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      Successful Treatment of Infectious Endocarditis Associated Glomerulonephritis Mimicking C3 Glomerulonephritis in a Case with No Previous Cardiac Disease

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          Abstract

          We report a 42-year-old man with subacute infectious endocarditis (IE) with septic pulmonary embolism, presenting rapidly progressive glomerulonephritis and positive proteinase 3-anti-neutrophil cytoplasmic antibody (PR3-ANCA). He had no previous history of heart disease. Renal histology revealed diffuse endocapillary proliferative glomerulonephritis with complement 3- (C3-) dominant staining and subendothelial electron dense deposit, mimicking C3 glomerulonephritis. Successful treatment of IE with valve plastic surgery gradually ameliorated hypocomplementemia and renal failure; thus C3 glomerulonephritis-like lesion in this case was classified as postinfectious glomerulonephritis. IE associated glomerulonephritis is relatively rare, especially in cases with no previous history of valvular disease of the heart like our case. This case also reemphasizes the broad differential diagnosis of renal involvement in IE.

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          Most cited references22

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          C3 glomerulopathy: consensus report

          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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            C3 glomerulopathy: a new classification.

            Several distinct pathological patterns of glomerular inflammation are associated with abnormal regulation of the complement system, specifically, with dysregulation of the alternative pathway of the complement system. However, these conditions share the pathological finding of complement C3 (C3) deposited within the glomerulus in the absence of substantial immunoglobulin. This finding has alerted us and others to the possible presence of genetic and acquired complement dysregulation in individual patients. This article summarizes our current understanding of the relationship between dysregulation of the complement system and glomerular inflammation. Here, we suggest that glomerular pathologies that are characterized by the isolated deposition of C3 could usefully be classified by the term C3 glomerulopathy. In our view, this classification would alert the pathologist and nephrologist to the importance of screening for acquired and genetic abnormalities in complement regulation. In the future, it could help to identify individuals who might benefit from therapeutic inhibition of the complement system.
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              Atypical post-infectious glomerulonephritis is associated with abnormalities in the alternative pathway of complement

              Post-infectious glomerulonephritis is a common disorder that develops following an infection. In the majority of cases, there is complete recovery of renal function within a few days to weeks following resolution of the infection. In a small percentage of patients, however, the glomerulonephritis takes longer to resolve resulting in persistent hematuria and proteinuria, or even progression to end-stage kidney disease. In some cases of persistent hematuria and proteinuria, kidney biopsies show findings of a post-infectious glomerulonephritis even in the absence of any evidence of a preceding infection. The cause of such ‘atypical’ post-infectious glomerulonephritis, with or without evidence of preceding infection, is unknown. Here, we show that most patients diagnosed with this ‘atypical’ post-infectious glomerulonephritis have an underlying defect in the regulation of the alternative pathway of complement. These defects include mutations in complement regulating proteins and antibodies to the C3 convertase known as C3 nephritic factors. As a result, the activated alternative pathway is not brought under control even after resolution of the infection. Hence, the sequela is continual glomerular deposition of complement factors with resultant inflammation and development of an ‘atypical’ post-infectious glomerulonephritis.
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                Author and article information

                Journal
                Case Rep Nephrol
                Case Rep Nephrol
                CRIN
                Case Reports in Nephrology
                Hindawi Publishing Corporation
                2090-6641
                2090-665X
                2014
                23 November 2014
                : 2014
                : 569047
                Affiliations
                1Department of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605, Japan
                2Department of Pathology, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605, Japan
                3Yamaguchi's Pathology Laboratory, 20-31-1 Minoridai, Matsudo-shi, Chiba 270-2231, Japan
                Author notes

                Academic Editor: Kouichi Hirayama

                Author information
                http://orcid.org/0000-0003-2803-9161
                http://orcid.org/0000-0003-0486-3965
                Article
                10.1155/2014/569047
                4259083
                25506445
                4f226f46-3b93-4b12-ac7f-958a6b8f1055
                Copyright © 2014 Yosuke Kawamorita et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 14 August 2014
                : 6 November 2014
                Categories
                Case Report

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