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1. Proteinuria as a Biomarker for COVID-19 Severity

Author

Hajar Ouahmi, Johan Courjon, Lucas Morand, Juliette François, Vincent Bruckert, Romain Lombardi, Vincent Esnault, Barbara Seitz-Polski, Elisa Demonchy, Jean Dellamonica, and Sonia Boyer-Suavet

Subjects
acute kidney injury, biomarker, COVID-19, proteinuria, SARS-CoV-2, kidney involvement, Physiology, QP1-981
Abstract

BackgroundRenal involvement in syndrome coronavirus 2 (SARS-CoV-2) infection has been retrospectively described, especially acute kidney injury (AKI). However, quantitative proteinuria assessment and its implication in coronavirus disease 2019 (COVID-19) remain unknown.MethodsIn this prospective, multicenter study in France, we collected clinical and biological data including urinary protein to creatine ratio (UPCR) in patients presenting with moderate to severe COVID-19. Clinical outcome was analyzed according to the level of UPCR.Results42/45 patients (93.3%) had renal involvement (abnormal urinary sediment and/or AKI). Significant proteinuria occurred in 60% of patients. Urine protein electrophoresis showed tubular protein excretion in 83.8% of patients with proteinuria. Inflammatory parametersand D-dimer concentrations correlated with proteinuria level. Patients who required intensive care unit (ICU) admission had higher proteinuria (p = 0.008). On multivariate analysis, proteinuria greater than 0.3 g/g was related to a higher prevalence of ICU admission [OR = 4.72, IC95 (1.16–23.21), p = 0.03], acute respiratory distress syndrome (ARDS) [OR = 6.89, IC95 (1.41–53.01, p = 0.02)], nosocomial infections [OR = 3.75, IC95 (1.11–13.55), p = 0.03], longer inpatient hospital stay (p = 0.003).ConclusionRenal involvement is common in moderate to severe SARS-CoV-2 infection. Proteinuria at baseline is an independent risk factor for increased hospitalization duration and ICU admission in patients with COVID-19.

Published
2021
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2. Anti-PLA2R1 Antibodies Containing Sera Induce In Vitro Cytotoxicity Mediated by Complement Activation

Author

Maël Lateb, Hajar Ouahmi, Christine Payré, Vesna Brglez, Kevin Zorzi, Guillaume Dolla, Mohamad Zaidan, Sonia Boyer-Suavet, Bertrand Knebelmann, Thomas Crépin, Cécile Courivaud, Noémie Jourde-Chiche, Vincent Esnault, Gérard Lambeau, and Barbara Seitz-Polski

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

The phospholipase A2 receptor (PLA2R1) is the major autoantigen in idiopathic membranous nephropathy (MN). However, the pathogenic role of anti-PLA2R1 autoantibodies is unclear. Our aim was to evaluate the in vitro cytotoxicity of anti-PLA2R1 antibodies mediated by complement. Forty-eight patients with PLA2R1-related MN from the prospective cohort SOURIS were included. Anti-PLA2R1 titer, epitope profile, and anti-PLA2R1 IgG subclasses were characterized by ELISA. Cell cytotoxicity was evaluated by immunofluorescence in HEK293 cells overexpressing PLA2R1 incubated with patient or healthy donor sera in the presence or absence of rabbit complement or complement inhibitors. Mean cytotoxicity of anti-PLA2R1 sera for HEK293 cells overexpressing PLA2R1 was 2±2%, which increased to 24±6% after addition of rabbit complement (p

Published
2019
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3. Anti-PLA2R1 Antibodies Containing Sera Induce In Vitro Cytotoxicity Mediated by Complement Activation

Author

Kévin Zorzi, Vincent L.M. Esnault, Gérard Lambeau, Cécile Courivaud, Barbara Seitz-Polski, Noémie Jourde-Chiche, Thomas Crepin, Guillaume Dolla, Christine Payré, Hajar Ouahmi, M. Lateb, Mohamad Zaidan, Bertrand Knebelmann, Vesna Brglez, Sonia Boyer-Suavet, Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Département de Néphrologie - Hôpital Pasteur [Nice], Hôpital Pasteur [Nice] (CHU), Centre Hospitalier Universitaire de Nice (CHU Nice), Néphrologie [CHU Bicêtre], AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Service de Néphrologie [CHRU Besançon], Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Centre recherche en CardioVasculaire et Nutrition = Center for CardioVascular and Nutrition research (C2VN), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Centre de néphrologie et transplantation rénale [Hôpital de la Conception - APHM], Assistance Publique - Hôpitaux de Marseille (APHM)-Hôpital de la Conception [CHU - APHM] (LA CONCEPTION), Hôpital l'Archet, Fondation pour la Recherche Médicale (FRMING20140129210, SPF20150934219, FDT201805005509, and DEQ20180339193), and the Fondation du Rein (award and grant FdR 2018/FRM/G.L), ANR-11-LABX-0028,SIGNALIFE,Réseau d'Innovation sur les Voies de Signalisation en Sciences de la Vie(2011), ANR-17-CE17-0012,MNaims,Dissection moléculaire de la glomérulonéphrite extramembraneuse liée à PLA2R1: vers l'identification de nouveaux biomarqueurs cliniques(2017), HAL AMU, Administrateur, Centres d'excellences - Réseau d'Innovation sur les Voies de Signalisation en Sciences de la Vie - - SIGNALIFE2011 - ANR-11-LABX-0028 - LABX - VALID, Dissection moléculaire de la glomérulonéphrite extramembraneuse liée à PLA2R1: vers l'identification de nouveaux biomarqueurs cliniques - - MNaims2017 - ANR-17-CE17-0012 - AAPG2017 - VALID, Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)

Subjects
Cytotoxicity, Immunologic, Male, 0301 basic medicine, PROGNOSIS, [SDV]Life Sciences [q-bio], 030232 urology & nephrology, Autoantigens, Glomerulonephritis, Membranous, Immunoglobulin G, Epitope, Cohort Studies, Epitopes, Complement inhibitor, 0302 clinical medicine, SUBCLASS, BINDING, Immunology and Allergy, Prospective Studies, Cytotoxicity, Complement Activation, biology, Podocytes, Chemistry, General Medicine, Middle Aged, 3. Good health, [SDV] Life Sciences [q-bio], Titer, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Rabbits, Antibody, Rituximab, Research Article, lcsh:Immunologic diseases. Allergy, DOMAIN-CONTAINING 7A, IGG4, Adult, [SDV.IMM] Life Sciences [q-bio]/Immunology, Article Subject, Cell Survival, Immunology, GLOMERULAR-DISEASES, PHOSPHOLIPASE-A2 RECEPTOR AUTOANTIBODIES, 03 medical and health sciences, GLOMERULONEPHRITIS, Animals, Humans, Aged, Autoantibodies, Receptors, Phospholipase A2, Complement System Proteins, Molecular biology, Complement system, HEK293 Cells, 030104 developmental biology, MEMBRANOUS NEPHROPATHY, biology.protein, Alternative complement pathway, lcsh:RC581-607
Abstract

The phospholipase A2 receptor (PLA2R1) is the major autoantigen in idiopathic membranous nephropathy (MN). However, the pathogenic role of anti-PLA2R1 autoantibodies is unclear. Our aim was to evaluate the in vitro cytotoxicity of anti-PLA2R1 antibodies mediated by complement. Forty-eight patients with PLA2R1-related MN from the prospective cohort SOURIS were included. Anti-PLA2R1 titer, epitope profile, and anti-PLA2R1 IgG subclasses were characterized by ELISA. Cell cytotoxicity was evaluated by immunofluorescence in HEK293 cells overexpressing PLA2R1 incubated with patient or healthy donor sera in the presence or absence of rabbit complement or complement inhibitors. Mean cytotoxicity of anti-PLA2R1 sera for HEK293 cells overexpressing PLA2R1 was 2±2%, which increased to 24±6% after addition of rabbit complement (p<0.001) (n=48). GVB-EDTA, which inhibits all complement activation pathways, completely blocked cell cytotoxicity, whereas Mg-EGTA, which only inhibits the classical and lectin pathways, highly decreased suggesting a limited role of the alternative pathway. A higher diversity of IgG subclasses beyond IgG4 and high titer of total IgG anti-PLA2R1 were associated with increased cytotoxicity (p=0.01 and p=0.03 respectively). In a cohort of 37 patients treated with rituximab, high level of complement-mediated cytotoxicity was associated with less and delayed remission at month 6 after rituximab therapy (5/12 vs. 20/25 (p=0.03) in 8.5 months±4.4 vs. 4.8±4.0 (p=0.02)). Kaplan-Meier analysis demonstrated that high level of cytotoxicity (≥40%) (p=0.005), epitope spreading (defined by immunization beyond the immunodominant CysR domain) (p=0.002), and high titer of anti-PLA2R1 total IgG (p=0.01) were factors of poor renal prognosis. Anti-PLA2R1 antibodies containing sera can induce in vitro cytotoxicity mediated by complement activation, and the level of cytotoxicity increases with the diversity and the titer of anti-PLA2R1 IgG subclasses. These patients with high level of complement-mediated cytotoxicity could benefit from adjuvant therapy using complement inhibitor associated with rituximab to induce earlier remission and less podocyte injury.

Published
2019

4. Cohort study: 'Outcomes of kidney transplantation in patients with prosthetic heart valves'

Author

Ouahmi, Hajar, Moceri, Pamela, Zorzi, Kevin, Albano, Laetitia, Durand, Matthieu, Karimi, Fatimaezzahra, Morelon, Emmanuel, Buron, Fanny, Le Quintrec, Moglie, Pernin, Vincent, Ladriere, Marc, Girerd, Sophie, Dantal, Jacques, Loupy, Alexandre, Couzi, Lionel, Ferrari, Emile, Esnault, Vincent, Merville, Pierre, Legendre, Christophe, Giral, Magali, Sicard, Antoine, Badet, Lionel, Brunet, Maria, Cahen, Rémi, Codas, Ricardo, Daoud, Sameh, Dubois, Valérie, Fournie, Coralie, Grégoire, Arnaud, Koenig, Alice, Lévi, Charlène, Pouteil‐Noble, Claire, Rabeyrin, Maud, Rimmelé, Thomas, Thaunat, Olivier, Abdo, Nicolas, Delmas, Sylvie, Perrochia, Hélène, Serre, Jean‐Emmanuel, Szwarc, Ilan, Aarnink, Alice, Alla, Asma, Eschwege, Pascal, Frimat, Luc, Hubert, Jacques, Kormann, Raphaël, Lagrange, François, Laurain, Emmanuelle, Lecoanet, Pierre, Lemelle, Jean‐Louis, Mannuguerra, Anthony, Mazeaud, Charles, Peres, Michael, Blancho, Gilles, Branchereau, Julien, Cantarovich, Diego, Chapelet, Agnès, Deltombe, Clément, Figueres, Lucile, Garandeau, Claire, Gourraud‐Vercel, Caroline, Hourmant, Maryvonne, Karam, Georges, Kerleau, Clarisse, Meurette, Aurélie, Ville, Simon, Kandell, Christine, Moreau, Anne, Renaudin, Karine, Cesbron, Anne, Delbos, Florent, Walencik, Alexandre, Devis, Anne, Chevallier, Daniel, Tibi, Brannwel, Ahallal, Younes, Amrouche, Lucile, Anglicheau, Dany, Aubert, Olivier, Bererhi, Lynda, Martinez, Frank, Sberro‐Soussan, Rébecca, Scemla, Anne, Tinel, Claire, Zuber, Julien, Glotz, Denis, Lefaucheur, Carmen, Université Côte d'Azur - Faculté de Médecine (UCA Faculté Médecine), Université Côte d'Azur (UCA), Centre Hospitalier Universitaire de Nice (CHU Nice), CIC CHU Lyon (inserm), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM), Réseau CENTAURE, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Service de Néphrologie [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Centre de Recherche en Transplantation et Immunologie - Center for Research in Transplantation and Translational Immunology (U1064 Inserm - CR2TI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Nantes Université - UFR de Médecine et des Techniques Médicales (Nantes Univ - UFR MEDECINE), Nantes Université - pôle Santé, Nantes Université (Nantes Univ)-Nantes Université (Nantes Univ)-Nantes Université - pôle Santé, Nantes Université (Nantes Univ)-Nantes Université (Nantes Univ), CHU Bordeaux [Bordeaux], Immunology from Concept and Experiments to Translation (ImmunoConcept), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de PhysioMédecine Moléculaire (LP2M), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), DIVAT Consortium: Lionel Badet, Maria Brunet, Fanny Buron, Rémi Cahen, Ricardo Codas, Sameh Daoud, Valérie Dubois, Coralie Fournie, Arnaud Grégoire, Alice Koenig, Charlène Lévi, Emmanuel Morelon, Claire Pouteil-Noble, Maud Rabeyrin, Thomas Rimmelé, Olivier Thaunat, Nicolas Abdo, Sylvie Delmas, Moglie Le Quintrec, Vincent Pernin, Hélène Perrochia, Jean-Emmanuel Serre, Ilan Szwarc, Alice Aarnink, Asma Alla, Pascal Eschwege, Luc Frimat, Sophie Girerd, Jacques Hubert, Raphaël Kormann, Marc Ladriere, François Lagrange, Emmanuelle Laurain, Pierre Lecoanet, Jean-Louis Lemelle, Anthony Mannuguerra, Charles Mazeaud, Michael Peres, Gilles Blancho, Julien Branchereau, Diego Cantarovich, Agnès Chapelet, Jacques Dantal, Clément Deltombe, Lucile Figueres, Claire Garandeau, Magali Giral, Caroline Gourraud-Vercel, Maryvonne Hourmant, Georges Karam, Clarisse Kerleau, Aurélie Meurette, Simon Ville, Christine Kandell, Anne Moreau, Karine Renaudin, Anne Cesbron, Florent Delbos, Alexandre Walencik, Anne Devis, Laetitia Albano, Fatimaezzahra Karimi, Antoine Sicard, Hajar Ouahmi, Daniel Chevallier, Brannwel Tibi, Matthieu Durand, Younes Ahallal, Lucile Amrouche, Dany Anglicheau, Olivier Aubert, Lynda Bererhi, Christophe Legendre, Alexandre Loupy, Frank Martinez, Rébecca Sberro-Soussan, Anne Scemla, Claire Tinel, Julien Zuber, Denis Glotz, Carmen Lefaucheur, and Retiveau, Nolwenn

Subjects
medicine.medical_specialty, medicine.medical_treatment, MESH: Heart Valves, Postoperative Hemorrhage, MESH: Kidney Transplantation, Cohort Studies, Diabetes mellitus, Internal medicine, Biological heart valve, Medicine, Endocarditis, Humans, Prospective Studies, MESH: Cohort Studies, Kidney transplantation, Dialysis, Retrospective Studies, Kidney, Transplantation, MESH: Humans, business.industry, Cardiac valve replacement, End-stage kidney disease, MESH: Postoperative Hemorrhage, MESH: Retrospective Studies, medicine.disease, Heart Valves, Kidney Transplantation, MESH: Prospective Studies, [SDV.TOX] Life Sciences [q-bio]/Toxicology, medicine.anatomical_structure, Prosthetic heart valve, Mechanical heart valve, [SDV.TOX]Life Sciences [q-bio]/Toxicology, Cohort, Cardiology, business, Cohort study
Abstract

Main problem The number of kidney transplant candidates with prosthetic heart valves (PHVs) is increasing. Yet, outcomes of kidney transplantation in these patients are still unclear. This is the first report of post-transplant outcomes in patients with PHVs at time of kidney transplantation. Methods We conducted a matched cohort study among recipients from the multicentric and prospective DIVAT cohort to compare outcomes in patients with left-sided PHVs at time of transplantation and a group of recipients without PHV matched according to age, dialysis time, initial disease, pre-transplant DSA, diabetes and cardiovascular events. Results Of 23018 patients, 92 patients with PHVs were included and compared to 276 patients without PHV. Delayed graft function and post-operative bleeding occurred more frequently in patients with PHVs. Kidney graft survival was similar between groups. 5-year overall survival was 68.5 % in patients with PHV versus 87.9 % in patients without PHV (HR, 2.72[1.57-4.70], p=0.0004). Deaths from infection, endocarditis and bleeding were more frequent in patients with PHV. Mechanical valves, but not bioprosthetic valves, were independent risk factors for mortality (HR, 2.89[1.68-4.97], p=0.0001). Conclusions Patients with PHV have high mortality rates after kidney transplantation. These data suggest that mechanical valves, but not biological valves, increase risks of post-transplant mortality.

Published
2021
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