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      Elevated Interleukin-18 Levels in the Urine of Nephrotic Patients

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          Abstract

          Background/Aim: The etiology of minimal-change nephritic syndrome (MCNS) is obscure. It has been speculated that T cells play a role in the pathogenesis of MCNS. Interleukin (IL)-18, a novel immunoregulatory cytokine with potent inferon-γ-inducing activities, may play an important role in T-helper type 1-mediated immune responses. To examine further the possible role of IL-18 in nephrotic syndrome (NS), in the present study we measured IL-18 levels in the urine in different clinical stages of MCNS. The aim of this study was to investigate the involvement of IL-18 in MCNS. Methods: Urine samples were obtained from 20 MCNS patients. The disease controls included 20 patients with IgA nephropathy. The samples were assayed for IL-18 protein by a sandwich enzyme-linked immunosorbent assay. Results: Compared with normal controls, significantly increased urinary levels of IL-18 were detected in MCNS patients with the NS. The urinary IL-18 (uIL-18) levels correlated with the degree of proteinuria in MCNS patients. Moreover, when individual MCNS patients were followed through their clinical illness, uIL-18 levels were increased during the active phase and decreased as the patients went into remission. Conclusions: These results indicate that uIL- 18 is detectable in a subgroup of patients with active NS and correlates to their disease activity in patients with MCNS. Our findings support the notion that IL-18 may play a role in the pathophysiology of NS.

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          Most cited references 5

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          Interleukin-18 Binding Protein

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            Anti-inflammatory actions of steroids: molecular mechanisms

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              Th1 and Th2 T helper cell subsets affect patterns of injury and outcomes in glomerulonephritis.

              The recognition that human immune responses can be directed by two different subsets of T helper cells (Th1 and Th2) has been an important development in modern immunology. Immune responses polarized by either the Th1 or Th2 subset predominance result in different inflammatory effector pathways and disease outcomes. Many autoimmune diseases are associated with either Th1- or Th2- polarized immune responses. Although these different immune response patterns are relevant to glomerulonephritis (GN), little attention has been paid to the consequences of Th1 or Th2 predominance of nephritogenic immune responses for the pattern and outcome of GN. Unlike other autoimmune conditions, GN results from a variety of different immune responses and has a range of histologic features and immune effectors in glomeruli. This review assesses the data available from studies of experimental and human GN that address the Th1 or Th2 predominance of nephritogenic immune responses and their relevance to the different histopathological patterns and outcomes of GN. In particular, the evidence that Th1-predominant nephritogenic immune responses are associated with severe proliferative and crescentic GN is presented.
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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2001
                2001
                25 July 2001
                : 88
                : 4
                : 334-339
                Affiliations
                aDepartment of Medical Technology, College of Medical Sciences, Saitama Prefectural University, Koshigaya, and bSecond Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan
                Article
                46017 Nephron 2001;88:334–339
                10.1159/000046017
                11474228
                © 2001 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: 4, Tables: 1, References: 14, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/46017
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                Original Paper

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