The introduction of new immunosuppressive drugs in the 1980s able to minimize cellular rejection enabled successful solid organ transplantation and improved graft survival rates, even where Human Leucocyte Antigen (HLA) mismatched donor organs were transplanted (Muntean & Lucan, 2013;Thurman et al., 2019). While organ allocation schemes strive to minimize HLA mismatches, it is accepted that most transplants will have some level of HLA mismatch to ensure the effective utilization of a finite resource (Montgomery et al., 2018;NHS Blood & Transplant, 2019).Although HLA mismatches are permissible in solid organ transplantation, the presence of circulating antibodies directed against mismatched donor HLA antigens at the time of transplant can initiate acute antibody-mediated rejection (AMR), leading to graft dysfunction, endothelial inflammation and potential graft loss (Stites et al., 2015). These pre-transplant donor-specific HLA antibodies (DSA) can damage the organ through the activation of the complement cascade, through antibody-dependent cell-mediated cytotoxicity (ADCC) via Natural Killer (NK) cells and/or by direct opsonization