**3. Donor Specific Antibodies (DSAs)**

Great advances have occurred in solid organ transplantation since the pioneering observation of Kissmeyer et al.[17] in the 1960s, of the deleterious impact of allo-antibodies in kidney grafts. About three decades later, the team of Edmonton described rejection episodes following kidney transplantation related to the presence of anti-HLA donor specific antibodies (DSA) [18]. The presence of DSAs and positive crossmatches with donors has long been considered a contraindication to proceeding with transplantation as ABMR and graft loss is highly likely to occur in such situations[4]. However, recent data by Montgomery *et al.*[19] demonstrated a significant reduction in the risk of mortality among highly sensitized patients who underwent desensitization and transplantation compared with a well-controlled group of patients who remained on dialysis. These authors concluded that desensitization followed by living-donor transplantation offered significant survival benefit and that the survival advantage more than doubled by 8 years.

In addition to DSAs existing prior to transplant, it has been realised that they can emerge at any time after transplant, thus mediating allograft injury [14]. These *de novo* DSAs are different in their pathogenicity. They are active against class II HLA and are associated with a worse prognosis than DSAs against Class I HLA [14].

DSAs can cause all types of ABMR, including chronic ABMR, otherwise known as transplant glomerulopathy.[4, 5, 7-10, 20]
