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      Proliferative glomerulonephritis with monoclonal IgG deposits in two kidney allografts successfully treated with rituximab

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          Abstract

          Proliferative glomerulonephritis with monoclonal immunoglobulin G deposit (PGNMID), a recently described pathologic entity in native kidneys, has been recognized in kidney transplant patients, where it can present as either recurrent or de novo disease. There is no definitive treatment to date, in either population. Here, we present two cases of PGNMID in kidney allografts that illustrate the challenges of diagnostic approach and highlight the allograft outcome after treatment with rituximab as a potential treatment of this condition.

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          Proliferative glomerulonephritis with monoclonal IgG deposits.

          G. Markowitz, D A Valeri, Anjali Satoskar … (2009)
          Dysproteinemias that result in monoclonal glomerular deposits of IgG are relatively uncommon. Here, we report the largest series of proliferative glomerulonephritis with monoclonal IgG deposits, a form of renal involvement by monoclonal gammopathy that mimics immune-complex glomerulonephritis. We retrospectively identified 37 patients, most of whom were white (81%), female (62%), or older than 50 yr (65%). At presentation, 49% had nephrotic syndrome, 68% had renal insufficiency, and 77% had hematuria. In 30% of the patients, we identified a monoclonal serum protein with the same heavy- and light-chain isotypes as the glomerular deposits (mostly IgG1 or IgG2), but only one patient had myeloma. Histologic patterns were predominantly membranoproliferative (57%) or endocapillary proliferative (35%) with membranous features. Electron microscopy revealed granular, nonorganized deposits, and immunofluorescence demonstrated glomerular deposits that stained for a single light-chain isotype and a single heavy-chain subtype, most commonly IgG3kappa (53%). During an average of 30.3 mo of follow-up for 32 patients with available data, 38% had complete or partial recovery, 38% had persistent renal dysfunction, and 22% progressed to ESRD. Correlates of ESRD on univariate analysis were higher creatinine at biopsy, percentage of glomerulosclerosis, and degree of interstitial fibrosis but not immunomodulatory treatment or presence of a monoclonal spike. On multivariate analysis, higher percentage of glomerulosclerosis was the only independent predictor of ESRD. Only one patient lacking a monoclonal spike at presentation subsequently developed a monoclonal spike and no patient with a monoclonal spike at presentation subsequently developed a hematologic malignancy. We conclude that proliferative glomerulonephritis with monoclonal IgG deposits does not seem to be a precursor of myeloma in the vast majority of patients.
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            Proliferative glomerulonephritis with monoclonal IgG deposits: a distinct entity mimicking immune-complex glomerulonephritis.

            Samih Nasr, Pierre Aucouturier, M. Stokes … (2003)
            Renal disease related to the deposition of monoclonal immunoglobulins containing both heavy and light chains can occur in type 1 cryoglobulinemia, Randall type light and heavy chain deposition disease (LHCDD), and immunotactoid glomerulonephritis. We report a novel phenotype of glomerular injury that does not conform to any of the previously described patterns of glomerular involvement by monoclonal gammopathy. Ten cases of unclassifiable proliferative glomerulonephritis manifesting glomerular monoclonal immunoglobulin G (IgG) deposits were identified retrospectively from the archives of the Renal Pathology Laboratory of Columbia University over the past 3 years (biopsy incidence 0.21%). The monoclonal immunoglobulins formed granular electron dense deposits in mesangial, subendothelial, and subepithelial sites, mimicking ordinary immune complex-mediated glomerulonephritis and producing a diffuse endocapillary proliferative or membranoproliferative glomerulonephritis. However, by immunofluorescence, the deposits were monoclonal, staining for a single light chain isotype and a single gamma subclass (including two IgG1kappa, one IgG1lambda, one IgG2lambda, four IgG3kappa, and one IgG3lambda). All cases stained for the three constant domains of the gamma heavy chain (CH1, CH2, and CH3), suggesting deposition of a nondeleted immunoglobulin molecule. Tissue fixation of complement was observed in 90% of cases, and 40% of patients had hypocomplementemia. Clinical presentations included renal insufficiency in 80% (mean serum creatinine 2.8 mg/dL, range 0.9 to 8.0), proteinuria in 100% (mean urine protein 5.8 g/day; range 1.9 to 13.0), nephrotic syndrome in 44%, and microhematuria in 60%. A monoclonal serum protein with the same heavy and light chain isotype as that of the glomerular deposits was identified in 50% of cases (including three IgGkappa and two IgGlambda); however, no patient had clinical or laboratory features of type 1 cryoglobulinemia. No patient had overt myeloma or lymphoma at presentation or over the course of follow-up (mean 12 months). Glomerular deposition of monoclonal IgG can produce a proliferative glomerulonephritis that mimics immune-complex glomerulonephritis by light and electron microscopy. Proper recognition of this entity requires confirmation of monoclonality by staining for the gamma heavy chain subclasses.
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              Posttransplant recurrence of primary glomerulonephritis.

              Claudio Ponticelli, Richard Glassock (2010)
              All forms of primary GN may recur after kidney transplantation and potentially jeopardize the survival of the graft. IgA nephritis (IgAN) may recur in approximately one third of patients, more frequently in younger patients and in those with a rapid progression of the original disease. However, with the exception of few patients with rapid progression, there is no evidence that recurrence of IgAN has a deleterious effect on graft survival at least up to 10 years. Recurrence of focal segmental glomerulosclerosis (FSGS) is often associated with nephrotic proteinuria and is more frequent in children, in patients with rapid progression of the original disease, and in those who lost a previous transplant from recurrence. The natural course of recurrent FSGS is usually unfavorable. Early and intensive plasmapheresis may obtain complete or partial response in several patients. Good results have also been reported with rituximab. Idiopathic membranous nephropathy (IMN) may recur in 30% to 40% of patients. The graft survival in patients with IMN is not different than that of patients with other renal diseases. Good results with rituximab have been reported. Membranoproliferative GN (MPGN) may recur in 27% to 65% of patients. The recurrence is more frequent and the prognosis is more severe in type II MPGN. Although recurrent GN is relatively frequent and may worsen the outcome of renal allografts in some patients, its effect is diluted by several other risk-factors that may have a greater effect than recurrent GN on the long-term graft survival.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Kidney J
                Journal ID (iso-abbrev): Clin Kidney J
                Journal ID (publisher-id): ckj
                Title: Clinical Kidney Journal
                Publisher: Oxford University Press
                ISSN (Print): 2048-8505
                ISSN (Electronic): 2048-8513
                Publication date (Print): June 2017
                Publication date (Electronic): 22 March 2017
                Publication date PMC-release: 22 March 2017
                Volume: 10
                Issue: 3
                Pages: 405-410
                Affiliations
                [1 ]Division of Kidney Disease and Hypertension, Department of Medicine, Rhode Island Hospital, Providence, RI, USA
                [2 ]Alpert Medical School, Brown University, Providence, RI, USA
                [3 ]University of Pennsylvania, Philadelphia, PA, USA
                [4 ]Department of Pathology, University of Chicago, Chicago, IL, USA
                Author notes
                Correspondence and offprint requests to: Basma Merhi; E-mail: bmerhi@ 123456lifespan.org
                Article
                Publisher ID: sfx001
                DOI: 10.1093/ckj/sfx001
                PMC ID: 5466084
                PubMed ID: 28616219
                SO-VID: be5ff26b-0f0b-4b68-892d-1e492fa8843b
                Copyright © © The Author 2017. Published by Oxford University Press on behalf of ERA-EDTA.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                Date received : 27 September 2016
                Date accepted : 29 December 2016
                Page count
                Pages: 6
                Categories
                Subject: Transplantation

                ScienceOpen disciplines: Nephrology
                Keywords: glomerulonephritis,graft function,graft survival,kidney biopsy,kidney transplantation,rituximab
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: glomerulonephritis, graft function, graft survival, kidney biopsy, kidney transplantation, rituximab

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