Validation of distinct pathogenic patterns in a cohort of membranoproliferative glomerulonephritis patients by cluster analysis
BackgroundA novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated membranoproliferative glomerulonephritis. Our aim was to replicate these observations in an independent cohort and elucidate disease pathophysiology with detailed...
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| Published in | Clinical Kidney Journal Vol. 13; no. 2; pp. 225 - 234 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Oxford University Press (OUP)
01.04.2020
Oxford University Press |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2048-8505 2048-8513 |
| DOI | 10.1093/ckj/sfz073 |
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| Abstract | BackgroundA novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated membranoproliferative glomerulonephritis. Our aim was to replicate these observations in an independent cohort and elucidate disease pathophysiology with detailed analysis of functional complement markers.MethodsA total of 92 patients with clinical, histological, complement and genetic data were involved in the study, and hierarchical cluster analysis was done by Ward method, where four clusters were generated.ResultsHigh levels of sC5b-9 (soluble membrane attack complex), low serum C3 levels and young age at onset (13 years) were characteristic for Cluster 1 with a high prevalence of likely pathogenic variations (LPVs) and C3 nephritic factor, whereas for Cluster 2—which is not reliable because of the small number of cases—strong immunoglobulin G staining, low C3 levels and high prevalence of nephritic syndrome at disease onset were observed. Low plasma sC5b-9 levels, decreased C3 levels and high prevalence of LPV and sclerotic glomeruli were present in Cluster 3, and patients with late onset of the disease (median: 39.5 years) and near-normal C3 levels in Cluster 4. A significant difference was observed in the incidence of end-stage renal disease during follow-up between the different clusters. Patients in Clusters 3–4 had worse renal survival than patients in Clusters 1–2.ConclusionsOur results confirm the main findings of the original cluster analysis and indicate that the observed, distinct pathogenic patterns are replicated in our cohort. Further investigations are necessary to analyse the distinct biological and pathogenic processes in these patient groups. |
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| AbstractList | A novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated membranoproliferative glomerulonephritis. Our aim was to replicate these observations in an independent cohort and elucidate disease pathophysiology with detailed analysis of functional complement markers.BACKGROUNDA novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated membranoproliferative glomerulonephritis. Our aim was to replicate these observations in an independent cohort and elucidate disease pathophysiology with detailed analysis of functional complement markers.A total of 92 patients with clinical, histological, complement and genetic data were involved in the study, and hierarchical cluster analysis was done by Ward method, where four clusters were generated.METHODSA total of 92 patients with clinical, histological, complement and genetic data were involved in the study, and hierarchical cluster analysis was done by Ward method, where four clusters were generated.High levels of sC5b-9 (soluble membrane attack complex), low serum C3 levels and young age at onset (13 years) were characteristic for Cluster 1 with a high prevalence of likely pathogenic variations (LPVs) and C3 nephritic factor, whereas for Cluster 2-which is not reliable because of the small number of cases-strong immunoglobulin G staining, low C3 levels and high prevalence of nephritic syndrome at disease onset were observed. Low plasma sC5b-9 levels, decreased C3 levels and high prevalence of LPV and sclerotic glomeruli were present in Cluster 3, and patients with late onset of the disease (median: 39.5 years) and near-normal C3 levels in Cluster 4. A significant difference was observed in the incidence of end-stage renal disease during follow-up between the different clusters. Patients in Clusters 3-4 had worse renal survival than patients in Clusters 1-2.RESULTSHigh levels of sC5b-9 (soluble membrane attack complex), low serum C3 levels and young age at onset (13 years) were characteristic for Cluster 1 with a high prevalence of likely pathogenic variations (LPVs) and C3 nephritic factor, whereas for Cluster 2-which is not reliable because of the small number of cases-strong immunoglobulin G staining, low C3 levels and high prevalence of nephritic syndrome at disease onset were observed. Low plasma sC5b-9 levels, decreased C3 levels and high prevalence of LPV and sclerotic glomeruli were present in Cluster 3, and patients with late onset of the disease (median: 39.5 years) and near-normal C3 levels in Cluster 4. A significant difference was observed in the incidence of end-stage renal disease during follow-up between the different clusters. Patients in Clusters 3-4 had worse renal survival than patients in Clusters 1-2.Our results confirm the main findings of the original cluster analysis and indicate that the observed, distinct pathogenic patterns are replicated in our cohort. Further investigations are necessary to analyse the distinct biological and pathogenic processes in these patient groups.CONCLUSIONSOur results confirm the main findings of the original cluster analysis and indicate that the observed, distinct pathogenic patterns are replicated in our cohort. Further investigations are necessary to analyse the distinct biological and pathogenic processes in these patient groups. BackgroundA novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated membranoproliferative glomerulonephritis. Our aim was to replicate these observations in an independent cohort and elucidate disease pathophysiology with detailed analysis of functional complement markers.MethodsA total of 92 patients with clinical, histological, complement and genetic data were involved in the study, and hierarchical cluster analysis was done by Ward method, where four clusters were generated.ResultsHigh levels of sC5b-9 (soluble membrane attack complex), low serum C3 levels and young age at onset (13 years) were characteristic for Cluster 1 with a high prevalence of likely pathogenic variations (LPVs) and C3 nephritic factor, whereas for Cluster 2—which is not reliable because of the small number of cases—strong immunoglobulin G staining, low C3 levels and high prevalence of nephritic syndrome at disease onset were observed. Low plasma sC5b-9 levels, decreased C3 levels and high prevalence of LPV and sclerotic glomeruli were present in Cluster 3, and patients with late onset of the disease (median: 39.5 years) and near-normal C3 levels in Cluster 4. A significant difference was observed in the incidence of end-stage renal disease during follow-up between the different clusters. Patients in Clusters 3–4 had worse renal survival than patients in Clusters 1–2.ConclusionsOur results confirm the main findings of the original cluster analysis and indicate that the observed, distinct pathogenic patterns are replicated in our cohort. Further investigations are necessary to analyse the distinct biological and pathogenic processes in these patient groups. Background. A novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated membranoproliferative glomerulonephritis. Our aim was to replicate these observations in an independent cohort and elucidate disease pathophysiology with detailed analysis of functional complement markers. Methods. A total of 92 patients with clinical, histological, complement and genetic data were involved in the study, and hierarchical cluster analysis was done by Ward method, where four clusters were generated. Results. High levels of sC5b-9 (soluble membrane attack complex), low serum C3 levels and young age at onset (13years) were characteristic for Cluster 1 with a high prevalence of likely pathogenic variations (LPVs) and C3 nephritic factor, whereas for Cluster 2--which is not reliable because of the small number of cases--strong immunoglobulin G staining, low C3 levels and high prevalence of nephritic syndrome at disease onset were observed. Low plasma sC5b-9 levels, decreased C3 levels and high prevalence of LPV and sclerotic glomeruli were present in Cluster 3, and patients with late onset of the disease (median: 39.5 years) and near-normal C3 levels in Cluster 4. A significant difference was observed in the incidence of end-stage renal disease during follow-up between the different clusters. Patients in Clusters 3-4 had worse renal survival than patients in Clusters 1-2. Conclusions. Our results confirm the main findings of the original cluster analysis and indicate that the observed, distinct pathogenic patterns are replicated in our cohort. Further investigations are necessary to analyse the distinct biological and pathogenic processes in these patient groups. Keywords: C3-glomerulopathy, C3-glomerulonephritis, complement, dense deposit disease, membranoproliferative glomerulonephritis A novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated membranoproliferative glomerulonephritis. Our aim was to replicate these observations in an independent cohort and elucidate disease pathophysiology with detailed analysis of functional complement markers. A total of 92 patients with clinical, histological, complement and genetic data were involved in the study, and hierarchical cluster analysis was done by Ward method, where four clusters were generated. High levels of sC5b-9 (soluble membrane attack complex), low serum C3 levels and young age at onset (13 years) were characteristic for Cluster 1 with a high prevalence of likely pathogenic variations (LPVs) and C3 nephritic factor, whereas for Cluster 2-which is not reliable because of the small number of cases-strong immunoglobulin G staining, low C3 levels and high prevalence of nephritic syndrome at disease onset were observed. Low plasma sC5b-9 levels, decreased C3 levels and high prevalence of LPV and sclerotic glomeruli were present in Cluster 3, and patients with late onset of the disease (median: 39.5 years) and near-normal C3 levels in Cluster 4. A significant difference was observed in the incidence of end-stage renal disease during follow-up between the different clusters. Patients in Clusters 3-4 had worse renal survival than patients in Clusters 1-2. Our results confirm the main findings of the original cluster analysis and indicate that the observed, distinct pathogenic patterns are replicated in our cohort. Further investigations are necessary to analyse the distinct biological and pathogenic processes in these patient groups. |
| Audience | Academic |
| Author | Inga Vainumäe Krešimir Galešić Adrian Catalin Lungu Christof Aigner Krisztina Rusai Michael A. Rudnicki Thomas Mueller Anna Pawłowska Ágnes Hartmann Attila Szabo Nóra Garam Mária Sinkó Simona Stancu Stefan Flaschberger Anamarija Meglic Ludmila Podracka Hana Flögelová Maarten Knechtelsdorfer Tamás Szabó Ágnes Szilágyi Alexandra Dumfarth Jürgen Brunner Viktor Janko Miroslav Tisljar György Reusz Eva Sládková Gert Mayer Rina Rus Nóra Klenk Daniel Cejka Ágnes Haris Dóra Bajcsi Johannes Hofer András Tislér Erika Szigeti Tomasz Stompór Martina Gaggl Zoltán Prohászka Tomáš Seeman Dániel Jakab Nika Kojc Gere Sunder-Plassmann Tanja Kersnik-Levart Jakub Zieg Marijan Saraga Romana Rysava Ernesta Macioniene Andreas Heilos Tomas Zaoral Mario Laganović Jana Reiterova Marius Miglinas Andrei Capitanescu Csaba Bereczki Martin Windpessl Alice Schmidt Galia Zlatanova Krisztina Kóbor Kata Kelen Klaus Arbeiter Dorottya Csuka |
| AuthorAffiliation | 12 Department of Pediatrics and Adolescent Medicine , Division of Pediatric Nephrology and Gastroenterology, Medical University of Vienna, Vienna, Austria 14 Research Institute for Developmental Medicine , Johannes Kepler University Linz, Linz, Austria 25 Department of Nephrology , Hypertension and Internal Medicine, School of Medicine, Collegium Medicum, University of Warmia and Mazury, Olsztyn, Poland 28 Nephrology Clinic , 1st Faculty of Medicine, Charles University, Prague, Czech Republic 1 Research Laboratory , 3rd Department of Internal Medicine, Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary 16 Medimapax – Center of Elimination Methods , Bratislava, Slovakia 34 Carol Davila Nephrology Hospital , Bucharest, Romania 26 Department of Pediatrics , Comenius University, Bratislava, Slovakia 33 Department of Pediatrics , Faculty of Medicine, Debrecen University, Debrecen, Hungary 17 1st Department of Pediatrics , Semmelweis University, Budapest, Hungary 35 Department |
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| BackLink | https://cir.nii.ac.jp/crid/1870302167948743168$$DView record in CiNii https://www.ncbi.nlm.nih.gov/pubmed/32296528$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Contributor | Semmelweis Egyetem SE/AOK/K/III. Sz. Belgyógyászati Klinika SE/AOK/K/BHK/MTA-SE Immunológiai és Hematológiai Kutatócsoport |
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| Copyright | The Author(s) 2019. Published by Oxford University Press on behalf of ERA-EDTA. 2019 The Author(s) 2019. Published by Oxford University Press on behalf of ERA-EDTA. COPYRIGHT 2020 Oxford University Press The Author(s) 2019. Published by Oxford University Press on behalf of ERA-EDTA. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Keywords | C3-glomerulonephritis dense deposit disease, membranoproliferative glomerulonephritis complement C3-glomerulopathy |
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| References_xml | – volume: 7 start-page: 265 year: 2012 ident: 2020041009153636600_sfz073-B11 article-title: Causes of alternative pathway dysregulation in dense deposit disease publication-title: Clin J Am Soc Nephrol doi: 10.2215/CJN.07900811 – volume: 118 start-page: 4705 year: 2011 ident: 2020041009153636600_sfz073-B19 article-title: Design and development of TT30, a novel C3d-targeted C3/C5 convertase inhibitor for treatment of human complement alternative pathway-mediated diseases publication-title: Blood doi: 10.1182/blood-2011-06-359646 – volume: 22 start-page: 1551 year: 2011 ident: 2020041009153636600_sfz073-B5 article-title: Allelic variants of complement genes associated with dense deposit disease publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2010080795 – volume: 84 start-page: 1079 year: 2013 ident: 2020041009153636600_sfz073-B3 article-title: C3 glomerulopathy: consensus report publication-title: Kidney Int doi: 10.1038/ki.2013.377 – volume: 27 start-page: 1245 year: 2016 ident: 2020041009153636600_sfz073-B2 article-title: High-throughput genetic testing for thrombotic microangiopathies and C3 glomerulopathies publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2015040385 – volume: 70 start-page: 834 year: 2017 ident: 2020041009153636600_sfz073-B8 article-title: C4 nephritic factors in C3 glomerulopathy: a case series publication-title: Am J Kidney Dis doi: 10.1053/j.ajkd.2017.07.004 – volume: 29 start-page: 9 year: 2018 ident: 2020041009153636600_sfz073-B18 article-title: Clusters not classifications: making sense of complement-mediated kidney injury publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2017111183 – volume: 36 start-page: 517 year: 2016 ident: 2020041009153636600_sfz073-B9 article-title: Testing the activity of complement convertases in serum/plasma for diagnosis of C4NeF-mediated C3 glomerulonephritis publication-title: J Clin Immunol doi: 10.1007/s10875-016-0290-5 – volume: 14 start-page: 205 year: 1984 ident: 2020041009153636600_sfz073-B16 article-title: A micromodification of the CH50 test for the classical pathway of complement publication-title: J Clin Lab Immunol – volume: 29 start-page: 283 year: 2018 ident: 2020041009153636600_sfz073-B15 article-title: Cluster analysis identifies distinct pathogenetic patterns in C3 glomerulopathies/immune complex-mediated membranoproliferative GN publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2017030258 – volume: 71 start-page: 131 year: 2016 ident: 2020041009153636600_sfz073-B1 article-title: Complement gene variants determine the risk of immunoglobulin-associated MPGN and C3 glomerulopathy and predict long-term renal outcome publication-title: Mol Immunol doi: 10.1016/j.molimm.2016.01.010 – volume: 82 start-page: 465 year: 2012 ident: 2020041009153636600_sfz073-B10 article-title: C3 glomerulonephritis: clinicopathological findings, complement abnormalities, glomerular proteomic profile, treatment, and follow-up publication-title: Kidney Int doi: 10.1038/ki.2012.212 – volume: 85 start-page: 450 year: 2014 ident: 2020041009153636600_sfz073-B12 article-title: Toward a working definition of C3 glomerulopathy by immunofluorescence publication-title: Kidney Int doi: 10.1038/ki.2013.340 – volume: 25 start-page: 2425 year: 2014 ident: 2020041009153636600_sfz073-B6 article-title: Characterization of a factor H mutation that perturbs the alternative pathway of complement in a family with membranoproliferative GN publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2013070732 – volume: 82 start-page: 454 year: 2012 ident: 2020041009153636600_sfz073-B14 article-title: Acquired and genetic complement abnormalities play a critical role in dense deposit disease and other C3 glomerulopathies publication-title: Kidney Int doi: 10.1038/ki.2012.63 – volume: 51 start-page: 101 year: 1982 ident: 2020041009153636600_sfz073-B17 article-title: A new screening test for C3 nephritis factor based on a stable cell bound convertase on sheep erythrocytes publication-title: J Immunol Methods doi: 10.1016/0022-1759(82)90386-6 – volume: 70 start-page: 42 year: 2006 ident: 2020041009153636600_sfz073-B4 article-title: Deletion of Lys224 in regulatory domain 4 of Factor H reveals a novel pathomechanism for dense deposit disease (MPGN II) publication-title: Kidney Int doi: 10.1038/sj.ki.5000269 – volume: 28 start-page: 1603 year: 2017 ident: 2020041009153636600_sfz073-B7 article-title: Anti-factor B and Anti-C3b Autoantibodies in C3 glomerulopathy and Ig-associated membranoproliferative GN publication-title: J Am Soc Nephrol doi: 10.1681/ASN.2016030343 – volume: 45 start-page: 2326 year: 2014 ident: 2020041009153636600_sfz073-B13 article-title: Heterogeneous histologic and clinical evolution in 3 cases of dense deposit disease with long-term follow-up publication-title: Hum Pathol doi: 10.1016/j.humpath.2014.07.021 |
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| Snippet | BackgroundA novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated membranoproliferative... A novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated membranoproliferative... Background. A novel data-driven cluster analysis identified distinct pathogenic patterns in C3-glomerulopathies and immune complex-mediated... |
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| SubjectTerms | Analysis Biopsy C3-glomerulonephritis C3-glomerulonephritis ; C3-glomerulopathy ; complement ; dense deposit disease, membranoproliferative glomerulonephritis C3-glomerulopathy Chronic kidney failure Cluster analysis complement dense deposit disease, membranoproliferative glomerulonephritis Diagnosis Glomerulonephritis Hemodialysis Hospitals Hypertension Immunoglobulins Internal medicine Medical research Medicine Medicine, Experimental Microscopy Nephrology Original Original Articles Pathogenesis Pathology Patients Pediatrics Physiological aspects Transplants & implants |
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| Title | Validation of distinct pathogenic patterns in a cohort of membranoproliferative glomerulonephritis patients by cluster analysis |
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