ABSTRACT
The less steep rate of attrition of donor organs that are well matched for recipient HLA antigens compared with that of poorly matched grafts supports the notion that immunological mechanisms are important determinations of long-term outcome.3,4 On
the other hand, in kidney transplantation at least, the remarkable similarity between the excellent success rates o f grafts from living u related and from related sources suggests that various nonspecific factors associated with procurement and storage of organs from brain dead cadavers may influence their less satisfactory success rate. The putative role of alloantigen-independent events in chronic graft dysfunction is also illustrated by the observation that renal transplants from identical human twins as well as long-term kidney isografts in rats may develop, albeit at a slower rate, progressive functional and morphologic changes that resemble the lesions of chronically rejecting allografts.5'7 The even tual failure (10 years) of 40% of the human isografts was originally thought to result from recurrent nephritis, although the original investigators also suggested the effect o f other undetermined causes. In further experimen tal studies, retransplantation o f organ allografts into the original donor strain prevents the development o f structural changes commensurate with chronic rejection if performed within a critical time period; late retransplantation does not alter the continu ous progression of the chronic process despite removal o f the host immunological drive.8,9 This latter finding emphasizes the notion that tissue injury beyond a certain point may lead to autonomous and programmed propagation and advancement of the lesions. Thus, the early stages of chronic rejection appear alloantigen dependent and reversible, whereas the
Transplant-Associated Coronary Artery Vasculopathy, edited by Marlene L. Rose. ©2001 Eurekah.com.
