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1. Renal Recovery for Patients with ANCA-Associated Vasculitis and Low eGFR in the ADVOCATE Trial of Avacopan

Author

Peh, C. Au, Chakera, A., Cooper, B., Kurtkoti, J., Langguth, D., Levidiotis, V., Luxton, G., Mount, P., Mudge, D., Noble, E., Phoon, R., Ranganathan, D., Ritchie, A., Ryan, J., Suranyi, M., Rosenkranz, A., Lhotta, K., Kronbichler, A., Demoulin, N., Bovy, C., Hellemans, R., Hougardy, J., Sprangers, B., Wissing, K., Pagnoux, C., Barbour, S., Brachemi, S., Cournoyer, S., Girard, L., Laurin, L., Liang, P., Philibert, D., Walsh, M., Tesar, V., Becvar, R., Horak, P., Rychlik, I., Szpirt, W., Dieperink, H., Gregersen, J., Ivarsen, P., Krarup, E., Lyngsoe, C., Rigothier, C., Augusto, J., Belot, A., Chauveau, D., Cornec, D., Jourde-Chiche, N., Ficheux, M., Karras, A., Klein, A., Maurier, F., Mesbah, R., Moranne, O., Neel, A., Quemeneur, T., Saadoun, D., Terrier, B., Zaoui, P., Schaier, M., Benck, U., Bergner, R., Busch, M., Floege, J., Grundmann, F., Haller, H., Haubitz, M., Hellmich, B., Henes, J., Hohenstein, B., Hugo, C., Iking-Konert, C., Arndt, F., Kubacki, T., Kotter, I., Lamprecht, P., Lindner, T., Halbritter, J., Mehling, H., Schönermarck, U., Venhoff, N., Vielhauer, V., Witzke, O., Szombati, I., Szucs, G., Garibotto, G., Alberici, F., Brunetta, E., Dagna, L., De Vita, S., Emmi, G., Gabrielli, A., Manenti, L., Pieruzzi, F., Roccatello, D., Salvarani, C., Dobashi, H., Atsumi, T., Fujimoto, S., Hagino, N., Ihata, A., Kaname, S., Kaneko, Y., Katagiri, A., Katayama, M., Kirino, Y., Kitagawa, K., Komatsuda, A., Kono, H., Kurasawa, T., Matsumura, R., Mimura, T., Morinobu, A., Murakawa, Y., Naniwa, T., Nanki, T., Ogawa, N., Oshima, H., Sada, K., Sugiyama, E., Takeuchi, T., Taki, H., Tamura, N., Tsukamoto, T., Yamagata, K., Yamamura, M., van Daele, P., Rutgers, A., Teng, Y., Walker, R., Chua, I., Collins, M., Rabindranath, K., de Zoysa, J., Svensson, M., Grevbo, B., Kalstad, S., Little, M., Clarkson, M., Molloy, E., Pamplona, I. Agraz, Anton, J., Lucia, V. Barrio, Ciggaran, S., Cid, M. Cinta, Encarnacion, M. Diaz, Oliveras, X. Fulladosa, Soler, M. Jose, Rusinol, H. Marco, Praga, M., Porras, L. Quintana, Segarra, A., Bruchfeld, A., Segelmark, M., Soveri, I., Thomaidi, E., Westman, K., Neumann, T., Burnier, M., Daikeler, T., Dudler, J., Hauser, T., Seeger, H., Vogt, B., Jayne, D., Burton, J., Al Jayyousi, R., Amin, T., Andrews, J., Baines, L., Brogan, P., Dasgupta, B., Doulton, T., Flossmann, O., Griffin, S., Harper, J., Harper, L., Kidder, D., Klocke, R., Lanyon, P., Luqmani, R., McLaren, J., Makanjuola, D., McCann, L., Nandagudi, A., Selvan, S., O'Riordan, E., Patel, M., Patel, R., Pusey, C., Rajakariar, R., Robson, J., Robson, M., Salama, A., Smyth, L., Sznajd, J., Taylor, J., Merkel, P., Sreih, A., Belilos, E., Bomback, A., Carlin, J., Chen Lin, Y. Chang, Derebail, V., Dragoi, S., Dua, A., Forbess, L., Geetha, D., Gipson, P., Gohh, R., Greenwood, G.T., Hugenberg, S., Jimenez, R., Kaskas, M., Kermani, T., Kivitz, A., Koening, C., Langford, C., Marder, G., Mohamed, A., Monach, P., Neyra, N., Niemer, G., Niles, J., Obi, R., Owens, C., Parks, D., Podoll, A., Rovin, B., Sam, R., Shergy, W., Silva, A., Specks, U., Spiera, R., Springer, J., Striebich, C., Swarup, A., Thakar, S., Tiliakos, A., Tsai, Y., Waguespack, D., Wasko, M. Chester, Cortazar, Frank B., Niles, John L., Jayne, David R.W., Merkel, Peter A., Bruchfeld, Annette, Yue, Huibin, Schall, Thomas J., and Bekker, Pirow

Published
2023
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3. Renal Recovery for Patients with ANCA-Associated Vasculitis and Low eGFR in the ADVOCATE Trial of Avacopan

Author

Cortazar, F. B., Niles, J. L., Jayne, D. R. W., Merkel, P. A., Bruchfeld, A., Yue, H., Schall, T. J., Bekker, P., Peh, C. A., Chakera, A., Cooper, B., Kurtkoti, J., Langguth, D., Levidiotis, V., Luxton, G., Mount, P., Mudge, D., Noble, E., Phoon, R., Ranganathan, D., Ritchie, A., Ryan, J., Suranyi, M., Rosenkranz, A., Lhotta, K., Kronbichler, A., Demoulin, N., Bovy, C., Hellemans, R., Hougardy, J., Sprangers, B., Wissing, K., Pagnoux, C., Barbour, S., Brachemi, S., Cournoyer, S., Girard, L., Laurin, L., Liang, P., Philibert, D., Walsh, M., Tesar, V., Becvar, R., Horak, P., Rychlik, I., Szpirt, W., Dieperink, H., Gregersen, J., Ivarsen, P., Krarup, E., Lyngsoe, C., Rigothier, C., Augusto, J., Belot, A., Chauveau, D., Cornec, D., Jourde-Chiche, N., Ficheux, M., Karras, A., Klein, A., Maurier, F., Mesbah, R., Moranne, O., Neel, A., Quemeneur, T., Saadoun, D., Terrier, B., Zaoui, P., Schaier, M., Benck, U., Bergner, R., Busch, M., Floege, J., Grundmann, F., Haller, H., Haubitz, M., Hellmich, B., Henes, J., Hohenstein, B., Hugo, C., Iking-Konert, C., Arndt, F., Kubacki, T., Kotter, I., Lamprecht, P., Lindner, T., Halbritter, J., Mehling, H., Schonermarck, U., Venhoff, N., Vielhauer, V., Witzke, O., Szombati, I., Szucs, G., Garibotto, G., Alberici, F., Brunetta, E., Dagna, L., De Vita, S., Emmi, G., Gabrielli, A., Manenti, L., Pieruzzi, F., Roccatello, D., Salvarani, C., Dobashi, H., Atsumi, T., Fujimoto, S., Hagino, N., Ihata, A., Kaname, S., Kaneko, Y., Katagiri, A., Katayama, M., Kirino, Y., Kitagawa, K., Komatsuda, A., Kono, H., Kurasawa, T., Matsumura, R., Mimura, T., Morinobu, A., Murakawa, Y., Naniwa, T., Nanki, T., Ogawa, N., Oshima, H., Sada, K., Sugiyama, E., Takeuchi, T., Taki, H., Tamura, N., Tsukamoto, T., Yamagata, K., Yamamura, M., van Daele, P., Rutgers, A., Teng, Y., Walker, R., Chua, I., Collins, M., Rabindranath, K., de Zoysa, J., Svensson, M., Grevbo, B., Kalstad, S., Little, M., Clarkson, M., Molloy, E., Pamplona, I. A., Anton, J., Lucia, V. B., Ciggaran, S., Cid, M. C., Encarnacion, M. D., Oliveras, X. F., Soler, M. J., Rusinol, H. M., Praga, M., Porras, L. Q., Segarra, A., Segelmark, M., Soveri, I., Thomaidi, E., Westman, K., Neumann, T., Burnier, M., Daikeler, T., Dudler, J., Hauser, T., Seeger, H., Vogt, B., Jayne, D., Burton, J., Al Jayyousi, R., Amin, T., Andrews, J., Baines, L., Brogan, P., Dasgupta, B., Doulton, T., Flossmann, O., Griffin, S., Harper, J., Harper, L., Kidder, D., Klocke, R., Lanyon, P., Luqmani, R., Mclaren, J., Makanjuola, D., Mccann, L., Nandagudi, A., Selvan, S., O'Riordan, E., Patel, M., Patel, R., Pusey, C., Rajakariar, R., Robson, J., Robson, M., Salama, A., Smyth, L., Sznajd, J., Taylor, J., Merkel, P., Sreih, A., Belilos, E., Bomback, A., Carlin, J., Chen Lin, Y. C., Derebail, V., Dragoi, S., Dua, A., Forbess, L., Geetha, D., Gipson, P., Gohh, R., Greenwood, G. T., Hugenberg, S., Jimenez, R., Kaskas, M., Kermani, T., Kivitz, A., Koening, C., Langford, C., Marder, G., Mohamed, A., Monach, P., Neyra, N., Niemer, G., Niles, J., Obi, R., Owens, C., Parks, D., Podoll, A., Rovin, B., Sam, R., Shergy, W., Silva, A., Specks, U., Spiera, R., Springer, J., Striebich, C., Swarup, A., Thakar, S., Tiliakos, A., Tsai, Y., Waguespack, D., Wasko, M. C., Cortazar, F, Niles, J, Jayne, D, Merkel, P, Bruchfeld, A, Yue, H, Schall, T, Bekker, P, Peh, C, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schonermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, De Vita, S, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, van Daele, P, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, de Zoysa, J, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, Pamplona, I, Anton, J, Lucia, V, Ciggaran, S, Cid, M, Encarnacion, M, Oliveras, X, Soler, M, Rusinol, H, Praga, M, Porras, L, Segarra, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Burton, J, Al Jayyousi, R, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Chen Lin, Y, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, and Wasko, M

Subjects
avacopan, Clinical Research, renal recovery, Nephrology, low eGFR, complement 5a receptor, complement, ANCA-associated vasculiti
Abstract

INTRODUCTION: In the 330-patient ADVOCATE trial of avacopan for the treatment of antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis, in which 81% of patients had renal involvement, estimated glomerular filtration rate (eGFR) increased on average 7.3 ml/min per 1.73 m(2) in the avacopan group and 4.1 ml/min per 1.73 m(2) in the prednisone group (P = 0.029) at week 52. This new analysis examines the results in the patient subgroup with severe renal insufficiency at enrollment into the trial, i.e., eGFR ≤20 ml/min per 1.73 m(2). METHODS: eGFR was determined at baseline and over the course of the trial. Changes in eGFR were compared between the 2 treatment groups. RESULTS: In ADVOCATE, 27 of 166 patients (16%) in the avacopan group and 23 of 164 patients (14%) in the prednisone group had a baseline eGFR ≤20 ml/min per 1.73 m(2). At week 52, eGFR increased on average 16.1 and 7.7 ml/min per 1.73 m(2) in the avacopan and prednisone groups, respectively (P = 0.003). The last eGFR value measured during the 52-week treatment period was ≥2-fold higher than baseline in 41% of patients in the avacopan group compared to 13% in the prednisone group (P = 0.030). More patients in the avacopan group versus prednisone group had increases in eGFR above 20, 30, and 45 ml/min per 1.73 m(2), respectively. Serious adverse events occurred in 13 of 27 patients (48%) in the avacopan group and 16 of 23 patients (70%) in the prednisone group. CONCLUSION: Among patients with baseline eGFR ≤20 ml/min per 1.73 m(2) in the ADVOCATE trial, eGFR improved more in the avacopan group than in the prednisone group.

Published
2023

4. Renal Recovery for Patients with ANCA-Associated Vasculitis and Low eGFR in the ADVOCATE Trial of Avacopan

Author

Cortazar, F, Niles, J, Jayne, D, Merkel, P, Bruchfeld, A, Yue, H, Schall, T, Bekker, P, Peh, C, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schonermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, De Vita, S, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, van Daele, P, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, de Zoysa, J, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, Pamplona, I, Anton, J, Lucia, V, Ciggaran, S, Cid, M, Encarnacion, M, Oliveras, X, Soler, M, Rusinol, H, Praga, M, Porras, L, Segarra, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Burton, J, Al Jayyousi, R, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Chen Lin, Y, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, Wasko, M, Cortazar F. B., Niles J. L., Jayne D. R. W., Merkel P. A., Bruchfeld A., Yue H., Schall T. J., Bekker P., Peh C. A., Chakera A., Cooper B., Kurtkoti J., Langguth D., Levidiotis V., Luxton G., Mount P., Mudge D., Noble E., Phoon R., Ranganathan D., Ritchie A., Ryan J., Suranyi M., Rosenkranz A., Lhotta K., Kronbichler A., Demoulin N., Bovy C., Hellemans R., Hougardy J., Sprangers B., Wissing K., Pagnoux C., Barbour S., Brachemi S., Cournoyer S., Girard L., Laurin L., Liang P., Philibert D., Walsh M., Tesar V., Becvar R., Horak P., Rychlik I., Szpirt W., Dieperink H., Gregersen J., Ivarsen P., Krarup E., Lyngsoe C., Rigothier C., Augusto J., Belot A., Chauveau D., Cornec D., Jourde-Chiche N., Ficheux M., Karras A., Klein A., Maurier F., Mesbah R., Moranne O., Neel A., Quemeneur T., Saadoun D., Terrier B., Zaoui P., Schaier M., Benck U., Bergner R., Busch M., Floege J., Grundmann F., Haller H., Haubitz M., Hellmich B., Henes J., Hohenstein B., Hugo C., Iking-Konert C., Arndt F., Kubacki T., Kotter I., Lamprecht P., Lindner T., Halbritter J., Mehling H., Schonermarck U., Venhoff N., Vielhauer V., Witzke O., Szombati I., Szucs G., Garibotto G., Alberici F., Brunetta E., Dagna L., De Vita S., Emmi G., Gabrielli A., Manenti L., Pieruzzi F., Roccatello D., Salvarani C., Dobashi H., Atsumi T., Fujimoto S., Hagino N., Ihata A., Kaname S., Kaneko Y., Katagiri A., Katayama M., Kirino Y., Kitagawa K., Komatsuda A., Kono H., Kurasawa T., Matsumura R., Mimura T., Morinobu A., Murakawa Y., Naniwa T., Nanki T., Ogawa N., Oshima H., Sada K., Sugiyama E., Takeuchi T., Taki H., Tamura N., Tsukamoto T., Yamagata K., Yamamura M., van Daele P., Rutgers A., Teng Y., Walker R., Chua I., Collins M., Rabindranath K., de Zoysa J., Svensson M., Grevbo B., Kalstad S., Little M., Clarkson M., Molloy E., Pamplona I. A., Anton J., Lucia V. B., Ciggaran S., Cid M. C., Encarnacion M. D., Oliveras X. F., Soler M. J., Rusinol H. M., Praga M., Porras L. Q., Segarra A., Segelmark M., Soveri I., Thomaidi E., Westman K., Neumann T., Burnier M., Daikeler T., Dudler J., Hauser T., Seeger H., Vogt B., Jayne D., Burton J., Al Jayyousi R., Amin T., Andrews J., Baines L., Brogan P., Dasgupta B., Doulton T., Flossmann O., Griffin S., Harper J., Harper L., Kidder D., Klocke R., Lanyon P., Luqmani R., McLaren J., Makanjuola D., McCann L., Nandagudi A., Selvan S., O'Riordan E., Patel M., Patel R., Pusey C., Rajakariar R., Robson J., Robson M., Salama A., Smyth L., Sznajd J., Taylor J., Merkel P., Sreih A., Belilos E., Bomback A., Carlin J., Chen Lin Y. C., Derebail V., Dragoi S., Dua A., Forbess L., Geetha D., Gipson P., Gohh R., Greenwood G. T., Hugenberg S., Jimenez R., Kaskas M., Kermani T., Kivitz A., Koening C., Langford C., Marder G., Mohamed A., Monach P., Neyra N., Niemer G., Niles J., Obi R., Owens C., Parks D., Podoll A., Rovin B., Sam R., Shergy W., Silva A., Specks U., Spiera R., Springer J., Striebich C., Swarup A., Thakar S., Tiliakos A., Tsai Y., Waguespack D., Wasko M. C., Cortazar, F, Niles, J, Jayne, D, Merkel, P, Bruchfeld, A, Yue, H, Schall, T, Bekker, P, Peh, C, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schonermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, De Vita, S, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, van Daele, P, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, de Zoysa, J, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, Pamplona, I, Anton, J, Lucia, V, Ciggaran, S, Cid, M, Encarnacion, M, Oliveras, X, Soler, M, Rusinol, H, Praga, M, Porras, L, Segarra, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Burton, J, Al Jayyousi, R, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Chen Lin, Y, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, Wasko, M, Cortazar F. B., Niles J. L., Jayne D. R. W., Merkel P. A., Bruchfeld A., Yue H., Schall T. J., Bekker P., Peh C. A., Chakera A., Cooper B., Kurtkoti J., Langguth D., Levidiotis V., Luxton G., Mount P., Mudge D., Noble E., Phoon R., Ranganathan D., Ritchie A., Ryan J., Suranyi M., Rosenkranz A., Lhotta K., Kronbichler A., Demoulin N., Bovy C., Hellemans R., Hougardy J., Sprangers B., Wissing K., Pagnoux C., Barbour S., Brachemi S., Cournoyer S., Girard L., Laurin L., Liang P., Philibert D., Walsh M., Tesar V., Becvar R., Horak P., Rychlik I., Szpirt W., Dieperink H., Gregersen J., Ivarsen P., Krarup E., Lyngsoe C., Rigothier C., Augusto J., Belot A., Chauveau D., Cornec D., Jourde-Chiche N., Ficheux M., Karras A., Klein A., Maurier F., Mesbah R., Moranne O., Neel A., Quemeneur T., Saadoun D., Terrier B., Zaoui P., Schaier M., Benck U., Bergner R., Busch M., Floege J., Grundmann F., Haller H., Haubitz M., Hellmich B., Henes J., Hohenstein B., Hugo C., Iking-Konert C., Arndt F., Kubacki T., Kotter I., Lamprecht P., Lindner T., Halbritter J., Mehling H., Schonermarck U., Venhoff N., Vielhauer V., Witzke O., Szombati I., Szucs G., Garibotto G., Alberici F., Brunetta E., Dagna L., De Vita S., Emmi G., Gabrielli A., Manenti L., Pieruzzi F., Roccatello D., Salvarani C., Dobashi H., Atsumi T., Fujimoto S., Hagino N., Ihata A., Kaname S., Kaneko Y., Katagiri A., Katayama M., Kirino Y., Kitagawa K., Komatsuda A., Kono H., Kurasawa T., Matsumura R., Mimura T., Morinobu A., Murakawa Y., Naniwa T., Nanki T., Ogawa N., Oshima H., Sada K., Sugiyama E., Takeuchi T., Taki H., Tamura N., Tsukamoto T., Yamagata K., Yamamura M., van Daele P., Rutgers A., Teng Y., Walker R., Chua I., Collins M., Rabindranath K., de Zoysa J., Svensson M., Grevbo B., Kalstad S., Little M., Clarkson M., Molloy E., Pamplona I. A., Anton J., Lucia V. B., Ciggaran S., Cid M. C., Encarnacion M. D., Oliveras X. F., Soler M. J., Rusinol H. M., Praga M., Porras L. Q., Segarra A., Segelmark M., Soveri I., Thomaidi E., Westman K., Neumann T., Burnier M., Daikeler T., Dudler J., Hauser T., Seeger H., Vogt B., Jayne D., Burton J., Al Jayyousi R., Amin T., Andrews J., Baines L., Brogan P., Dasgupta B., Doulton T., Flossmann O., Griffin S., Harper J., Harper L., Kidder D., Klocke R., Lanyon P., Luqmani R., McLaren J., Makanjuola D., McCann L., Nandagudi A., Selvan S., O'Riordan E., Patel M., Patel R., Pusey C., Rajakariar R., Robson J., Robson M., Salama A., Smyth L., Sznajd J., Taylor J., Merkel P., Sreih A., Belilos E., Bomback A., Carlin J., Chen Lin Y. C., Derebail V., Dragoi S., Dua A., Forbess L., Geetha D., Gipson P., Gohh R., Greenwood G. T., Hugenberg S., Jimenez R., Kaskas M., Kermani T., Kivitz A., Koening C., Langford C., Marder G., Mohamed A., Monach P., Neyra N., Niemer G., Niles J., Obi R., Owens C., Parks D., Podoll A., Rovin B., Sam R., Shergy W., Silva A., Specks U., Spiera R., Springer J., Striebich C., Swarup A., Thakar S., Tiliakos A., Tsai Y., Waguespack D., and Wasko M. C.

Abstract

Introduction: In the 330-patient ADVOCATE trial of avacopan for the treatment of antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis, in which 81% of patients had renal involvement, estimated glomerular filtration rate (eGFR) increased on average 7.3 ml/min per 1.73 m2 in the avacopan group and 4.1 ml/min per 1.73 m2 in the prednisone group (P = 0.029) at week 52. This new analysis examines the results in the patient subgroup with severe renal insufficiency at enrollment into the trial, i.e., eGFR ≤20 ml/min per 1.73 m2. Methods: eGFR was determined at baseline and over the course of the trial. Changes in eGFR were compared between the 2 treatment groups. Results: In ADVOCATE, 27 of 166 patients (16%) in the avacopan group and 23 of 164 patients (14%) in the prednisone group had a baseline eGFR ≤20 ml/min per 1.73 m2. At week 52, eGFR increased on average 16.1 and 7.7 ml/min per 1.73 m2 in the avacopan and prednisone groups, respectively (P = 0.003). The last eGFR value measured during the 52-week treatment period was ≥2-fold higher than baseline in 41% of patients in the avacopan group compared to 13% in the prednisone group (P = 0.030). More patients in the avacopan group versus prednisone group had increases in eGFR above 20, 30, and 45 ml/min per 1.73 m2, respectively. Serious adverse events occurred in 13 of 27 patients (48%) in the avacopan group and 16 of 23 patients (70%) in the prednisone group. Conclusion: Among patients with baseline eGFR ≤20 ml/min per 1.73 m2 in the ADVOCATE trial, eGFR improved more in the avacopan group than in the prednisone group.

Published
2023

8. Avacopan for the Treatment of ANCA-Associated Vasculitis

Author

Jayne, David R W, Merkel, Peter A, Schall, Thomas J, Bekker, Pirow, ADVOCATE Study Group:, C Au Peh, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schönermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, S De Vita, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, P van Daele, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, J de Zoysa, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, I Agraz Pamplona, Anton, J, V Barrio Lucia, Ciggaran, S, M Cinta Cid, M Diaz Encarnacion, X Fulladosa Oliveras, M Soler, J, H Rusinol, M, Praga, M, L Quintana Porras, Segarra, A, Bruchfeld, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Jayne, D, Burton, J, R Al Jayyousi, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Merkel, P, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Y Chang Chen Lin, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, T Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Niles, J, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, M Chester Wasko, Internal Medicine, Immunology, Jayne, D, Merkel, P, Schall, T, Bekker, P, Pieruzzi, F, Jayne, David RW [0000-0002-1712-0637], Apollo - University of Cambridge Repository, and Translational Immunology Groningen (TRIGR)

Subjects
Male, Receptor, Anaphylatoxin C5a/antagonists & inhibitors, Anaphylatoxin C5a, Anaphylatoxin C5a/antagonists & inhibitors, Nipecotic Acids, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculiti, Administration, Oral, Azathioprine, Kaplan-Meier Estimate, 030204 cardiovascular system & hematology, urologic and male genital diseases, Gastroenterology, C5a receptor, Cyclophosphamide/administration & dosage, Rituximab/administration & dosage, Immunosuppressive Agent, renal vasculitis, Prednisone/administration & dosage, 0302 clinical medicine, Glucocorticoid, immune system diseases, Prednisone, Recurrence, Medicine, 030212 general & internal medicine, skin and connective tissue diseases, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/drug therapy, Aniline Compounds, Remission Induction, General Medicine, Aniline Compound, Middle Aged, Administration, Combination, Rituximab, Drug Therapy, Combination, Female, Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis, Cyclophosphamide, Double-Blind Method, Glucocorticoids, Humans, Immunosuppressive Agents, Receptor, Anaphylatoxin C5a, Vasculitis, Receptor, medicine.drug, Human, Azathioprine/administration & dosage, Oral, medicine.medical_specialty, Nipecotic Acid, ANCA-Associated Vasculitis, 03 medical and health sciences, Drug Therapy, Internal medicine, Aniline Compounds/adverse effects, cardiovascular diseases, Immunosuppressive Agents/administration & dosage, Anti-neutrophil cytoplasmic antibody, business.industry, Glucocorticoids/administration & dosage, medicine.disease, Nipecotic Acids/adverse effects, respiratory tract diseases, business
Abstract

BACKGROUND: The C5a receptor inhibitor avacopan is being studied for the treatment of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.METHODS: In this randomized, controlled trial, we assigned patients with ANCA-associated vasculitis in a 1:1 ratio to receive oral avacopan at a dose of 30 mg twice daily or oral prednisone on a tapering schedule. All the patients received either cyclophosphamide (followed by azathioprine) or rituximab. The first primary end point was remission, defined as a Birmingham Vasculitis Activity Score (BVAS) of 0 (on a scale from 0 to 63, with higher scores indicating greater disease activity) at week 26 and no glucocorticoid use in the previous 4 weeks. The second primary end point was sustained remission, defined as remission at both weeks 26 and 52. Both end points were tested for noninferiority (by a margin of 20 percentage points) and for superiority.RESULTS: A total of 331 patients underwent randomization; 166 were assigned to receive avacopan, and 165 were assigned to receive prednisone. The mean BVAS at baseline was 16 in both groups. Remission at week 26 (the first primary end point) was observed in 120 of 166 patients (72.3%) receiving avacopan and in 115 of 164 patients (70.1%) receiving prednisone (estimated common difference, 3.4 percentage points; 95% confidence interval [CI], -6.0 to 12.8; PCONCLUSIONS: In this trial involving patients with ANCA-associated vasculitis, avacopan was noninferior but not superior to prednisone taper with respect to remission at week 26 and was superior to prednisone taper with respect to sustained remission at week 52. All the patients received cyclophosphamide or rituximab. The safety and clinical effects of avacopan beyond 52 weeks were not addressed in the trial. (Funded by ChemoCentryx; ADVOCATE ClinicalTrials.gov number, NCT02994927.).

Published
2021

10. Single-center experience of patients with interstitial lung diseases during the early days of the COVID-19 pandemic

Author

Ancion, A., Bouquegneau, A., Bovy, C., Darcis, G., Defraigne, J.O., Duysinx, B., Ghuysen, A., Gilbert, A., Heinen, V., Lambermont, B., Malaise, O., Martin, M., Misset, B., Moutschen, M., Nguyen Dang, D., Piazza, J., Szecel, J., Vaillant, F., Van Cauwenberge, H., Von Frenckell, C., Vroonen, L., Guiot, J., Henket, M., Frix, A.N., Delvaux, M., Denis, A., Giltay, L., Thys, M., Gester, F., Corhay, J.L., and Louis, R.

Published
2020
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12. POS-196 PATIENTS WITH COVID-19 MOSTLY RECOVER FROM TUBULAR PROTEINURIA AND ACUTE KIDNEY INJURY AFTER HOSPITAL DISCHARGE

Author

Bouquegneau, A., primary, Huart, J., additional, Lutteri, L., additional, Erpicum, P., additional, Grosch, S., additional, Résimont, G., additional, Wiesen, P., additional, Rousseau, A.F., additional, Bovy, C., additional, Krzesinski, J.M., additional, Thys, M., additional, Lambermont, B., additional, Misset, B., additional, Pottel, H., additional, Darcis, G., additional, Cavalier, E., additional, Jouret, F., additional, and Delanaye, P., additional

Published
2021
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13. Single-center experience of patients with interstitial lung diseases during the early days of the COVID-19 pandemic

Author

Guiot, J., primary, Henket, M., additional, Frix, A.N., additional, Delvaux, M., additional, Denis, A., additional, Giltay, L., additional, Thys, M., additional, Gester, F., additional, Moutschen, M., additional, Corhay, J.L., additional, Louis, R., additional, Ancion, A., additional, Bouquegneau, A., additional, Bovy, C., additional, Darcis, G., additional, Defraigne, J.O., additional, Duysinx, B., additional, Ghuysen, A., additional, Gilbert, A., additional, Heinen, V., additional, Lambermont, B., additional, Malaise, O., additional, Martin, M., additional, Misset, B., additional, Nguyen Dang, D., additional, Piazza, J., additional, Szecel, J., additional, Vaillant, F., additional, Van Cauwenberge, H., additional, Von Frenckell, C., additional, and Vroonen, L., additional

Published
2020
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16. [18F]FDG PET/CT imaging disproves renal allograft acute rejection in kidney transplant recipients with acute kidney dysfunction: a validation cohort.

Author

Lovinfosse, P., Weekers, L., Pottel, H., Bouquegneau, A., Bonvoisin, C., Bovy, C., Grosch, S., Hustinx, R., and Jouret, Francois

Subjects
KIDNEY transplantation, ACUTE kidney failure, HOMOGRAFTS, TUKEY'S test, KIDNEY failure
Abstract

Purpose: [18F]FDG PET/CT may predict the absence of acute allograft rejection (AR) in kidney transplant recipients (KTRs) with acute kidney injury (AKI). Still, the proposed threshold of 1.6 of the mean of mean standardized uptake values (mSUVmean) in the renal parenchyma needs validation. Methods: We prospectively performed 86 [18F]FDG PET/CT in 79 adult KTRs who underwent per-cause transplant biopsy for suspected AR. Biopsy-proven polyoma BK nephropathies (n = 7) were excluded. PET/CT was performed 192 ± 18 min after administration of 254.4 ± 30.4 MBq of [18F]FDG. The SUVmean was measured in both upper and lower poles of the renal allograft. One-way analysis of variance (ANOVA) and Tukey's studentized range test were sequentially performed. The receiver operating characteristic (ROC) curve was drawn to discriminate "AR" from non-pathological ("normal" + "borderline") conditions. Results: The median age of the cohort was 55 [43; 63] years, with M/F gender ratio of 47/39. The mean eGFR was 31.9 ± 14.6 ml/min/1.73m2. Biopsies were categorized in 4 groups: "normal" (n = 54), "borderline" (n = 9), "AR" (n = 14), or "others" (n = 2). The median [min; max] mSUVmean reached 1.72 [1.02; 2.07], 1.97 [1.55; 2.11], 2.13 [1.65, 3.12], and 1.84 [1.57; 2.12] in "normal," "borderline," "AR," and "others" groups, respectively. ANOVA demonstrated a significant difference of mSUVmean among groups (F = 13.25, p < 0.0001). The ROC area under the curve was 0.86. Test sensitivity and specificity corresponding to the threshold value of 1.6 were 100% and 30%, respectively. Conclusion: [18F]FDG PET/CT may help noninvasively prevent inessential transplant biopsies in KTR with AKI. [ABSTRACT FROM AUTHOR]

Published
2021
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17. YKL-40 as a new promising prognostic marker of severity in COVID infection.

Author

Schoneveld, Lauranne, Ladang, Aurélie, Henket, Monique, Frix, Anne-Noëlle, Cavalier, Etienne, Guiot, Julien, the COVID-19 clinical investigators of the CHU de Liège, Schoneveld, L., Ladang, A., Henket, M., Frix, A., Cavalier, E., Guiot, J., Ancion, A., Berg, J., Bonhomme, O., Bouquegneau, A., Bovy, C., Bruls, S., and Darcis, G.

Published
2021
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24. Comparaison de l'évaluation des propriétés de transport transpéritonéal au moyen d'un dialysat 'conventionnel' par rapport à un nouveau dialysat dit 'biocompatible'

Author

UCL - SSS/IREC/NEFR - Pôle de Néphrologie, UCL - (SLuc) Service de néphrologie, Van Overmeire, L., Goffin, Eric, Bovy, P., Cornet, G., Krzesinski, J.M., Bovy, C., 12e Réunion commune de la Société de Néphrologie (SN) et de la Société Francophone de Dialyse (SFD), UCL - SSS/IREC/NEFR - Pôle de Néphrologie, UCL - (SLuc) Service de néphrologie, Van Overmeire, L., Goffin, Eric, Bovy, P., Cornet, G., Krzesinski, J.M., Bovy, C., and 12e Réunion commune de la Société de Néphrologie (SN) et de la Société Francophone de Dialyse (SFD)

Published
2010

30. Fluorodeoxyglucose F18Positron Emission Tomography Coupled With Computed Tomography in Suspected Acute Renal Allograft Rejection

Author

Lovinfosse, P., Weekers, L., Bonvoisin, C., Bovy, C., Grosch, S., Krzesinski, J.‐M., Hustinx, R., and Jouret, F.

Abstract

Management of kidney transplant recipients (KTRs) with suspected acute rejection (AR) ultimately relies on kidney biopsy; however, noninvasive tests predicting nonrejection would help avoid unnecessary biopsy. AR involves recruitment of leukocytes avid for fluorodeoxyglucose F18(18F‐FDG), thus 18F‐FDG positron emission tomography (PET) coupled with computed tomography (CT) may noninvasively distinguish nonrejection from AR. From January 2013 to February 2015, we prospectively performed 32 18F‐FDG PET/CT scans in 31 adult KTRs with suspected AR who underwent transplant biopsy. Biopsies were categorized into four groups: normal (n = 8), borderline (n = 10), AR (n = 8), or other (n = 6, including 3 with polyoma BK nephropathy). Estimated GFR was comparable in all groups. PET/CT was performed 201 ± 18 minutes after administration of 3.2 ± 0.2 MBq/kg of 18F‐FDG, before any immunosuppression change. Mean standard uptake values (SUVs) of both upper and lower renal poles were measured. Mean SUVs reached 1.5 ± 0.2, 1.6 ± 0.3, 2.9 ± 0.8, and 2.2 ± 1.2 for the normal, borderline, AR, and other groups, respectively. One‐way analysis of variance demonstrated a significant difference of mean SUVs among groups. A positive correlation between mean SUV and acute composite Banff score was found, with r2= 0.49. The area under the receiver operating characteristic curve was 0.93, with 100% sensitivity and 50% specificity using a mean SUV threshold of 1.6. In conclusion, 18F‐FDG PET/CT may help noninvasively prevent avoidable transplant biopsies in KTRs with suspected AR. 18FDG‐PET/CTimaging noninvasively identifies nonrejection in kidney transplant recipients with suspected acute rejection, and may allow selected patients to forgo renal transplant biopsy.

Published
2016
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31. Comparaison des taux de BNP et NT-proBNP chez des patients insuffisants rénaux pour prévenir l’insuffisance cardiaque.

Author

Goff, C., Kaux, J., Bovy, C., Silva, A., and Chapelle, J.

Abstract

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Published
2010
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35. [Diagnosis and management of renal allograft rejection]

Author

Erpicum P, Bonvoisin C, Grosch S, Bovy C, Tiago Pinto Coelho, Detry O, Jouret F, Weekers L, and Bouquegneau A

Subjects
Graft Rejection, Graft Survival, Humans, Allografts, Kidney, Kidney Transplantation
Abstract

Renal allograft rejection involves many mechanisms of innate and adaptive immunity, responsible for parenchymal inflammatory lesions that negatively impact the long-term outcomes of the renal allograft. The heterogeneous presentations of rejections in terms of clinical, biological and histological aspects make them difficult to manage in daily clinical practice. Indeed, current therapeutic strategies are disappointing in term of long-term outcomes, including graft survival. In this article, we will discuss the main effector mechanisms of rejection and their histological classification, as well as the existing treatments and those currently under evaluation.: Le rejet du greffon rénal fait intervenir de nombreux mécanismes de l’immunité innée et adaptative, responsables de lésions inflammatoires parenchymateuses impactant négativement le devenir au long cours du greffon rénal. La grande hétérogénéité dans la présentation clinique, biologique et histologique des rejets de greffe en fait des entités difficiles à prendre en charge en pratique clinique quotidienne. En effet, les stratégies thérapeutiques actuelles montrent des résultats assez décevants pour le traitement des rejets, ce qui a comme conséquence une diminution significative de la survie des greffons. Nous aborderons dans cet article les principaux mécanismes effecteurs des rejets, leur classification histologique ainsi que les traitements existants et en cours de validation.

41. Kidney biopsy for the diagnosis and treatment of kidney diseases. Recommendations from the French speaking Society of Nephrology (SFNDT) and French National Authority for Health (HAS) 2022

Author

de Laforcade L, Bobot M, Boffa JJ, Bovy C, Cartery C, Chauveau D, Gueutin V, Isnard-Bagnis C, Jourde Chiche N, Karras A, Meftah A, Müller C, Sié P, Stehlé T, Vrigneaud L, Vuiblet V, and Guerrot D

Subjects
Humans, France, Kidney pathology, Biopsy, Nephrology, Kidney Diseases diagnosis, Kidney Diseases therapy, Kidney Diseases pathology
Abstract

Kidney Biopsy (KB) is a crucial diagnostic tool in the field of renal diseases and is routinely performed in nephrology departments. A previous survey conducted by the Société Francophone de Néphrologie Dialyse Transplantation (SFNDT) revealed significant disparities in clinical practices, sometimes conflicting with the existing literature and recently published recommendations. In response, the SFNDT wished to promote the development of best practice guidelines, under the auspices of the French National Authority for Health (HAS), to establish a standardized framework for performing kidney biopsies in France.

Published
2024
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42. The uptake of [ 18 F]-fluorodeoxyglucose by the renal allograft correlates with the acute Banff scores of cortex inflammation but not with the 1-year graft outcomes.

Author

Fank H, Weekers L, Lovinfosse P, Pottel H, Seidel L, Jadoul A, Bouquegneau A, Bonvoisin C, Bovy C, Grosch S, Erpicum P, Hustinx R, and Jouret F

Abstract

Introduction: [ 18 F]FDG PET/CT noninvasively disproves acute kidney allograft rejection (AR) in kidney transplant recipients (KTRs) with suspected AR. However, the correlation of biopsy-based Banff vs. PET/CT-based scores of acute inflammation remains unknown, as does the prognostic performance of [ 18 F]FDG PET/CT at one year post suspected AR., Methods: From 2012 to 2019, 114 [ 18 F]FDG-PET/CTs were prospectively performed in 105 adult KTRs who underwent per cause transplant biopsies. Ordinal logistic regression assessed the correlation between the extent of histological inflammation and the mean standardized [ 18 F]FDG uptake values (mSUV mean ). Functional outcomes of kidney allografts were evaluated at one year post per cause biopsy and correlated to mSUVmean., Results: A significant correlation between mSUV mean and acute Banff score was found, with an adjusted R 2 of 0.25. The mSUV mean was significantly different between subgroups of "total i", with 2.30 ± 0.71 in score 3 vs. 1.68 ± 0.24 in score 0. Neither the function nor the survival of the graft at one year was statistically related to mSUV mean ., Discussion: [ 18 F]FDG-PET/CT may help noninvasively assess the severity of kidney allograft inflammation in KTRs with suspected AR, but it does not predict graft outcomes at one year., 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., (© 2023 Fank, Weekers, Lovinfosse, Pottel, Seidel, Jadoul, Bouquegneau, Bonvoisin, Bovy, Grosch, Erpicum, Hustinx and Jouret.)

Published
2023
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43. [The glomerulus in all its states].

Author

Grosch S, Erpicum P, Bouquegneau A, Jouret F, and Bovy C

Subjects
Hematuria etiology, Hematuria pathology, Humans, Kidney Glomerulus pathology, Proteinuria etiology, Glomerulonephritis diagnosis, Glomerulonephritis therapy, Kidney Diseases complications, Nephrotic Syndrome diagnosis, Nephrotic Syndrome etiology, Nephrotic Syndrome therapy
Abstract

Glomerulonephritis are the result of an inflammatory hit to the glomerulus. They are rare and heterogeneous renal diseases. Each glomerular compartment can be affected. The clinical manifestations present with hematuria, proteinuria and/or impaired renal function, either isolated or combined. Two main clinico-biological syndromes are described: nephrotic syndrome and nephritic syndrome. The latter can present in a more severe form i.e. rapidly progressive glomerulonephritis with the worst prognosis. These different clinical pictures are related to specific glomerular lesions. Thus, podocytic damage is mainly responsible for nephrotic syndromes, mesangial damage is responsible for proteinuria and hematuria and, finally, endothelial damage is responsible for nephritic syndrome and rapidly progressive glomerulonephritis. Therapeutic approaches include non-specific measures, combining both life-style and pharmacological interventions with the aim to reduce risk factors, and specific measures with the use of different immunosuppressive agents.

Published
2022

44. [Diagnosis and management of renal allograft rejection].

Author

Erpicum P, Bonvoisin C, Grosch S, Bovy C, Pinto Coelho T, Detry O, Jouret F, Weekers L, and Bouquegneau A

Subjects
Allografts, Graft Survival, Humans, Kidney, Graft Rejection diagnosis, Graft Rejection therapy, Kidney Transplantation adverse effects
Abstract

Renal allograft rejection involves many mechanisms of innate and adaptive immunity, responsible for parenchymal inflammatory lesions that negatively impact the long-term outcomes of the renal allograft. The heterogeneous presentations of rejections in terms of clinical, biological and histological aspects make them difficult to manage in daily clinical practice. Indeed, current therapeutic strategies are disappointing in term of long-term outcomes, including graft survival. In this article, we will discuss the main effector mechanisms of rejection and their histological classification, as well as the existing treatments and those currently under evaluation.

Published
2022

46. Survivors of COVID-19 mostly recover from tubular proteinuria and acute kidney injury after hospital discharge.

Author

Bouquegneau A, Huart J, Lutteri L, Erpicum P, Grosch S, Résimont G, Wiesen P, Rousseau AF, Bovy C, Krzesinski JM, Thys M, Lambermont B, Misset B, Pottel H, Darcis G, Cavalier E, Jouret F, and Delanaye P

Subjects
Hospitals, Humans, Patient Discharge, Proteinuria diagnosis, SARS-CoV-2, Survivors, Acute Kidney Injury diagnosis, Acute Kidney Injury therapy, COVID-19
Published
2021
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47. Proteinuria in COVID-19: prevalence, characterization and prognostic role.

Author

Huart J, Bouquegneau A, Lutteri L, Erpicum P, Grosch S, Résimont G, Wiesen P, Bovy C, Krzesinski JM, Thys M, Lambermont B, Misset B, Pottel H, Mariat C, Cavalier E, Burtey S, Jouret F, and Delanaye P

Subjects
Aged, Aged, 80 and over, Belgium epidemiology, Biomarkers urine, COVID-19 epidemiology, COVID-19 urine, Female, Humans, Male, Middle Aged, Prevalence, Prognosis, Proteinuria etiology, Proteinuria urine, Retrospective Studies, Survival Rate trends, COVID-19 complications, Proteinuria epidemiology
Abstract

Background: Proteinuria has been commonly reported in patients with COVID-19. However, only dipstick tests have been frequently used thus far. Here, the quantification and characterization of proteinuria were investigated and their association with mortality was assessed., Methods: This retrospective, observational, single center study included 153 patients, hospitalized with COVID-19 between March 28th and April 30th, 2020, in whom total proteinuria and urinary α 1 -microglobulin (a marker of tubular injury) were measured. Association with mortality was evaluated, with a follow-up until May 7th, 2020., Results: According to the Kidney Disease Improving Global Outcomes staging, 14% (n = 21) of the patients had category 1 proteinuria (< 150 mg/g of urine creatinine), 42% (n = 64) had category 2 (between 150 and 500 mg/g) and 44% (n = 68) had category 3 proteinuria (over 500 mg/g). Urine α 1 -microglobulin concentration was higher than 15 mg/g in 89% of patients. After a median follow-up of 27 [14;30] days, the mortality rate reached 18%. Total proteinuria and urinary α 1 -microglobulin were associated with mortality in unadjusted and adjusted models. This association was stronger in subgroups of patients with normal renal function and without a urinary catheter., Conclusions: Proteinuria is frequent in patients with COVID-19. Its characterization suggests a tubular origin, with increased urinary α 1 -microglobulin. Tubular proteinuria was associated with mortality in COVID-19 in our restropective, observational study.

Published
2021
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48. COVID-19-associated Nephropathy Includes Tubular Necrosis and Capillary Congestion, with Evidence of SARS-CoV-2 in the Nephron.

Author

Bouquegneau A, Erpicum P, Grosch S, Habran L, Hougrand O, Huart J, Krzesinski JM, Misset B, Hayette MP, Delvenne P, Bovy C, Kylies D, Huber TB, Puelles VG, Delanaye P, and Jouret F

Subjects
Aged, Aged, 80 and over, Capillaries pathology, Humans, In Situ Hybridization, Fluorescence, Kidney Glomerulus pathology, Male, Middle Aged, Necrosis, SARS-CoV-2, Acute Kidney Injury diagnosis, COVID-19 complications
Abstract

Background: Kidney damage has been reported in patients with COVID-19. Despite numerous reports about COVID-19-associated nephropathy, the factual presence of the SARS-CoV-2 in the renal parenchyma remains controversial., Methods: We consecutively performed 16 immediate (≤3 hours) postmortem renal biopsies in patients diagnosed with COVID-19. Kidney samples from five patients who died from sepsis not related to COVID-19 were used as controls. Samples were methodically evaluated by three pathologists. Virus detection in the renal parenchyma was performed in all samples by bulk RNA RT-PCR (E and N1/N2 genes), immunostaining (2019-nCOV N-Protein), fluorescence in situ hybridization (nCoV2019-S), and electron microscopy., Results: The mean age of our COVID-19 cohort was 68.2±12.8 years, most of whom were male (69%). Proteinuria was observed in 53% of patients, whereas AKI occurred in 60% of patients. Acute tubular necrosis of variable severity was found in all patients, with no tubular or interstitial inflammation. There was no difference in acute tubular necrosis severity between the patients with COVID-19 versus controls. Congestion in glomerular and peritubular capillaries was respectively observed in 56% and 88% of patients with COVID-19, compared with 20% of controls, with no evidence of thrombi. The 2019-nCOV N-Protein was detected in proximal tubules and at the basolateral pole of scattered cells of the distal tubules in nine out of 16 patients. In situ hybridization confirmed these findings in six out of 16 patients. RT-PCR of kidney total RNA detected SARS-CoV-2 E and N1/N2 genes in one patient. Electron microscopy did not show typical viral inclusions., Conclusions: Our immediate postmortem kidney samples from patients with COVID-19 highlight a congestive pattern of AKI, with no significant glomerular or interstitial inflammation. Immunostaining and in situ hybridization suggest SARS-CoV-2 is present in various segments of the nephron., Competing Interests: F. Jouret reports having consultancy agreements with ORGENESIS; reports receiving honoraria from AMGEN and OTSUKA; and reports being a scientific advisor or member of the Belgian Society of Nephrology. J.-M. Krzesinski reports having consultancy agreements with Bayer, Boehringer, Menarini, and Vifor Pharma; and reports receiving honoraria from Bayer, Boehringer, Menarini, and Vifor. P. Delanaye reports having consultancy agreements with ARK Biosciences and Immunodiagnostic Systems; and reports receiving honoraria from Amgen, AstraZeneca, Bayer, Fresenius, Menarini, Sanofi, and Siemens. T. Huber reports having consultancy agreements with AstraZeneca, Bayer, Boehringer-Ingelheim, DaVita, Deerfield, Fresenius Medical Care, GoldfinchBio, Mantrabio, Novartis, and Retrophin; reports receiving research funding from Amicus Therapeutics and Fresenius Medical Care; and reports being a scientific advisor or member of Kidney International (Journal; Editorial board) and Nature Review Nephrology (Journal, Advisory Board). All remaining authors have nothing to disclose., (Copyright © 2021 by the American Society of Nephrology.)

Published
2021
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49. [Therapeutic innovation in nephrology : 10 years of progress].

Author

Bovy C, Delanaye P, Jouret F, and Krzesinski JM

Subjects
Disease Progression, Glomerular Filtration Rate, Humans, Kidney, Quality of Life, Tolvaptan, Nephrology trends, Renal Insufficiency, Chronic therapy
Abstract

Chronic kidney disease (CKD) impairs the quality of life and increases the risk for cardiovascular morbimortality. Intensive research is conducted in order to slow down CKD development and progression. During the past decade, a better understanding of the pathophysiological mechanisms of glomerular diseases has highlighted the benefits of rituximab. Progresses have also been made in the understanding of the mechanisms of autosomal polycystic kidney disease, the most frequent inherited kidney disease. These observations led to the discovery and validation of tolvaptan, a blocker of the V2 receptor of the antidiuretic hormone as an innovative treatment. Type 2 diabetic disease is the leading cause worldwide of endstage kidney disease and dialysis. The development of new drugs, such as the gliflozins (inhibiting the sodium glucose reabsorption in the proximal tubule), has contributed to an improvement in the management of the cardiovascular and renal risks especially reducing congestive heart failure rate. Another important progress in nephrology since the beginning of the new century concerns a more precise estimation of the kidney function, which allows to better evaluate the slope of CKD progression and test the influence of different therapeutic approaches aiming at correcting anemia, hyperkalemia, metabolic acidosis and disturbances of calcium and phosphate. The present review summarizes all of these major advances in the field of CKD diagnosis and treatment, and envisions the future of nephrology for the next decade.

Published
2020

50. [Kidney injury in COVID-19].

Author

Erpicum P, Grosch S, Bouquegneau A, Huart J, Résimont G, Bovy C, Habran L, Delvenne P, Krzesinski JM, Burtey S, Delanaye P, and Jouret F

Subjects
COVID-19, Humans, SARS-CoV-2, Acute Kidney Injury complications, Betacoronavirus, Coronavirus Infections complications, Coronavirus Infections epidemiology, Pandemics, Pneumonia, Viral
Abstract

The SARS-CoV-2 virus causes a respiratory distress syndrome, the main symptom of COVID-19 (for "COronaVIrus Disease 2019"). This infectious disease has been causing a major health and socio-economic pandemic since December 2019. The pulmonary alveolus is regarded as the main target of SARS-CoV-2. However, this coronavirus is capable of directly or indirectly affecting other organs, including the kidneys. Here, we summarize the presumed pathophysiology of COVID-19 renal disease. The incidence of acute kidney injury ranges from 0,5 to 22 % of all patients infected with SARS-CoV-2. The need for renal replacement therapy is reported in 5-9 % of patients in intensive care. Histological analysis of renal biopsies mainly shows acute tubular necrosis of varying severity, as well as the congestion of glomerular and peri-tubular capillaries. Endothelitis has been described in few cases. Evidence for a factual inflammation of the glomerulus remains controversial. The medium/long term consequences of COVID-19 nephropathy are unknown and will deserve a tight follow-up.

Published
2020

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