**4.1. Indolent ABMR**

Modern therapies can efficiently reverse acute renal dysfunction from ABMR, but they usually fail to deplete antibody-secreting plasma cells from the spleen and bone marrow of allograft recipients.[25] Hence, after a clinical episode of acute ABMR, DSAs remain in circulation and cause slowly progressive microvascular abnormalities without acute compromise of graft function, at least initially. This truncated form of antibody-mediated injury is called subclinical or indolent ABMR. [26, 27]
