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2. [Use of antiplatelet therapy and direct oral anticoagulants in candidates for renal transplantation: The French guidelines from the CTAFU]

Author

Timsit, M.-O., Branchereau, J., Matillon, X., Verhoest, G., Bessede, T., Lequintrec, M., Boissier, R., Badet, L., Smadja, D.M., Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Centre hospitalier universitaire de Nantes (CHU Nantes), Hôpital Edouard Herriot [CHU - HCL], Hospices Civils de Lyon (HCL), CHU Pontchaillou [Rennes], Hôpital Bicêtre, Hôpital Lapeyronie [Montpellier] (CHU), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Aix Marseille Université (AMU), and Hôpital de la Conception [CHU - APHM] (LA CONCEPTION)

Subjects
MESH: Humans, Antiplatelet therapy, [SDV]Life Sciences [q-bio], Anticoagulants, MESH: Preoperative Period, Kidney Transplantation, MESH: Kidney Transplantation, Agents antiplaquettaires, MESH: Platelet Aggregation Inhibitors, Preoperative Period, Renal Transplantation, Transplantation rénale, Humans, MESH: Factor Xa Inhibitors, Platelet Aggregation Inhibitors, Factor Xa Inhibitors
Abstract

International audience; Objective: To define guidelines for the use of antiplatelet therapy (AT) and direct oral anticoagulants (DOAC) in candidates for kidney allotransplantation.Method: A review of the medical literature following a systematic approach was conducted by the CTAFU to report the use of AT and DOAC before major surgery and in the setting of advanced chronic kidney disease, defining their managment prior to kidney transplantation with the corresponding level of evidence.Results: DOAC are not recommended in patients under dialysis. Aspirin therapy, but not anti-P2Y12 and DOAC, may be maintained during renal transplantation. Anti-P2Y12 and DOAC should not be use in patients awaiting a kidney transplant, except when a living donor is scheduled, therefore authorizing treatment interruption in optimal conditions. Further data regarding DOAC reversion and monitoring may improve their use in this setting. Global level of evidence is weak.Conclusion: These French recommendations should contribute to improve surgical management of kidney transplant candidates exposed to AT or DOA.

Published
2020

5. Airway microbiota signals anabolic and catabolic remodeling in the transplanted lung

Author

Mouraux, Stéphane, primary, Bernasconi, Eric, additional, Pattaroni, Céline, additional, Koutsokera, Angela, additional, Aubert, John-David, additional, Claustre, Johanna, additional, Pison, Christophe, additional, Royer, Pierre-Joseph, additional, Magnan, Antoine, additional, Kessler, Romain, additional, Benden, Christian, additional, Soccal, Paola M., additional, Marsland, Benjamin J., additional, Nicod, Laurent P., additional, Jougon, J., additional, Velly, J.-F., additional, Rozé, H., additional, Blanchard, E., additional, Dromer, C., additional, Antoine, M., additional, Cappello, M., additional, Ruiz, M., additional, Sokolow, Y., additional, Vanden Eynden, F., additional, Van Nooten, G., additional, Barvais, L., additional, Berré, J., additional, Brimioulle, S., additional, De Backer, D., additional, Créteur, J., additional, Engelman, E., additional, Huybrechts, I., additional, Ickx, B., additional, Preiser, T.J.C., additional, Tuna, T., additional, Van Obberghe, L., additional, Vancutsem, N., additional, Vincent, J.-L., additional, De Vuyst, P., additional, Etienne, I., additional, Féry, F., additional, Jacobs, F., additional, Knoop, C., additional, Vachiéry, J.L., additional, Van den Borne, P., additional, Wellemans, I., additional, Amand, G., additional, Collignon, L., additional, Giroux, M., additional, Angelescu, D., additional, Chavanon, O., additional, Hacini, R., additional, Pirvu, A., additional, Porcu, P., additional, Albaladejo, P., additional, Allègre, C., additional, Bataillard, A., additional, Bedague, D., additional, Briot, E., additional, Casez-Brasseur, M., additional, Colas, D., additional, Dessertaine, G., additional, Durand, M., additional, Francony, G., additional, Hebrard, A., additional, Marino, M.R., additional, Oummahan, B., additional, Protar, D., additional, Rehm, D., additional, Robin, S., additional, Rossi-Blancher, M., additional, Augier, C., additional, Bedouch, P., additional, Boignard, A., additional, Bouvaist, H., additional, Briault, A., additional, Camara, B., additional, Claustre, J., additional, Chanoine, S., additional, Dubuc, M., additional, Quétant, S., additional, Maurizi, J., additional, Pavèse, P., additional, Pison, C., additional, Saint-Raymond, C., additional, Wion, N., additional, Chérion, C., additional, Grima, R., additional, Jegaden, O., additional, Maury, J.-M., additional, Tronc, F., additional, Flamens, C., additional, Paulus, S., additional, Mornex, J.-F., additional, Philit, F., additional, Senechal, A., additional, Glérant, J.-C., additional, Turquier, S., additional, Gamondes, D., additional, Chalabresse, L., additional, Thivolet-Bejui, F., additional, Barnel, C., additional, Dubois, C., additional, Tiberghien, A., additional, Le Pimpec-Barthes, F., additional, Bel, A., additional, Mordant, P., additional, Achouh, P., additional, Boussaud, V., additional, Guillemain, R., additional, Méléard, D., additional, Bricourt, M.O., additional, Cholley, B., additional, Pezella, V., additional, Brioude, G., additional, D'Journo, X.B., additional, Doddoli, C., additional, Thomas, P., additional, Trousse, D., additional, Dizier, S., additional, Leone, M., additional, Papazian, L., additional, Bregeon, F., additional, Basire, A., additional, Coltey, B., additional, Dufeu, N., additional, Dutau, H., additional, Garcia, S., additional, Gaubert, J.Y., additional, Gomez, C., additional, Laroumagne, S., additional, Nieves, A., additional, Picard, L.C., additional, Reynaud-Gaubert, M., additional, Secq, V., additional, Mouton, G., additional, Baron, O., additional, Lacoste, P., additional, Perigaud, C., additional, Roussel, J.C., additional, Danner, I., additional, Haloun, A., additional, Magnan, A., additional, Tissot, A., additional, Lepoivre, T., additional, Treilhaud, M., additional, Botturi-Cavaillès, K., additional, Brouard, S., additional, Danger, R., additional, Loy, J., additional, Morisset, M., additional, Pain, M., additional, Pares, S., additional, Reboulleau, D., additional, Royer, P.-J., additional, Fabre, D., additional, Fadel, E., additional, Mercier, O., additional, Mussot, S., additional, Stephan, F., additional, Viard, P., additional, Cerrina, J., additional, Dorfmuller, P., additional, Ghigna, S.M., additional, Hervén, Ph., additional, Le Roy Ladurie, F., additional, Le Pavec, J., additional, Thomas de Montpreville, V., additional, Lamrani, L., additional, Castier, Y., additional, Cerceau, P., additional, Augustin, P., additional, Jean-Baptiste, S., additional, Boudinet, S., additional, Montravers, P., additional, Brugière, O., additional, Dauriat, G., additional, Jébrak, G., additional, Mal, H., additional, Marceau, A., additional, Métivier, A.-C., additional, Thabut, G., additional, Lhuillier, E., additional, Dupin, C., additional, Bunel, V., additional, Falcoz, P., additional, Massard, G., additional, Santelmo, N., additional, Ajob, G., additional, Collange, O., additional, Helms, O., additional, Hentz, J., additional, Roche, A., additional, Bakouboula, B., additional, Degot, T., additional, Dory, A., additional, Hirschi, S., additional, Ohlmann-Caillard, S., additional, Kessler, L., additional, Kessler, R., additional, Schuller, A., additional, Bennedif, K., additional, Vargas, S., additional, Stauder, J., additional, Ali-Azouaou, S., additional, Bonnette, P., additional, Chapelier, A., additional, Puyo, P., additional, Sage, E., additional, Bresson, J., additional, Caille, V., additional, Cerf, C., additional, Devaquet, J., additional, Dumans-Nizard, V., additional, Felten, M.-L., additional, Fischler, M., additional, Si Larbi, A.-G., additional, Leguen, M., additional, Ley, L., additional, Liu, N., additional, Trebbia, G., additional, De Miranda, S., additional, Douvry, B., additional, Gonin, F., additional, Grenet, D., additional, Hamid, A.M., additional, Neveu, H., additional, Parquin, F., additional, Picard, C., additional, Roux, A., additional, Stern, M., additional, Bouillioud, F., additional, Cahen, P., additional, Colombat, M., additional, Dautricourt, C., additional, Delahousse, M., additional, D'Urso, B., additional, Gravisse, J., additional, Guth, A., additional, Hillaire, S., additional, Honderlick, P., additional, Lequintrec, M., additional, Longchampt, E., additional, Mellot, F., additional, Scherrer, A., additional, Temagoult, L., additional, Tricot, L., additional, Vasse, M., additional, Veyrie, C., additional, Zemoura, L., additional, Berjaud, J., additional, Brouchet, L., additional, Dahan, M., additional, Mathe, F.O., additional, Benahoua, H., additional, DaCosta, M., additional, Serres, I., additional, Merlet-Dupuy, V., additional, Grigoli, M., additional, Didier, A., additional, Murris, M., additional, Crognier, L., additional, Fourcade, O., additional, Krueger, T., additional, Ris, H.B., additional, Gonzalez, M., additional, Jolliet, Ph., additional, Marcucci, C., additional, Chollet, M., additional, Gronchi, F., additional, Courbon, C., additional, Berutto, C., additional, Manuel, O., additional, Koutsokera, A., additional, Aubert, J.-D., additional, Nicod, L.P., additional, Mouraux, S., additional, Bernasconi, E., additional, Pattaroni, C., additional, Marsland, B.J., additional, Soccal, P.M., additional, Rochat, T., additional, Lücker, L.M., additional, Hillinger, S., additional, Inci, I., additional, Weder, W., additional, Schuepbach, R., additional, Zalunardo, M., additional, Benden, C., additional, Schuurmans, M.M., additional, Gaspert, A., additional, Holzmann, D., additional, Müller, N., additional, Schmid, C., additional, Vrugt, B., additional, Fritz, A., additional, Maier, D., additional, Deplanche, K., additional, Koubi, D., additional, Ernst, F., additional, Paprotka, T., additional, Schmitt, M., additional, Wahl, B., additional, Boissel, J.-P., additional, Olivera-Botello, G., additional, Trocmé, C., additional, Toussaint, B., additional, Bourgoin-Voillard, S., additional, Sève, M., additional, Benmerad, M., additional, Siroux, V., additional, Slama, R., additional, Auffray, C., additional, Charron, D., additional, Lefaudeux, D., additional, and Pellet, J., additional

Published
2018
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6. Blood CD9+B cell, a biomarker of bronchiolitis obliterans syndrome after lung transplantation

Author

Brosseau, Carole, Danger, Richard, Durand, Maxim, Durand, Eugénie, Foureau, Aurore, Lacoste, Philippe, Tissot, Adrien, Roux, Antoine, Reynaud‐Gaubert, Martine, Kessler, Romain, Mussot, Sacha, Dromer, Claire, Brugière, Olivier, Mornex, Jean François, Guillemain, Romain, Claustre, Johanna, Magnan, Antoine, Brouard, Sophie, Jougon, J., Velly, J.‐F., Rozé, H., Blanchard, E., Antoine, M., Cappello, M., Ruiz, M., Sokolow, Y., Vanden Eynden, F, Van Nooten, G., Barvais, L., Berré, J., Brimioulle, S., De Backer, D., Créteur, J., Engelman, E, Huybrechts, I., Ickx, B., Preiser, T.J.C., Tuna, T., Van Obberghe, L., Vancutsem, N., Vincent, J.‐L., De Vuyst, P., Etienne, I., Féry, F., Jacobs, F., Knoop, C., Vachiéry, J.L., Van den Borne, P., Wellemans, I., Amand, G., Collignon, L., Giroux, M., Angelescu, D., Chavanon, O., Hacini, R., Martin, C., Pirvu, A., Porcu, P., Albaladejo, P., Allègre, C., Bataillard, A., Bedague, D., Briot, E., Casez‐Brasseur, M., Colas, D., Dessertaine, G., Francony, G., Hebrard, A., Marino, M.R., Protar, D., Rehm, D., Robin, S, Rossi‐Blancher, M., Augier, C., Bedouch, P., Boignard, A., Bouvaist, H., Briault, A., Camara, B., Chanoine, S., Dubuc, M., Quétant, S., Maurizi, J., Pavèse, P., Pison, C., Saint‐Raymond, C., Wion, N., Chérion, C., Grima, R., Jegaden, O., Maury, J.‐M., Tronc, F., Flamens, C., Paulus, S., Philit, F., Senechal, A., Glérant, J.‐C., Turquier, S., Gamondes, D., Chalabresse, L., Thivolet‐Bejui, F., Barnel, C., Dubois, C., Tiberghien, A., Pimpec‐Barthes, F., Bel, A., Mordant, P., Achouh, P., Boussaud, V., Méléard, D., Bricourt, M.O., Cholley, B., Pezella, V., Brioude, G., D'Journo, X.B., Doddoli, C., Thomas, P., Trousse, D., Dizier, S., Leone, M., Papazian, L., Bregeon, F., Coltey, B., Dufeu, N., Dutau, H., Garcia, S., Gaubert, J.Y., Gomez, C., Laroumagne, S., Mouton, G., Nieves, A., Picard, Ch., Rolain, J.M., Sampol, E., Secq, V., Perigaud, C., Roussel, J.C., Senage, T., Mugniot, A., Danner, I., Haloun, A., Abbes, S., Bry, C., Blanc, F.X., Lepoivre, T., Botturi‐Cavaillès, K., Loy, J., Bernard, M., Godard, E., Royer, P.‐J., Henrio, K., Dartevelle, Ph., Fabre, D., Fadel, E., Mercier, O., Stephan, F., Viard, P., Cerrina, J., Dorfmuller, P., Feuillet, S., Ghigna, M., Hervén, Ph., Le Roy Ladurie, F., Le Pavec, J., Thomas de Montpreville, V., Lamrani, L., Castier, Y., Mordant, P., Cerceau, P., Augustin, P., Jean‐Baptiste, S., Boudinet, S., Montravers, P., Dauriat, G., Jébrak, G., Mal, H., Marceau, A., Métivier, A.‐C., Thabut, G., Lhuillier, E., Dupin, C., Bunel, V., Falcoz, P., Massard, G., Santelmo, N., Ajob, G., Collange, O., Helms, O., Hentz, J., Roche, A., Bakouboula, B., Degot, T., Dory, A., Hirschi, S., Ohlmann‐Caillard, S., Kessler, L., Schuller, A., Bennedif, K., Vargas, S., Bonnette, P., Chapelier, A., Puyo, P., Sage, E., Bresson, J., Caille, V., Cerf, C., Devaquet, J., Dumans‐Nizard, V., Felten, M.L., Fischler, M., Si Larbi, A.G., Leguen, M., Ley, L., Liu, N., Trebbia, G., De Miranda, S., Douvry, B., Gonin, F., Grenet, D., Hamid, A.M., Neveu, H., Parquin, F., Picard, C., Stern, M., Bouillioud, F., Cahen, P., Colombat, M., Dautricourt, C., Delahousse, M., D'Urso, B., Gravisse, J., Guth, A., Hillaire, S., Honderlick, P., Lequintrec, M., Longchampt, E., Mellot, F., Scherrer, A., Temagoult, L., Tricot, L., Vasse, M., Veyrie, C., Zemoura, L., Dahan, M., Murris, M., Benahoua, H., Berjaud, J., Le Borgne Krams, A., Crognier, L., Brouchet, L., Mathe, O., Didier, A., Krueger, T., Ris, H.B., Gonzalez, M., Aubert, J.‐D., Nicod, L.P., Marsland, B.J., Berutto, T.C., Rochat, T., Soccal, P., Jolliet, Ph., Koutsokera, A., Marcucci, C., Manuel, O., Bernasconi, E., Chollet, M., Gronchi, F., Courbon, C., Hillinger, S., Inci, I., Kestenholz, P., Weder, W., Schuepbach, R., Zalunardo, M., Benden, C., Buergi, U., Huber, L.C., Isenring, B., Schuurmans, M.M., Gaspert, A., Holzmann, D., Müller, N., Schmid, C., Vrugt, B., Rechsteiner, T., Fritz, A., Maier, D., Deplanche, K., Koubi, D., Ernst, F., Paprotka, T., Schmitt, M., Wahl, B., Boissel, J.‐P., Olivera‐Botello, G., Trocmé, C., Toussaint, B., Bourgoin‐Voillard, S., Séve, M., Benmerad, M., Siroux, V., Slama, R., Auffray, C., Charron, D., Lefaudeux, D., and Pellet, J.

Abstract

Bronchiolitis obliterans syndrome is the main limitation for long‐term survival after lung transplantation. Some specific B cell populations are associated with long‐term graft acceptance. We aimed to monitor the B cell profile during early development of bronchiolitis obliterans syndrome after lung transplantation. The B cell longitudinal profile was analyzed in peripheral blood mononuclear cells from patients with bronchiolitis obliterans syndrome and patients who remained stable over 3 years of follow‐up. CD24hiCD38hitransitional B cells were increased in stable patients only, and reached a peak 24 months after transplantation, whereas they remained unchanged in patients who developed a bronchiolitis obliterans syndrome. These CD24hiCD38hitransitional B cells specifically secrete IL‐10 and express CD9. Thus, patients with a total CD9+B cell frequency below 6.6% displayed significantly higher incidence of bronchiolitis obliterans syndrome (AUC = 0.836, PPV = 0.75, NPV = 1). These data are the first to associate IL‐10‐secreting CD24hiCD38hitransitional B cells expressing CD9 with better allograft outcome in lung transplant recipients. CD9‐expressing B cells appear as a contributor to a favorable environment essential for the maintenance of long‐term stable graft function and as a new predictive biomarker of bronchiolitis obliterans syndrome–free survival. In lung transplant patients with bronchiolitis obliterans syndrome and patients who remained stable over 3 years of follow‐up, IL‐10–secreting CD24hiCD38hi transitional B cells expressing CD9 are associated with better allograft outcome, suggesting CD9‐expressing B cells as a new predictive biomarker of bronchiolitis obliterans syndrome–free survival.

Published
2019
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8. T Cells Promote Bronchial Epithelial Cell Secretion of Matrix Metalloproteinase‐9 via a C‐C Chemokine Receptor Type 2 Pathway: Implications for Chronic Lung Allograft Dysfunction

Author

Pain, M., Royer, P.‐J., Loy, J., Girardeau, A., Tissot, A., Lacoste, P., Roux, A., Reynaud‐Gaubert, M., Kessler, R., Mussot, S., Dromer, C., Brugière, O., Mornex, J.‐F., Guillemain, R., Dahan, M., Knoop, C., Botturi, K., Pison, C., Danger, R., Brouard, S., Magnan, A., Jougon, J., Velly, J.‐F., Rozé, H., Blanchard, E., Antoine, M., Cappello, M., Souilamas, R., Ruiz, M., Sokolow, Y., Vanden Eynden, F., Van Nooten, G., Barvais, L., Berré, J., Brimioulle, S., De Backer, D., Créteur, J., Engelman, E., Huybrechts, I., Ickx, B., Preiser, T.J.C., Tuna, T., Van Obberghe, L., Vancutsem, N., Vincent, J.‐L., De Vuyst, P., Etienne, I., Féry, F., Jacobs, F., Vachiéry, J.L., Van den Borne, P., Wellemans, I., Amand, G., Collignon, L., Giroux, M., Arnaud‐Crozat, E., Bach, V., Brichon, P.‐Y., Chaffanjon, P., Chavanon, O., de Lambert, A., Fleury, J.P., Guigard, S., Hireche, K., Pirvu, A., Porcu, P., Hacini, R., Albaladejo, P., Allègre, C., Bataillard, A., Bedague, D., Briot, E., Casez‐Brasseur, M., Colas, D., Dessertaine, G., Durand, M., Francony, G., Hebrard, A., Marino, M.R., Oummahan, B., Protar, D., Rehm, D., Robin, S., Rossi‐Blancher, M., Bedouch, P., Boignard, A., Bouvaist, H., Briault, A., Camara, B., Chanoine, S., Dubuc, M., Lantuéjoul, S., Quétant, S., Maurizi, J., Pavèse, P., Saint‐Raymond, C., Wion, N., Chérion, C., Grima, R., Jegaden, O., Maury, J.‐M., Tronc, F., Flamens, C., Paulus, S., Philit, F., Senechal, A., Glérant, J.‐C., Turquier, S., Gamondes, D., Chalabresse, L., Thivolet‐Bejui, F., Barnel, C., Dubois, C., Tiberghien, A., Le Pimpec‐Barthes, F., Bel, A., Mordant, P., Achouh, P., Boussaud, V., Méléard, D., Bricourt, M.O., Cholley, B., Pezella, V., Adda, M., Badier, M., Bregeon, F., Coltey, B., D'Journo, X.B., Dizier, S., Doddoli, C., Dufeu, N., Dutau, H., Forel, J.M., Gaubert, J.Y., Gomez, C., Leone, M., Nieves, A., Orsini, B., Papazian, L., Picard, C., Roch, A., Rolain, J.M., Sampol, E., Secq, V., Thomas, P., Trousse, D., Yahyaoui, M., Baron, O., Perigaud, C., Roussel, J.C., Danner, I., Haloun, A., Lepoivre, T., Treilhaud, M., Botturi‐Cavaillès, K., Morisset, M., Pares, S., Reboulleau, D., Dartevelle, P., Fabre, D., Fadel, E., Mercier, O., Stephan, F., Viard, P., Cerrina, J., Dorfmuller, P., Feuillet, S., Ghigna, M., Hervén, P., Le Roy Ladurie, F., Le Pavec, J., Thomas de Montpreville, V., Lamrani, L., Castier, Y., Cerceau, P., Francis, F., Lesèche, G., Allou, N., Augustin, P., Boudinet, S., Desmard, M., Dufour, G., Montravers, P., Dauriat, G., Jébrak, G., Mal, H., Marceau, A., Métivier, A.‐C., Thabut, G., Ait Ilalne, B., Falcoz, P., Massard, G., Santelmo, N., Ajob, G., Collange, O., Helms, O., Hentz, J., Roche, A., Bakouboula, B., Degot, T., Dory, A., Hirschi, S., Ohlmann‐Caillard, S., Kessler, L., Schuller, A., Bennedif, K., Vargas, S., Bonnette, P., Chapelier, A., Puyo, P., Sage, E., Bresson, J., Caille, V., Cerf, C., Devaquet, J., Dumans‐Nizard, V., Felten, M.L., Fischler, M., Si Larbi, A.G., Leguen, M., Ley, L., Liu, N., Trebbia, G., De Miranda, S., Douvry, B., Gonin, F., Grenet, D., Hamid, A.M., Neveu, H., Parquin, F., Picard, C., Stern, M., Bouillioud, F., Cahen, P., Colombat, M., Dautricourt, C., Delahousse, M., D'Urso, B., Gravisse, J., Guth, A., Hillaire, S., Honderlick, P., Lequintrec, M., Longchampt, E., Mellot, F., Scherrer, A., Temagoult, L., Tricot, L., Vasse, M., Veyrie, C., Zemoura, L., Berjaud, J., Brouchet, L., Le Balle, F, Mathe, O., Benahoua, H., Didier, A., Goin, A.L., Murris, M., Crognier, L., and Fourcade, O.

Abstract

Chronic lung allograft dysfunction (CLAD) is the major limitation of long‐term survival after lung transplantation. CLADmanifests as bronchiolitis obliterans syndrome (BOS) or restrictive allograft syndrome (RAS). Alloimmune reactions and epithelial‐to‐mesenchymal transition have been suggested in BOS. However, little is known regarding the role of allogenicity in epithelial cell differentiation. Primary human bronchial epithelial cells (BECs) were treated with activated T cells in the presence or absence of transforming growth factor (TGF)‐β. The expression of epithelial and mesenchymal markers was investigated. The secretion of inflammatory cytokines and matrix metalloproteinase (MMP)‐9 was measured in culture supernatants and in plasma from lung transplant recipients (LTRs): 49 stable, 29 with BOS,and 16 with RAS. We demonstrated that C‐C motif chemokine 2 secreted by T cells supports TGF‐β–induced MMP‐9 production by BECsafter binding to C‐C chemokine receptor type 2. Longitudinal investigation in LTRsrevealed a rise in plasma MMP‐9 before CLADonset. Multivariate analysis showed that plasma MMP‐9 was independently associated with BOS(odds ratio [OR] =6.19, p = 0.002) or RAS(OR= 3.9, p = 0.024) and predicted the occurrence of CLAD12 months before the functional diagnosis. Thus, immune cells support airway remodeling through the production of MMP‐9. Plasma MMP‐9 is a potential predictive biomarker of CLAD. The authors investigate the production of matrix metalloproteinase‐9 by primary bronchial epithelial cells after interaction with activated T cells and show that plasma matrix metalloproteinase‐9 can serve as a predictor of chronic lung allograft dysfunction 12 months before clinical diagnosis.

Published
2017
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10. Corrigendum: Impaired antigen-specific B-cell responses after Influenza vaccination in kidney transplant recipients receiving co-stimulation blockade with Belatacept.

Author

Pernin V, Meneghini M, Torija A, Jouve T, Del Bello A, Sanz-Muñoz I, Eiros JM, Donadeu L, Polo C, Morandeira F, Navarro S, Masuet C, Favà A, LeQuintrec M, Kamar N, Crespo E, and Bestard O

Abstract

[This corrects the article DOI: 10.3389/fimmu.2022.918887.]., (Copyright © 2024 Pernin, Meneghini, Torija, Jouve, Del Bello, Sanz-Muñoz, Eiros, Donadeu, Polo, Morandeira, Navarro, Masuet, Favà, LeQuintrec, Kamar, Crespo and Bestard.)

Published
2024
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11. Impaired antigen-specific B-cell responses after Influenza vaccination in kidney transplant recipients receiving co-stimulation blockade with Belatacept.

Author

Pernin V, Meneghini M, Torija A, Jouve T, Del Bello A, Sanz-Muñoz I, Eiros JM, Donadeu L, Polo C, Morandeira F, Navarro S, Masuet C, Favà A, LeQuintrec M, Kamar N, Crespo E, and Bestard O

Subjects
Abatacept pharmacology, Abatacept therapeutic use, Humans, Transplant Recipients, Vaccination, Influenza A Virus, H1N1 Subtype, Kidney Transplantation adverse effects
Abstract

Emerging data suggest that costimulation blockade with belatacept effectively controls humoral alloimmune responses. However, whether this effect may be deleterious for protective anti-infectious immunity remains poorly understood. We performed a mechanistic exploratory study in 23 kidney transplant recipients receiving either the calcineurin-inhibitor tacrolimus (Tac, n=14) or belatacept (n=9) evaluating different cellular immune responses after influenza vaccination such as activated T follicular Helper (Tfh), plasmablasts and H1N1 hemagglutinin (HA)-specific memory B cells (HA + mBC) by flow-cytometry, and anti-influenza antibodies by hemagglutination inhibition test (HI), at baseline and days 10, 30 and 90 post-vaccination. The proportion of CD4+CD54RA-CXCR5+ Tfh was lower in belatacept than Tac patients at baseline (1.86%[1.25-3.03] vs 4.88%[2.40-8.27], p=0.01) and remained stable post-vaccination. At M3, HA + mBc were significantly higher in Tac-treated patients (0.56%[0.32-1.49] vs 0.27%[0.13-0.44], p=0.04) and correlated with activated Tfh numbers. When stratifying patients according to baseline HA + mBc frequencies, belatacept patients with low HA + mBC displayed significantly lower HA + mBc increases after vaccination than Tac patients (1.28[0.94-2.4] vs 2.54[1.73-5.70], p=0.04). Also, belatacept patients displayed significantly lower seroprotection rates against H1N1 at baseline than Tac-treated patients (44.4% vs 84.6%) as well as lower seroconversion rates at days 10, 30 and 90 after vaccination (50% vs 0%, 63.6% vs 0%, and 63.6% vs 0%, respectively). We show the efficacy of belatacept inhibiting T-dependent antigen-specific humoral immune responses, active immunization should be highly encouraged before starting belatacept therapy., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Pernin, Meneghini, Torija, Jouve, Del Bello, Sanz-Muñoz, Eiros, Donadeu, Polo, Morandeira, Navarro, Masuet, Favà, LeQuintrec, Kamar, Crespo and Bestard.)

Published
2022
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12. [Use of antiplatelet therapy and direct oral anticoagulants in candidates for renal transplantation: The French guidelines from the CTAFU].

Author

Timsit MO, Branchereau J, Matillon X, Verhoest G, Bessede T, LeQuintrec M, Boissier R, Badet L, and Smadja DM

Subjects
Humans, Preoperative Period, Factor Xa Inhibitors therapeutic use, Kidney Transplantation, Platelet Aggregation Inhibitors therapeutic use
Abstract

Objective: To define guidelines for the use of antiplatelet therapy (AT) and direct oral anticoagulants (DOAC) in candidates for kidney allotransplantation., Method: A review of the medical literature following a systematic approach was conducted by the CTAFU to report the use of AT and DOAC before major surgery and in the setting of advanced chronic kidney disease, defining their managment prior to kidney transplantation with the corresponding level of evidence., Results: DOAC are not recommended in patients under dialysis. Aspirin therapy, but not anti-P2Y 12 and DOAC, may be maintained during renal transplantation. Anti-P2Y 12 and DOAC should not be use in patients awaiting a kidney transplant, except when a living donor is scheduled, therefore authorizing treatment interruption in optimal conditions. Further data regarding DOAC reversion and monitoring may improve their use in this setting. Global level of evidence is weak., Conclusion: These French recommendations should contribute to improve surgical management of kidney transplant candidates exposed to AT or DOA., (Copyright © 2020 Elsevier Masson SAS. All rights reserved.)

Published
2021
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13. A Randomized Prospective Study Comparing Anti-T-Lymphocyte Igs to Basiliximab in Highly Sensitized Kidney Transplant Patients.

Author

Kamar N, Lepage B, Couzi L, Albano L, Durrbach A, Pernin V, Esposito L, Hebral AL, Darres A, Lequintrec M, Cassuto E, Merville P, Congy N, and Del Bello A

Abstract

Background: Two prospective studies that were performed before the era of highly sensitive solid-phase assays have shown a lower incidence of acute rejection in highly sensitized kidney-transplant patients given polyclonal antibodies compared with those given anti-CD25 monoclonal antibodies., Methods: This prospective pilot randomized French multicenter study aimed to compare anti-T-lymphocyte Ig (ATLG) ( n  = 32) and basiliximab ( n  = 27) in highly sensitized kidney-transplant patients without preformed donor-specific antibodies (pDSAs) as assessed by a Luminex Single-Antigen flow bead assay. Only patients with a calculated panel reactive antibody ≥50%, with at least 1 antibody with a mean fluorescence intensity ≥5000 and without a historical pDSA and without a pDSA on the day of transplantation were included., Results: Treatment failure as defined by biopsy-proven acute rejection, patient lost to follow-up, graft loss, and death was observed in 18.8% (95% confidence interval [CI], 8.9%-37.1%) and 18.8% (95% CI, 8.9%-37.1%) in patients who received ATLG and 14.8% (95% CI, 5.8%-34.8%) and 28.2% (95% CI, 14.2%-51.2%) of patients who received basiliximab, respectively at 6 ( P  = 0.66) and 12 ( P  = 0.62) months post-transplantation. One T cell-mediated rejection was observed in ATLG-treated patients (3.1%). One antibody-mediated rejection due to a de novo donor-specific antibody (DSA) occurred in basiliximab-treated patients (3.7%). Patient survival, graft survival, kidney parameters, and infection rate were similar in the 2 groups., Conclusion: This pilot study indicates that in highly sensitized kidney-transplant patients without pDSAs, both ATLG and basiliximab can be used efficiently and safely. However, because of the lack of power, these results should be interpreted with caution., (© 2020 International Society of Nephrology. Published by Elsevier Inc.)

Published
2020
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14. The clinicopathologic characteristics of kidney diseases related to monotypic IgA deposits.

Author

Vignon M, Cohen C, Faguer S, Noel LH, Guilbeau C, Rabant M, Higgins S, Hummel A, Hertig A, Francois H, Lequintrec M, Vilaine E, Knebelmann B, Pourrat J, Chauveau D, Goujon JM, Javaugue V, Touchard G, El Karoui K, and Bridoux F

Subjects
Adult, Aged, Aged, 80 and over, Biomarkers analysis, Biopsy, Cell Proliferation, Diagnosis, Differential, Disease Progression, Female, Fluorescent Antibody Technique, France, Glomerulonephritis drug therapy, Glomerulonephritis pathology, Glomerulonephritis, IGA drug therapy, Glomerulonephritis, IGA pathology, Heavy Chain Disease drug therapy, Heavy Chain Disease pathology, Humans, Immunoglobulin alpha-Chains analysis, Immunoglobulin gamma-Chains analysis, Kidney drug effects, Kidney ultrastructure, Male, Middle Aged, Multiple Myeloma drug therapy, Multiple Myeloma pathology, Predictive Value of Tests, Prognosis, Retrospective Studies, Time Factors, Glomerulonephritis immunology, Glomerulonephritis, IGA immunology, Heavy Chain Disease immunology, Immunoglobulin A analysis, Kidney immunology, Multiple Myeloma immunology
Abstract

Monoclonal gammopathy of renal significance (MGRS) regroups renal disorders caused by a monoclonal immunoglobulin without overt hematological malignancy. MGRS includes tubular disorders, glomerular disorders with organized deposits, and glomerular disorders with non-organized deposits, such as proliferative glomerulonephritis with monoclonal IgG deposits. Since glomerular involvement related to monotypic IgA deposits is poorly described we performed retrospective analysis and defined clinico-biological characteristics, renal pathology, and outcome in 19 referred patients. This analysis allowed distinction between 2 types of glomerulopathies, α-heavy chain deposition disease (5 patients) and glomerulonephritis with monotypic IgA deposits (14 patients) suggestive of IgA-proliferative glomerulonephritis with monoclonal immunoglobulin deposits in 12 cases. Clinicopathologic characteristics of α-heavy chain deposition disease resemble those of the γ-heavy chain disease, except for a higher frequency of extra-capillary proliferation and extra-renal involvement. IgA-proliferative glomerulonephritis with monoclonal immunoglobulin deposits should be differentiated from diseases with polytypic IgA deposits, given distinct clinical, histological, and pathophysiological features. Similarly to IgG-proliferative glomerulonephritis with monoclonal immunoglobulin deposits, overt hematological malignancy was infrequent, but sensitive serum and bone marrow studies revealed a subtle plasma cell proliferation in most patients with IgA-proliferative glomerulonephritis with monoclonal immunoglobulin deposits. Anti-myeloma agents appeared to favorably influence renal prognosis. Thus, potential progression towards symptomatic IgA multiple myeloma suggests that careful hematological follow-up is mandatory. This series expands the spectrum of renal disease in MGRS., (Copyright © 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Published
2017
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15. Primary glomerulonephritis with isolated C3 deposits: a new entity which shares common genetic risk factors with haemolytic uraemic syndrome.

Author

Servais A, Frémeaux-Bacchi V, Lequintrec M, Salomon R, Blouin J, Knebelmann B, Grünfeld JP, Lesavre P, Noël LH, and Fakhouri F

Subjects
Adolescent, Adult, Aged, Child, Complement C3 Nephritic Factor analysis, Complement Factor H analysis, Complement Factor H genetics, Female, Fibrinogen analysis, Fibrinogen genetics, Genetic Predisposition to Disease, Glomerulonephritis classification, Glomerulonephritis immunology, Glomerulonephritis metabolism, Glomerulonephritis pathology, Glomerulonephritis, Membranoproliferative genetics, Glomerulonephritis, Membranoproliferative immunology, Glomerulonephritis, Membranoproliferative metabolism, Glomerulonephritis, Membranoproliferative pathology, Humans, Male, Membrane Cofactor Protein genetics, Mesangial Cells chemistry, Mesangial Cells ultrastructure, Middle Aged, Retrospective Studies, Risk Factors, Complement C3 analysis, Complement Pathway, Alternative genetics, Glomerulonephritis genetics, Hemolytic-Uremic Syndrome genetics
Abstract

Introduction: Abnormal control of the complement alternative pathway (CAP) (factor H, factor I and membrane cofactor protein (MCP) deficiencies) is a well established risk factor for the occurrence of haemolytic uraemic syndrome (HUS). In some instances, HUS may be associated with an unusual glomerulonephritis with isolated C3 deposits (glomerulonephritis C3). We determined whether HUS and glomerulonephritis C3 share common genetic susceptibility factors., Methods: We identified 19 patients with glomerulonephritis C3. We measured levels of circulating complement components, performed assays for the detection of C3 nephritic factor (C3NeF) and screened factor H, factor I and MCP coding genes for the presence of mutations., Results: Patients were divided in two groups based on renal pathology findings: group I (n = 13) had typical features of type I membranoproliferative glomerulonephritis (glomerulonephritis C3 with membranoproliferative glomerulonephritis (MPGN)) and group II (n = 6) was characterised by mesangial and epimembranous C3 deposits in the absence of mesangial proliferation (glomerulonephritis C3 without MPGN). Mutations in complement regulatory genes were detected in 4/6 patients with glomerulonephritis C3 without MPGN (heterozygous mutations in factor H gene (two patients) with low factor H antigenic level in one case, heterozygous mutations in factor I gene (two patients)) and in only 2/13 patients with glomerulonephritis C3 with MPGN (heterozygous mutations in factor H gene (one patient) and double heterozygous mutation in CD 46 gene (one patient)). In contrast, C3NeF was present in 5/13 patients with glomerulonephritis C3 with MPGN and in 2/6 patients with glomerulonephritis C3 without MPGN, one of whom had a factor H mutation., Conclusion: HUS and glomerulonephritis C3 without MPGN share common genetic risk factors. Constitutional or acquired dysregulation of the CAP is probably associated with a wide spectrum of diseases, ranging from HUS to glomerulonephritis C3 with MPGN.

Published
2007
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