Complement as the enabler of carfilzomib‐induced thrombotic microangiopathy
Miquel Blasco, Alexandra Martínez‐Roca, Luis Gerardo Rodríguez‐Lobato, Adriana García‐Herrera, Laura Rosiñol, Pedro Castro, Sara Fernández, Luís F. Quintana, María Teresa Cibeira, Joan Bladé, Carlos Fernández de Larrea, Natalia Tovar, Raquel Jimenez, Esteban Poch, Elena Guillén, Josep M. Campistol, Enric Carreras, Maribel Díaz‐Ricart, Marta Palomo
Abstract
Carfilzomib has been associated with the development of thrombotic microangiopathy (TMA) in relapsed/refractory multiple myeloma patients, a severe disease with no currently available aetiological treatment. We evaluated the potential role of terminal complement pathway in four patients with carfilzomib-induced TMA. Membrane attack complex (C5b-9) deposition on endothelial cells in culture exposed to plasma from patients during the acute phase of the disease suggests complement overactivation as a mechanism of potential endothelial damage in three out of four patients. If confirmed in larger cohorts, C5b-9 evaluation will allow early identification of patients who could benefit from complement blockade and treatment monitoring.