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[PMID]: 29510921
[Au] Autor:Gu QH; Jia XY; Hu SY; Wang SX; Zou WZ; Cui Z; Zhao MH
[Ad] Address:Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China; Institute of Nephrology, Peking University, Beijing, China; Key Laboratory of Renal Disease, Ministry of Health of China, Beijing, China; Key Laboratory of CKD Prevention and Treatment, Ministry of Education of
[Ti] Title:The Clinical and Immunologic Features of Patients With Combined Anti-GBM Disease and Castleman Disease.
[So] Source:Am J Kidney Dis;, 2018 Mar 03.
[Is] ISSN:1523-6838
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Patients with both anti-glomerular basement membrane (anti-GBM) disease and Castleman disease have been rarely reported. In this study, we report 3 patients with this combination. They had immunologic features similar to patients with classic anti-GBM disease. Sera from the 3 patients recognized the noncollagenous (NC) domain of the α3 chain of type IV collagen (α3(IV)NC1) and its 2 major epitopes, EA and EB. All 4 immunogloblin G (IgG) subclasses against α3(IV)NC1 were detectable, with predominance of IgG1. In one patient with lymph node biopsy specimens available, sporadic plasma cells producing α3(IV)NC1-IgG were found, suggesting a causal relationship between the 2 diseases. One patient, who achieved remission with antibody clearance and normalization of serum creatinine and interleukin 6 concentrations after plasma exchange and 3 cycles of chemotherapy, experienced recurrence of anti-GBM antibodies and an increase in interleukin 6 concentration after chemotherapy discontinuation because of adverse effects, but both returned to normal after another cycle of chemotherapy. This clinical course and the pathologic findings support the hypothesis that the Castleman disease-associated tumor cells are the source of the anti-GBM autoantibodies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher

  2 / 2497 MEDLINE  
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[PMID]: 28467828
[Au] Autor:Ooi JD; Petersen J; Tan YH; Huynh M; Willett ZJ; Ramarathinam SH; Eggenhuizen PJ; Loh KL; Watson KA; Gan PY; Alikhan MA; Dudek NL; Handel A; Hudson BG; Fugger L; Power DA; Holt SG; Coates PT; Gregersen JW; Purcell AW; Holdsworth SR; La Gruta NL; Reid HH; Rossjohn J; Kitching AR
[Ad] Address:Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria 3168, Australia.
[Ti] Title:Dominant protection from HLA-linked autoimmunity by antigen-specific regulatory T cells.
[So] Source:Nature;545(7653):243-247, 2017 05 11.
[Is] ISSN:1476-4687
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Susceptibility and protection against human autoimmune diseases, including type I diabetes, multiple sclerosis, and Goodpasture disease, is associated with particular human leukocyte antigen (HLA) alleles. However, the mechanisms underpinning such HLA-mediated effects on self-tolerance remain unclear. Here we investigate the molecular mechanism of Goodpasture disease, an HLA-linked autoimmune renal disorder characterized by an immunodominant CD4 T-cell self-epitope derived from the α3 chain of type IV collagen (α3 ). While HLA-DR15 confers a markedly increased disease risk, the protective HLA-DR1 allele is dominantly protective in trans with HLA-DR15 (ref. 2). We show that autoreactive α3 -specific T cells expand in patients with Goodpasture disease and, in α3 -immunized HLA-DR15 transgenic mice, α3 -specific T cells infiltrate the kidney and mice develop Goodpasture disease. HLA-DR15 and HLA-DR1 exhibit distinct peptide repertoires and binding preferences and present the α3 epitope in different binding registers. HLA-DR15-α3 tetramer T cells in HLA-DR15 transgenic mice exhibit a conventional T-cell phenotype (T ) that secretes pro-inflammatory cytokines. In contrast, HLA-DR1-α3 tetramer T cells in HLA-DR1 and HLA-DR15/DR1 transgenic mice are predominantly CD4 Foxp3 regulatory T cells (T cells) expressing tolerogenic cytokines. HLA-DR1-induced T cells confer resistance to disease in HLA-DR15/DR1 transgenic mice. HLA-DR15 and HLA-DR1 healthy human donors display altered α3 -specific T-cell antigen receptor usage, HLA-DR15-α3 tetramer Foxp3 T and HLA-DR1-α3 tetramer Foxp3 CD25 CD127 T dominant phenotypes. Moreover, patients with Goodpasture disease display a clonally expanded α3 -specific CD4 T-cell repertoire. Accordingly, we provide a mechanistic basis for the dominantly protective effect of HLA in autoimmune disease, whereby HLA polymorphism shapes the relative abundance of self-epitope specific T cells that leads to protection or causation of autoimmunity.
[Mh] MeSH terms primary: Anti-Glomerular Basement Membrane Disease/immunology
Autoimmunity/immunology
T-Lymphocytes, Regulatory/immunology
[Mh] MeSH terms secundary: Animals
Anti-Glomerular Basement Membrane Disease/pathology
Base Sequence
CD4-Positive T-Lymphocytes/immunology
Collagen Type IV/chemistry
Collagen Type IV/immunology
Cytokines/immunology
Female
Forkhead Transcription Factors/metabolism
HLA-DR Serological Subtypes/immunology
HLA-DR1 Antigen/immunology
Humans
Immunodominant Epitopes
Male
Mice
Mice, Transgenic
Models, Molecular
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Collagen Type IV); 0 (Cytokines); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (HLA-DR Serological Subtypes); 0 (HLA-DR1 Antigen); 0 (HLA-DR15 antigen); 0 (Immunodominant Epitopes)
[Em] Entry month:1709
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[Js] Journal subset:IM
[Da] Date of entry for processing:170504
[St] Status:MEDLINE
[do] DOI:10.1038/nature22329

  3 / 2497 MEDLINE  
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[PMID]: 29453850
[Au] Autor:Tecklenborg J; Clayton D; Siebert S; Coley SM
[Ad] Address:School of Medicine, University of Glasgow, Glasgow, UK.
[Ti] Title:The role of the immune system in kidney disease.
[So] Source:Clin Exp Immunol;, 2018 Feb 17.
[Is] ISSN:1365-2249
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The immune system and the kidneys are closely linked. In health the kidneys contribute to immune homeostasis, while components of the immune system mediate many acute forms of renal disease and play a central role in progression of chronic kidney disease. A dysregulated immune system can have either direct or indirect renal effects. Direct immune-mediated kidney diseases are usually a consequence of autoantibodies directed against a constituent renal antigen, such as collagen IV in anti-glomerular basement membrane disease. Indirect immune-mediated renal disease often follows systemic autoimmunity with immune complex formation, but can also be due to uncontrolled activation of the complement pathways. Though the range of mechanisms of immune dysregulation leading to renal disease is broad, the pathways leading to injury are similar. Loss of immune homeostasis in renal disease results in perpetual immune cell recruitment and worsening damage to the kidney. Uncoordinated attempts at tissue repair, after immune-mediated disease or non-immune mediated injury, result in fibrosis of structures important for renal function, eventually leading to kidney failure. As renal disease often only manifests clinically when substantial damage has already occurred, new diagnostic methods and indeed treatments must be identified to inhibit further progression and promote appropriate tissue repair. Studying cases in which immune homeostasis is re-established may reveal new treatment possibilities. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180217
[Lr] Last revision date:180217
[St] Status:Publisher
[do] DOI:10.1111/cei.13119

  4 / 2497 MEDLINE  
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[PMID]: 29275837
[Au] Autor:Krebs CF; Panzer U
[Ad] Address:III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Germany. Electronic address: c.krebs@uke.de.
[Ti] Title:Plasticity and heterogeneity of Th17 in immune-mediated kidney diseases.
[So] Source:J Autoimmun;87:61-68, 2018 Feb.
[Is] ISSN:1095-9157
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Anti-neutrophil cytoplasmatic antibody (ANCA)-associated glomerulonephritis, anti-glomerular basement membrane (GBM) glomerulonephritis and lupus nephritis are the most common causes of rapid progressive glomerulonephritis (RPGN) in the Western world. These aggressive forms of autoimmune kidney diseases significantly contribute to end-stage renal disease and are associated with high morbidity and mortality. Moreover, patients show significant heterogeneity with respect to clinical outcome and response to therapy. T cell infiltration is a morphological hallmark of RPGN and it is a critical driver of kidney injury. Different CD4 T cell subsets that are endowed with distinct regulatory and effector functions are involved in this detrimental inflammatory process. In particular, the identification and functional characterization of IL-17-expressing CD4 Th17 cells have substantially advanced our understanding of organ-specific autoimmunity. In experimental models of crescentic and proliferative GN, including ANCA-associated GN, anti-GBM-GN and lupus nephritis, the Th17/IL-17 axis significantly contributes to renal tissue damage. In patients with ANCA-associated GN or lupus nephritis, IL-17 serum levels correlated with disease activity. Moreover, Th17 cells are present in the kidneys of these patients and represents a topic of intense ongoing clinical and basic research. Importantly, recent studies have challenged the view of CD4 T cells subsets as terminally differentiated homogenous cells, showing that T cells, in particular Th17 cells, are much more flexible and heterogeneous than previously thought. However, analysis of Th17 cell fate in mouse models of autoimmune kidney disease revealed a high degree of stability within these cells, an observation that is in contrast to Th17 cells in other models of autoimmune diseases including experimental autoimmune encephalomyelitis. Interestingly, anti-CD3 treatment interferes with stable Th17 cells and induces a potential regulatory phenotype in Th17 cells, highlighting the therapeutic potential of targeting pathogenic Th17 cells in autoimmunity. In this review, we discuss the current knowledge of Th17 cell plasticity and heterogeneity in autoimmune kidney diseases with a special focus on the underlying mechanisms of this process and debate if Th17 cell plasticity is beneficial or harmful to renal inflammation.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1712
[Cu] Class update date: 180206
[Lr] Last revision date:180206
[St] Status:In-Data-Review

  5 / 2497 MEDLINE  
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[PMID]: 28459999
[Au] Autor:Henderson SR; Salama AD
[Ad] Address:Centre for Nephrology, Division of Medicine, University College London, Royal Free Hospital, London, UK.
[Ti] Title:Diagnostic and management challenges in Goodpasture's (anti-glomerular basement membrane) disease.
[So] Source:Nephrol Dial Transplant;33(2):196-202, 2018 Feb 01.
[Is] ISSN:1460-2385
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Goodpasture's or anti-glomerular basement membrane (GBM) disease is classically characterized by the presence of circulating autoantibodies directed against the non-collagenous domain of the α3 chain of type IV collagen, targeting glomerular and alveolar basement membranes, and associated with rapidly progressive crescentic glomerulonephritis, with alveolar haemorrhage in over half the patients. However, there are increasing examples of variants or atypical presentations of this disease, and novel therapeutic options have been proposed, which nephrologists should be aware of. The pathophysiology of this condition has been understood through molecular analysis of the antibody-antigen interactions and the use of human leucocyte antigen-transgenic animals, while the association of anti-GBM antibodies with anti-neutrophil cytoplasm antibodies and their combined impact on disease phenotype is increasingly recognized, providing some insights into the basis of glomerular damage and autoimmunity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1705
[Cu] Class update date: 180205
[Lr] Last revision date:180205
[St] Status:In-Data-Review
[do] DOI:10.1093/ndt/gfx057

  6 / 2497 MEDLINE  
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[PMID]: 29293138
[Au] Autor:Holt E; Gough A; Prasad P; Chowdhury FU
[Ti] Title:18F-FDG PET/CT Imaging of Necrotizing Crescentic Glomerulonephritis With Anti-Glomerular Basement Membrane Disease.
[So] Source:Clin Nucl Med;43(3):e96-e97, 2018 Mar.
[Is] ISSN:1536-0229
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A 30-year-old woman presented with lethargy, night sweats, and fever with raised inflammatory markers. Anti-neutrophil cytoplasmic antibody was negative. Abdominopelvic CT was unremarkable. Subsequently, she underwent FDG PET/CT showing globally enlarged kidneys with diffuse hypermetabolic activity within the renal parenchyma bilaterally. Renal biopsies showed morphologic features of an active necrotizing crescentic glomerulonephritis, which was confirmed clinically and treated. This case demonstrates the role that FDG PET/CT can play in inflammatory conditions, such as glomerulonephritis, where it may be clinically useful when the presentation is atypical.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180201
[Lr] Last revision date:180201
[St] Status:In-Process
[do] DOI:10.1097/RLU.0000000000001960

  7 / 2497 MEDLINE  
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[PMID]: 29288482
[Au] Autor:Fijolek J; Wiatr E; Jakubowska L; Polubiec-Kownacka M; Kuca P; Roszkowski-Sliz K
[Ad] Address:The Third Department of Pneumonology,, Warsaw, Poland. jfijolek@op.pl.
[Ti] Title:Diffuse alveolar haemorrhage complicated by pulmonary embolism - problems with treatment.
[So] Source:Adv Respir Med;85(6):328-332, 2017.
[Is] ISSN:2451-4934
[Cp] Country of publication:Poland
[La] Language:eng
[Ab] Abstract:Diffuse alveolar haemorrhage (DAH) refers to a clinical syndrome resulting from injury of the alveolar capillaries, arterioles and venules leading to red blood cel accumulation in the distal air spaces. The conditions associated with DAH and underlying disease determine the prognosis and the treatment regimen. The coexistence of DAH with venous thromboembolism (VTE) is a seroius problem for clinicians and poses a challenge in the therapeutic management. We describe a young patient who developed massive DAH in the course of anti-glomerular basement membrane (anti-GBM) disease (formerly called Goodpasture's syndrome) complicated by pulmonary embolism (PE).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 171230
[Lr] Last revision date:171230
[St] Status:In-Process
[do] DOI:10.5603/ARM.2017.0056

  8 / 2497 MEDLINE  
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[PMID]: 29265054
[Au] Autor:Annamalai I; Chandramohan G; Srinivasa Prasad ND; Fernando E; Sujith S
[Ad] Address:Department of Nephrology, Government Stanley Hospital, Chennai, Tamil Nadu, India.
[Ti] Title:Rapidly progressive glomerulonephritis due to anti-glomerular basement membrane disease accompanied by IgA nephropathy: An unusual association.
[So] Source:Saudi J Kidney Dis Transpl;28(6):1404-1407, 2017 Nov-Dec.
[Is] ISSN:1319-2442
[Cp] Country of publication:Saudi Arabia
[La] Language:eng
[Ab] Abstract:Anti-glomerular basement membrane (anti-GBM) disease is a systemic autoimmune disorder characterized by circulating IgG antibodies (rarely IgA and IgM) to the carboxyterminal, noncollagenous 1 (NC1) domain of type IV collagen of GBM also known as Goodpasture antigen. Patients typically present with rapidly progressive glomerulonephritis (RPGN) and pulmonary hemorrhage in the presence of which it is referred to as Goodpasture's disease. Anti-GBM disease has been reported to coexist with pauci-immune antineutrophil cytoplasmic autoantibody-positive glomerulonephritis and membranous glomerulopathy. The sequential or concurrent presentation of anti-GBM disease with IgA nephropathy has been rarely described. We herein report a case of a 22-year-old female who presented with RPGN, and renal biopsy revealed crescentic glomerulonephritis with strong linear IgG (+2) staining of GBM and extensive mesangial IgA (+3) deposits. The patient was treated with three pulses of IV methylprednisolone followed by oral steroids. Plasmapheresis and cytotoxic agents were not included in the therapeutic armamentarium as the patient had no pulmonary hemorrhage and biopsy revealed established chronic changes. The association of anti-GBM disease with IgA nephropathy could open up new vistas on the implication of these IgA mesangial deposits in the pathogenesis and prognosis of anti-GBM disease.
[Pt] Publication type:CASE REPORTS
[Em] Entry month:1712
[Cu] Class update date: 171221
[Lr] Last revision date:171221
[St] Status:In-Data-Review
[do] DOI:10.4103/1319-2442.220866

  9 / 2497 MEDLINE  
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[PMID]: 27772636
[Au] Autor:Fogo AB; Lusco MA; Najafian B; Alpers CE
[Ad] Address:Department of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, TN. Electronic address: agnes.fogo@vanderbilt.edu.
[Ti] Title:AJKD Atlas of Renal Pathology: Anti-Glomerular Basement Membrane Antibody-Mediated Glomerulonephritis.
[So] Source:Am J Kidney Dis;68(5):e29-e30, 2016 Nov.
[Is] ISSN:1523-6838
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Anti-Glomerular Basement Membrane Disease/pathology
Glomerular Basement Membrane/pathology
Kidney/pathology
[Mh] MeSH terms secundary: Anti-Glomerular Basement Membrane Disease/metabolism
Bowman Capsule/metabolism
Bowman Capsule/pathology
Bowman Capsule/ultrastructure
Complement C3/metabolism
Glomerular Basement Membrane/metabolism
Glomerular Basement Membrane/ultrastructure
Humans
Immunoglobulin A/metabolism
Immunoglobulin G/metabolism
Immunoglobulin M/metabolism
Kidney/metabolism
Kidney/ultrastructure
Microscopy
Microscopy, Electron
Microscopy, Fluorescence
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Complement C3); 0 (Immunoglobulin A); 0 (Immunoglobulin G); 0 (Immunoglobulin M)
[Em] Entry month:1712
[Cu] Class update date: 171205
[Lr] Last revision date:171205
[Js] Journal subset:IM
[Da] Date of entry for processing:161025
[St] Status:MEDLINE

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[PMID]: 29162595
[Au] Autor:van Daalen EE; Jennette JC; McAdoo SP; Pusey CD; Alba MA; Poulton CJ; Wolterbeek R; Nguyen TQ; Goldschmeding R; Alchi B; Griffiths M; de Zoysa JR; Vincent B; Bruijn JA; Bajema IM
[Ad] Address:Departments of Pathology and e.e.van_daalen@lumc.nl.
[Ti] Title:Predicting Outcome in Patients with Anti-GBM Glomerulonephritis.
[So] Source:Clin J Am Soc Nephrol;, 2017 Nov 21.
[Is] ISSN:1555-905X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND OBJECTIVES: Large studies on long-term kidney outcome in patients with anti-glomerular basement membrane (anti-GBM) GN are lacking. This study aimed to identify clinical and histopathologic parameters that predict kidney outcome in these patients. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This retrospective analysis included a total of 123 patients with anti-GBM GN between 1986 and 2015 from six centers worldwide. Their kidney biopsy samples were classified according to the histopathologic classification for ANCA-associated GN. Clinical data such as details of treatment were retrieved from clinical records. The primary outcome parameter was the occurrence of ESRD. Kidney survival was analyzed using the log-rank test and Cox regression analyses. RESULTS: The 5-year kidney survival rate was 34%, with an improved rate observed among patients diagnosed after 2007 ( =0.01). In patients with anti-GBM GN, histopathologic class and kidney survival were associated ( <0.001). Only one of 15 patients with a focal class biopsy sample (≥50% normal glomeruli) developed ESRD. Patients with a sclerotic class biopsy sample (≥50% globally sclerotic glomeruli) and patients with 100% cellular crescents did not recover from dialysis dependency at presentation. In multivariable analysis, dialysis dependency at presentation (hazard ratio [HR], 3.17; 95% confidence interval [95% CI], 1.59 to 6.32), percentage of normal glomeruli (HR, 0.97; 95% CI, 0.95 to 0.99), and extent of interstitial infiltrate (HR, 2.02; 95% CI, 1.17 to 3.50) were predictors of ESRD during follow-up. CONCLUSIONS: Dialysis dependency, low percentage of normal glomeruli, and large extent of interstitial infiltrate are associated with poor kidney outcome in anti-GBM GN. Kidney outcome has improved during recent years; the success rate doubled after 2007. PODCAST: This article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2017_11_21_CJASNPodcast_18_1_v.mp3.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171122
[Lr] Last revision date:171122
[St] Status:Publisher


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