Nellie Bourse Chalvon1, Pauline Orquevaux1, Delphine Giusti2, Gregory Gatouillat2, Thierry Tabary2, Marcelle Tonye Libyh2, Jan Chrusciel3, Moustapha Drame4, Grace Stockton-Bliard5, Zahir Amoura6, Laurent Arnaud7, Hanns-Martin Lorenz8, Gilles Blaison9, Bernard Bonnotte10, Nadine Magy-Bertrand11, Sabine Revuz12, Reinhard Edmund Voll13, Oliver Hinschberger14, Andreas Schwarting15, Bach Nga Pham2, Thierry Martin16, Jean-Loup Pennaforte1, Amelie Servettaz1. 1. Département de médecine interne, Centre Hospitalier Universitaire de Reims, Reims, France. 2. Département d'immunologie biologique (laboratoire d'immunologie), Centre Hospitalier Universitaire de Reims, Reims, France. 3. Département d'information médicale et d'évaluation des performances, santé publique, Centre Hospitalier de Troyes, Troyes, France. 4. Département de Délégation à la Recherche Clinique et à l'Innovation, University Hospital of Martinique, Fort-de-France, Martinique. 5. Commission de la recherche, Université de Reims Champagne-Ardenne, Reims, France. 6. Service de Médecine interne, Assistance Publique Hôpitaux de Paris (APHP), Paris, France. 7. Service de Rhumatologie, Hôpitaux Universitaires de Strasbourg, Strasbourg, France. 8. Division of Rheumatology, Clinic for Hematology, Oncology and Rheumatology, Department of Internal Medicine V, University Hospital Heidelberg, Heidelberg, Germany. 9. Département de médecine interne, Hôpital Pasteur, Colmar, France. 10. Département de Médecine Interne et d'immunologie Clinique, Centre Hospitalier Regional Universitaire De Dijon, Dijon, France. 11. Département de médecine interne, Centre Hospitalier Universitaire de Besançon, Besancon, France. 12. Département de médecine interne, Hôpital Belle-Isle, Metz, France. 13. Department of Rheumatology and Clinical Immunology, Medical Center, University of Freiburg, Freiburg, Germany. 14. Département de médecine interne, Groupe Hospitalier de la Région de Mulhouse et Sud Alsace (GHRMSA), Mulhouse, France. 15. Universitäres Centrum für Autoimmunität Mainz, Johannes Gutenberg-Universität Mainz, Mainz, Germany. 16. Immunologie Clinique et Médecine Interne, Hôpitaux Universitaires de Strasbourg, Strasbourg, France.
Abstract
Introduction: Anti-glomerular basement membrane (GBM) antibodies are pathogenic antibodies first detected in renal-limited anti-GBM disease and in Goodpasture disease, the latter characterized by rapidly progressive crescentic glomerulonephritis combined with intra-alveolar hemorrhage. Studies have suggested that anti-GBM antibody positivity may be of interest in lupus nephritis (LN). Moreover, severe anti-GBM vasculitis cases in patients with systemic lupus erythematosus (SLE) have been described in the literature, but few studies have assessed the incidence of anti-GBM antibodies in SLE patients. Objective: The main study objective was to determine if positive anti-GBM antibodies were present in the serum of SLE patients with or without proliferative renal damage and compared to a healthy control group. Methodology: This retrospective study was performed on SLE patients' sera from a Franco-German European biobank, developed between 2011 and 2014, from 17 hospital centers in the Haut-Rhin region. Patients were selected according to their renal involvement, and matched by age and gender. The serum from healthy voluntary blood donors was also tested. Anti-GBM were screened by fluorescence enzyme immunoassay (FEIA), and then by indirect immunofluorescence (IIF) in case of low reactivity detection (titer >6 U/ml). Results: The cohort was composed of 100 SLE patients with proliferative LN (27% with class III, 67% with class IV, and 6% with class V), compared to 100 SLE patients without LN and 100 controls. Patients were mostly Caucasian and met the ACR 1997 criteria and/or the SLICC 2012 criteria. Among the 300 tested sera, no significant levels of anti-GBM antibodies were detected (>10 U/ml) by the automated technique, three sera were found "ambivalent" (>7 U/ml): one in the SLE with LN group and two in the SLE without LN group. Subsequent IIF assays did not detect anti-GBM antibodies. Conclusion: Anti-GBM antibodies were not detected in the serum of Caucasian patients with SLE, even in case of renal involvement, a situation favoring the antigenic exposure of glomerular basement membranes. Our results reaffirm the central role of anti-GBM antibodies as a specific diagnostic biomarker for Goodpasture vasculitis and therefore confirm that anti-GBM antibody must not be carried out in patients with SLE (with or without LN) in the absence of disease-suggestive symptoms.
Introduction: Anti-glomerular basement membrane (GBM) antibodies are pathogenic antibodies first detected in renal-limited anti-GBM disease and in Goodpasture disease, the latter characterized by rapidly progressive crescentic glomerulonephritis combined with intra-alveolar hemorrhage. Studies have suggested that anti-GBM antibody positivity may be of interest in lupus nephritis (LN). Moreover, severe anti-GBM vasculitis cases in patients with systemic lupus erythematosus (SLE) have been described in the literature, but few studies have assessed the incidence of anti-GBM antibodies in SLEpatients. Objective: The main study objective was to determine if positive anti-GBM antibodies were present in the serum of SLEpatients with or without proliferative renal damage and compared to a healthy control group. Methodology: This retrospective study was performed on SLEpatients' sera from a Franco-German European biobank, developed between 2011 and 2014, from 17 hospital centers in the Haut-Rhin region. Patients were selected according to their renal involvement, and matched by age and gender. The serum from healthy voluntary blood donors was also tested. Anti-GBM were screened by fluorescence enzyme immunoassay (FEIA), and then by indirect immunofluorescence (IIF) in case of low reactivity detection (titer >6 U/ml). Results: The cohort was composed of 100 SLEpatients with proliferative LN (27% with class III, 67% with class IV, and 6% with class V), compared to 100 SLEpatients without LN and 100 controls. Patients were mostly Caucasian and met the ACR 1997 criteria and/or the SLICC 2012 criteria. Among the 300 tested sera, no significant levels of anti-GBM antibodies were detected (>10 U/ml) by the automated technique, three sera were found "ambivalent" (>7 U/ml): one in the SLE with LN group and two in the SLE without LN group. Subsequent IIF assays did not detect anti-GBM antibodies. Conclusion: Anti-GBM antibodies were not detected in the serum of Caucasian patients with SLE, even in case of renal involvement, a situation favoring the antigenic exposure of glomerular basement membranes. Our results reaffirm the central role of anti-GBM antibodies as a specific diagnostic biomarker for Goodpasture vasculitis and therefore confirm that anti-GBM antibody must not be carried out in patients with SLE (with or without LN) in the absence of disease-suggestive symptoms.
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