TYPES OF SOLID ORGAN ALLOGRAFT REJECTION
In hyperacute rejection, thrombosis of the vasculature occurs immediately after anasto-mosis of the solid organ graft blood vessels and release of the surgical clamp, which is caused by the presence of preformed anti-bodies that bind to the endothelial anti-gens. In the early days of transplantation, ABO incompatibility was the main culprit. Because ABO incompatibility is largely avoided now, hyperacute rejection usually occurs when IgG antibodies react with for-eign M HC antigens or lesser-known alloan-tigens in the endothelium. The latter may be associated with accelerated hyperacute rejec-tion that lasts a few days. Adequate screen-ing for preformed anti-HLA antibodies and ABO testing should prevent hyperacute rejection.
Acute rejection is an inflammatory process affecting the vasculature and parenchyma of the allograft, which occurs a few days to a week after transplantation. Activated T cells can cause direct lysis of the graft or release cytokines that promote inflammation in the allograft. The endothelial cells appear to be the earliest targets for rejection with re-sultant endotheliitis. A humoral-mediated response causes binding of antibodies to the blood vessel wall with resultant necro-sis and occlusion of the arteries.
Fibrosis with intimal thickening and eventual occlusion of medium-sized arteries that supply the graft characterizes chronic rejection. The fibrosis seen in chronic rejection is presumed to be a by-product of previous inflammation from acute rejection or from cytokines that stimulated fibroblast produc-tion. Chronic allograft rejection accounts for the majority of allograft failures.