**2. Rejection**

Over the past two decades, our thinking has changed from considering rejection as a primarily T-cell-mediated process (one that is now increasingly better managed in the era of more potent calcineurin inhibitors and broader use of T-cell depleting therapies), to the realization that insufficient control of the humoral arm of a recipient's immune system by current immuno‐ suppressive regimens is now the pathogenic factor primarily responsible for allograft dys‐ function and loss.[13, 15, 16] This has changed our perception about allograft losses which were deemed to be caused by calcineurin inhibitor (CNI) toxicity and chronic allograft nephropathy (CAN).

Furthermore, the growing incidence of transplantation across HLA and ABO barriers by using desensitisation programs, but in the face of known DSAs, has led to increased incidence and a wider variety of ABMR. We are now exposed to a greater spectrum of antibody-mediated graft injury.
