Rejection of transplanted organs occurs because of the body's immune system. An allograft (transplant from another individual of the same species) will trigger rejection unless it is from the recipients (genetically) identical twin. The aim in transplantation is to match the donor organ with a recipient who is most likely to control their rejection with imumunosuppressants.
One of the main methods of improving graft survival is to match donor organs with recipients who have the best match of human lymphocyte antigens (HLA). HLA mismatch is often denoted using the number of mismatches corresponding to HLA-A, HLA-B and HLA-DR.
Living related donors (LRD) tend to be a better HLA matches than cadaveric donors (also referred to as deceased donors) and this lead to 10-15% increase in graft survival at 1 year.
Rejection occurs in three phases:
Due to pre-formed antibodies, this occurs the moment blood flows through the donor organ. Crossmatching of donor and recipient blood for lymphocytoxic antibodies should make this rare. It can be recognised by a rapid onset, mottled appearance of the transplanted organ leading to it becoming cyanotic.
This occurs anytime after about 1 week and may be seen up to several months post-op. Two forms are recognised: T-cell mediated rejection (TCR) and an antibody-mediated (i.e. humoral) rejection.
In the T-cell mediated form, there is interstitial infiltration of monocytes, leading to tubular destruction in the case of the kidney. Vascular infiltration is a feature of poorer prognosis. In the absence of cyclosporin, it presents with and acutely tender and swollen graft (if the graft is a kidney then hypertension will also be seen). In the presence of cyclosporin most patients will present with deteriorating graft function. Diagnosis and prognosis will be confirmed on biopsy (see also Banff classification).
Over many months and years some grafts suffer gradual and relentless loss of function. The mechanisms are not clearly defined and therapeutic options are limited.