayed for MIF protein by a sandwich enzyme-linked immunosorbent assay (ELISA). Results: The MIF levels in the urine of patients with IgAN examined were significantly higher than those of the healthy control subjects. In contrast, the levels of urinary MIF (uMIF) in patients with MCNS did not differ significantly from normal values. In IgAN patients, uMIF significantly correlated with the magnitude of proteinuria, but not with the grade of hematuria. We also investigated the relationship between uMIF levels and pathological features. Among patients with IgAN, uMIF levels were significantly correlated with the grade of glomerular crescent formation and that of mesangial cell proliferation. There was also a significant correlation between uMIF levels and the number of both intraglomerular and interstitial macrophages. Conclusion: Although the underlying mechanisms remain to be determined, these data provide evidence that urinary excretion of MIF is increased in IgAN patients with active renal lesions.

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          The Pathogenic Role of Macrophage Migration Inhibitory Factor in Immunologically Induced Kidney Disease in the Rat

          Macrophage migration inhibitory factor (MIF) plays a pivotal role in the inflammatory response in endotoxemia and in the delayed-type hypersensitivity response, but its potential as a regulator of immunologically induced disease is unknown. We have addressed this issue by administering a neutralizing anti-MIF antibody in a rat model of immunologically induced crescentic anti-glomerular basement membrane (GBM) glomerulonephritis. Six individual experiments using paired inbred littermates were performed. Rats were primed with rabbit immunoglobulin on day −5 and then injection with rabbit anti–rat GBM serum on day 0. Pairs of animals were treated with anti-MIF or a control monoclonal antibody from the time of anti-GBM serum administration until being killed 14 d later. Control antibody-treated animals developed severe proteinuria and renal function impairment with severe histological damage due to marked leukocytic infiltration and activation within the kidney. In contrast, anti-MIF treatment substantially reduced proteinuria, prevented the loss of renal function, significantly reduced histological damage including glomerular crescent formation, and substantially inhibited renal leukocytic infiltration and activation (all P <0.001 compared with control treatment). Inhibition of renal disease by anti-MIF treatment was attributed to preventing the marked upregulation of interleukin-1β, leukocyte adhesion molecules including intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, and inducible nitric oxide synthase expression seen in the control antibody-treated animals. This inhibition of progressive renal injury was mirrored by the complete suppression of the skin delayed-type hypersensitivity response to the challenge antigen (rabbit IgG). Interestingly, anti-MIF treatment did not effect the secondary antibody response or immune deposition within the kidney, indicating that MIF participates in cellular-based immunity in this primed macrophage-dependent anti-GBM glomerulonephritis. In conclusion, this study has demonstrated a key regulatory role for MIF in the pathogenesis of immunologically induced kidney disease. These results argue that blocking MIF activity may be of benefit in the treatment of human rapidly progressive glomerulonephritis, and suggest that MIF may be important in immune-mediated disease generally.
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            An essential regulatory role for macrophage migration inhibitory factor in T-cell activation.

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              Author and article information

              Journal
              NEF
              Nephron
              10.1159/issn.1660-8151
              Nephron
              S. Karger AG
              1660-8151
              2235-3186
              2002
              October 2002
              02 September 2002
              : 92
              : 2
              : 309-315
              Affiliations
              Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan
              Article
              63297 Nephron 2002;92:309–315
              10.1159/000063297
              12218308
              © 2002 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: 5, Tables: 1, References: 23, Pages: 7
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              Self URI (application/pdf): https://www.karger.com/Article/Pdf/63297
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              Original Paper

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