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      Monoclonal gammopathy of renal significance: Diagnostic workup

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          Abstract

          The clinical spectrum of diseases associated with monoclonal gammopathies is wide and they are most commonly the consequence of renal deposition of monoclonal immunoglobulin or its components. The differential diagnosis is difficult and renal biopsy is essential. To distinguish many of these pathologies is necessary to use techniques that are not always available, even in tertiary central hospitals. This review will discuss the clinical presentation, pathologic features, treatment, prognosis and common diagnostic difficulties of these entities.

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          C3 glomerulopathy: consensus report

          Matthew C. Pickering, Vivette D. D'Agati, Carla Nester … (2013)
          C3 glomerulopathy is a recently introduced pathological entity whose original definition was glomerular pathology characterized by C3 accumulation with absent or scanty immunoglobulin deposition. In August 2012, an invited group of experts (comprising the authors of this document) in renal pathology, nephrology, complement biology, and complement therapeutics met to discuss C3 glomerulopathy in the first C3 Glomerulopathy Meeting. The objectives were to reach a consensus on: the definition of C3 glomerulopathy, appropriate complement investigations that should be performed in these patients, and how complement therapeutics should be explored in the condition. This meeting report represents the current consensus view of the group.
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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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              Amyloidosis-associated kidney disease.

              Laura Dember (2006)
              The amyloidoses are a group of disorders in which soluble proteins aggregate and deposit extracellularly in tissues as insoluble fibrils, causing progressive organ dysfunction. The kidney is one of the most frequent sites of amyloid deposition in AL, AA, and several of the hereditary amyloidoses. Amyloid fibril formation begins with the misfolding of an amyloidogenic precursor protein. The misfolded variants self-aggregate in a highly ordered manner, generating protofilaments that interact to form fibrils. The fibrils have a characteristic appearance by electron microscopy and generate birefringence under polarized light when stained with Congo red dye. Advances in elucidating the mechanisms of amyloid fibril formation, tissue deposition, and tissue injury have led to new and more aggressive treatment approaches for these disorders. This article reviews the pathogenesis, diagnosis, clinical manifestations, and treatment of the amyloidoses, focusing heavily on the renal aspects of each of these areas.
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                Author and article information

                Journal
                Journal ID (nlm-ta): World J Nephrol
                Journal ID (publisher-id): WJN
                Title: World Journal of Nephrology
                Publisher: Baishideng Publishing Group Inc
                ISSN (Electronic): 2220-6124
                Publication date (Print): 6 March 2017
                Publication date (Electronic): 6 March 2017
                Volume: 6
                Issue: 2
                Pages: 72-78
                Affiliations
                Sofia O Correia, Sofia Santos, Jorge Malheiro, António Cabrita, La Salete Martins, Josefina Santos, Nephrology and Transplant Department, Centro Hospitalar do Porto, 4099-001 Porto, Portugal
                Author notes

                Author contributions: All authors equally contributed to this paper with literature review, critical revision and editing, and final approval of the final version.

                Correspondence to: Sofia O Correia, MD, Nephrology and Transplant Department, Centro Hospitalar do Porto, Largo Prof.Abel Salazar, 4099-001 Porto, Portugal. soacorreia@ 123456gmail.com

                Telephone: +351-222-077500 Fax: +351-222-033189

                Article
                Other ID: jWJN.v6.i2.pg72
                DOI: 10.5527/wjn.v6.i2.72
                PMC ID: 5339639
                SO-VID: 001d818c-6794-42e5-8b0b-694ce6a046ee
                Copyright © ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
                License:

                Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

                History
                Date received : 25 August 2016
                Date revision received : 28 December 2016
                Date accepted : 11 January 2017
                Categories
                Subject: Minireviews

                Keywords: algorithm,immunoglobulin,monoclonal gammopathy of renal significance,m protein,monoclonal gammopathy of undetermined significance
                Data availability:
                Keywords: algorithm, immunoglobulin, monoclonal gammopathy of renal significance, m protein, monoclonal gammopathy of undetermined significance

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