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

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      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Bucillamine-Induced Membranous Nephropathy with Crescent Formation in a Patient with Rheumatoid Arthritis: Case Report and Literature Review

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          Abstract

          Bucillamine is a disease-modifying antirheumatic drug that is structurally similar to <smlcap>D</smlcap>-penicillamine. The major renal side effect of bucillamine and <smlcap>D</smlcap>-penicillamine is proteinuria caused by membranous nephropathy (MN). In addition to MN, combined crescent formation has been occasionally reported in <smlcap>D</smlcap>-penicillamine-induced MN, while crescent formation has been rarely reported in bucillamine-treated cases. Here, we describe a 76-year-old female who presented with nephrotic syndrome and rapidly progressive glomerulonephritis. She was receiving bucillamine as initial treatment for recently diagnosed rheumatoid arthritis, and renal biopsy showed MN with crescent formation. To the best of our knowledge, this is the first report of bucillamine-induced MN with crescent formation in the English literature.

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          The role of complement in membranous nephropathy.

          Hong Ma, H. Beck, Dana G. Sandor (2013)
          Membranous nephropathy (MN) describes a histopathologic pattern of injury marked by glomerular subepithelial immune deposits and collectively represents one of the most common causes of adult nephrotic syndrome. Studies in Heymann nephritis, an experimental model of MN, have established a paradigm in which these deposits locally activate complement to cause podocyte injury, culminating in cytoskeletal reorganization, loss of slit diaphragms, and proteinuria. There is much circumstantial evidence for a prominent role of complement in human MN because C3 and C5b-9 are found consistently within immune deposits. Secondary MN often shows the additional presence of C1q, implicating the classic pathway of complement activation. Primary MN, however, is IgG4-predominant and IgG4 is considered incapable of binding C1q and activating the complement pathway. Recent studies have identified the M-type phospholipase A2 receptor (PLA2R) as the major target antigen in primary MN. Early evidence hints that IgG4 anti-PLA2R autoantibodies can bind mannan-binding lectin and activate the lectin complement pathway. The identification of anti-PLA2R antibodies as likely participants in the pathogenesis of disease will allow focused investigation into the role of complement in MN. Definitive therapy for MN is immunosuppression, although future therapeutic agents that specifically target complement activation may represent an effective temporizing measure to forestall further glomerular injury. © 2013 Elsevier Inc. All rights reserved.
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            Current views on collapsing glomerulopathy.

            Mamdouh Albaqumi, Laura Barisoni (2008)
            Collapsing glomerulopathy is a proliferative disease defined by segmental or global wrinkling of the glomerular basement membranes associated with podocyte proliferation. These lesions are particularly poor responders to standard therapies. First described as an idiopathic disorder or following HIV infection, it is now associated with a broad group of diseases and different pathogenetic mechanisms, which participate in podocyte injury and mitogenic stimulation. Because of this etiologic heterogeneity, there is clear need for new therapeutic approaches to target each variant of this entity. Historical background, terminology, morphologic and phenotypic features, and suggested mechanisms are reviewed in this manuscript.
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              Clinical and pathological features of renal involvement in propylthiouracil-associated ANCA-positive vasculitis.

              Ai-min Chen, Ming-Hui Zhao, Ying-Lian Gao … (2007)
              The kidney is one of the organs affected in patients with propylthiouracil (PTU)-associated antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis. We present a series of Chinese patients with renal involvement in PTU-associated ANCA-positive vasculitis and describe their clinical and pathological characteristics. Clinical and pathological data from patients with PTU-associated ANCA-positive vasculitis with renal involvement, diagnosed in Peking University First Hospital, were collected and analyzed retrospectively. Nineteen patients with PTU-associated ANCA-positive vasculitis were treated at Peking University First Hospital between December 1999 and December 2005, and 15 of them had renal involvement. Of the 15 patients, 13 were female and 2 were male, with an average age of 26.3 +/- 11.8 years. All 15 patients were perinuclear ANCA positive with specificities to myeloperoxidase (15 of 15), cathepsin G (9 of 15), human leukocyte elastase (8 of 15), lactoferrin (7 of 15), azurocidin (5 of 15), and proteinase 3 (4 of 15). Duration of PTU administration was 43.0 +/- 31.2 months. All 15 patients had clinical markers of renal involvement, including hematuria (100%), proteinuria (100%), and renal function abnormality (47%). All 15 patients underwent percutaneous renal biopsy. Ten patients had necrotizing crescentic glomerulonephritis, and 7 of these 10 patients had immune complex deposition. Three patients had minimal involvement, 2 patients had immunoglobulin A nephropathy, and 2 patients had membranous nephropathy. PTU treatment was discontinued in all 15 patients. All except 2 patients with minimal renal involvement received immunosuppressive treatment. Eleven of 15 patients achieved complete clinical remission. Renal involvement in our case series of patients with PTU-associated ANCA-positive vasculitis was heterogeneous, and nearly half our patients had renal immune complex deposition.
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                Author and article information

                Journal
                Journal ID (publisher-id): CND
                Journal ID (pmc): CND
                Journal ID (doi): 10.1159/issn.2296-9705
                Title: Case Reports in Nephrology and Dialysis
                Publisher: S. Karger AG
                ISSN (Electronic): 2296-9705
                Publication date Subscription-year: 2015
                Publication date Collection: January – April 2015
                Publication date (Electronic): 29 October 2014
                Volume: 5
                Issue: 1
                Pages: 30-38
                Affiliations
                Departments of aNephrology and bRheumatology, Yokohama Rosai Hospital, Yokohama, and cDepartment of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan
                Author notes
                *Kosaku Nitta, MD, PhD, Department of Medicine, Kidney Center, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666 (Japan), E-Mail knitta@kc.twmu.ac.jp
                Article
                Publisher ID: 368826 Pmcid ID: PMC4294451 Other ID: Case Rep Nephrol Dial 2015;5:30-38
                DOI: 10.1159/000368826
                PMC ID: PMC4294451
                PubMed ID: 25849672
                SO-VID: e67e3936-04af-40aa-93f9-8db31ac09288
                Copyright © © 2014 S. Karger AG, Basel
                License:

                Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) ( http://www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. 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: 3, Tables: 2, Pages: 9
                Categories
                Subject: Published: October 2014

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Crescent formation,Nephrotic syndrome,Rheumatoid arthritis,Membranous nephropathy,Bucillamine,Rapidly progressive glomerulonephritis
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Crescent formation, Nephrotic syndrome, Rheumatoid arthritis, Membranous nephropathy, Bucillamine, Rapidly progressive glomerulonephritis

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