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

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      A Case of Podocytic Infolding Glomerulopathy with Focal Segmental Glomerulosclerosis

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          Abstract

          Podocytic infolding glomerulopathy (PIG) has been proposed as a new disease entity. A 14-year-old girl underwent renal biopsy at our institution because of a chance finding of proteinuria. Light microscopic findings revealed a minor glomerular abnormality, but under a higher magnification, after periodic acid methenamine silver staining, a bubbling appearance in the glomerular basement membrane (GBM) was observed. An electron microscopic examination revealed microspheres in the GBM, which were sparse but global. The patient was diagnosed as having PIG. After 3 years, her urinary protein had increased and a second biopsy was performed, showing focal segmental glomerulosclerosis in addition to a lesser degree of podocytic infolding than at the first biopsy. This is the first report of a case complicated by a different type of glomerulonephritis after being diagnosed as PIG. A few cases of PIG are complicated by focal segmental glomerulosclerosis, suggesting several mechanisms for the disorder.

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          Proposal of podocytic infolding glomerulopathy as a new disease entity: a review of 25 cases from nationwide research in Japan.

          Ritsuko Katafuchi, Shinsuke Nomura, Yoshihide Fujigaki … (2008)
          A rare and peculiar glomerulopathy has begun to be recognized in Japan. The Japanese Society of Nephrology has established a research working group and has collected cases from all over Japan in an attempt to understand the complete spectrum of this glomerulopathy. The diagnostic criterion, which was needed to collect the cases, was proposed as a glomerulopathy showing microspheres or microtubular structures or both associated with podocytic infolding into the glomerular basement membrane (GBM) on electron microscopy. The lesion shows a non-argentaffin hole in the GBM with periodic acid methenamine silver staining and is similar to membranous glomerulonephritis. Twenty-five cases were collected from 17 institutions. Patients were 20-69 years old (19 women, 6 men). Seventeen patients also had collagen diseases such as lupus nephritis and Sjögren's syndrome. All patients had proteinuria. Proteinuria showed a remission in 15 of 23 patients within 12 months, but proteinuria remained higher than 1.0 g/day in five patients despite different types of therapy. Podocytic infolding including microspheres showed either positive or negative staining for immunoglobulins. Cluster formation of microspheres was found in 4 of 17 patients with collagen disease, and in five out eight patients without collagen disease. Electron-dense deposits in the GBM were also found in 6 of 17 patients with collagen disease but were not found in eight patients without collagen disease. Some patients might have a subtype of lupus nephritis, class V, or membranous glomerulonephritis. However, we propose a new disease entity, podocytic infolding glomerulopathy, as a common basis of all 25 patients, because we suspect that microspheres or microtubular structures or both can be derived from podocytic infolding.
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            Immunohistochemical study of the C5b-9 complex of complement in human kidneys.

            Nicole Hinglais, Michel D Kazatchkine, Sucharit Bhakdi … (1986)
            The presence and localization of the C5b-9 neoantigens of the terminal complement sequence, of antigens expressed by cleavage fragments of C3, and of Factor H antigens have been studied by immunohistochemical techniques in morphologically normal adult human kidneys and in biopsy specimens from patients with a wide range of renal diseases with and without immune deposits. In morphologically normal kidneys, C5b-9 neoantigens were observed within all connective matrices (arteriolar media, glomerular basement membrane (GBM), mesangial matrix and tubular basement membrane). The C3d and C3g antigens of the C3dg, and C3bi cleavage fragments of C3 and Factor H antigens were found in similar locations. None of the matrices stained for immunoglobulins. Immunoelectron microscopy demonstrated that C3d, C3g, H antigens and the C5b-9 neoantigens were localized on membranous and vesicular structures embedded in the connective matrices. These structures represent cell membranes shed from adjacent cells as evidenced by their ultrastructural appearance and by the fact that those which were in close vicinity to pedicles within the GBM expressed the C3b receptor antigen, a specific marker for podocyte membranes. Formation of C5b-9 complexes in the shielded environment of connective matrices may explain their persistence over long periods of time in the absence of apparent immunopathological consequences. Biopsies from pathological kidneys were classified into three groups based on the pattern of glomerular staining with anti-C5b-9 antibodies. In the first group, a sparse mesangial labeling was seen, similar to that observed in normal kidneys. In the second group, abundant clusters of C5b-9 were seen in the same location as immune deposits. Activation of the complement system to completion could be documented in the absence of detectable C3 (C3c) antigen in glomeruli. Immunoelectron microscopy demonstrated that C5b-9 neoantigens were present on cell remnants in connective matrices in all specimens that were studied. Labeled cell remnants were present in large amounts in sclerotic matrices. C5b-9 neoantigens were constantly found on old and large immune deposits, and absent or occasionally present on recent and small immune deposits. In membranous nephropathy stage I, proteinuria appeared to be independent of the presence or absence of detectable C5b-9 neoantigens on immune deposits. Thus, the presence of C5b-9 neoantigens in pathological renal tissue does not have an univocal significance, and requires analysis of the localization of the antigens and appropriate controls in order to assess the potential role of C5b-9 in tissue damage.
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              A nephrotic case of vesicoureteral reflux representing focal segmental glomerulosclerosis associated with podocytic infolding lesions.

              T Matsuo, T Sano, Kouju Kamata … (2008)
              The case was a 54-year-old woman who had suffered from occasional incontinence of urine after a craniotomy for subarachnoid hemorrhage in 1991. In June 1998 she was admitted for nephrotic syndrome without hematuria. Intravenous pyelography and voiding cystourethrography revealed bilateral hydronephrosis, atonic bladder, and vesicoureteral reflux (VUR). Renal biopsy demonstrated the presence of focal segmental glomerulosclerosis with cellular lesions. However, periodic-acid methenamine silver (PAM) staining revealed bubbling and spike appearance in the diffuse peripheral loops, although immunofluorescence microscopy showed negative findings in the glomeruli. Electron microscopy revealed diffuse thickening of the glomerular basement membrane (GBM) accompanying diffuse podocytic infolding lesions into the GBM and numerous spherical microstructures in the GBM. No findings of dense deposits were observed in the GBM and mesangium. Her urinary protein excretion decreased and renal function improved after placement of an urethral catheter for one year. A second renal biopsy revealed a remarkable decrease in podocytic infolding lesions, although microstructures in the GBM remained. Although mechanisms of the occurrence of these peculiar podocytic infolding lesions are unclear, it is speculated that podocyte damage due to hydronephrosis may have caused the lesions.
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                Author and article information

                Journal
                Journal ID (publisher-id): CRU
                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: 2013
                Publication date Collection: July – December 2013
                Publication date (Electronic): 08 August 2013
                Volume: 3
                Issue: 2
                Pages: 110-116
                Affiliations
                aDepartment of Internal Medicine, Nagaoka Red Cross Hospital, Nagaoka, and bDivision of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan
                Author notes
                *Akira Iguchi, MD, PhD, Department of Internal Medicine, Nagaoka Red Cross Hospital, Sensyu-2 297-1, Nagaoka City, Niigata 940-2085 (Japan), E-Mail igucci4444@yahoo.co.jp
                Article
                Publisher ID: 354591 Pmcid ID: PMC3770251 Other ID: Case Rep Nephrol Urol 2013;3:110-116
                DOI: 10.1159/000354591
                PMC ID: PMC3770251
                PubMed ID: 24027576
                SO-VID: 6b3ccbe8-0653-4283-a8d2-029d3e6ef0c1
                Copyright © © 2013 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: 1, Pages: 7
                Categories
                Subject: Published: August 2013

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Podocyte,Microspheres,Focal segmental glomerulosclerosis,Podocytic infolding glomerulopathy
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Podocyte, Microspheres, Focal segmental glomerulosclerosis, Podocytic infolding glomerulopathy

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