Abstract
Chronic rejection is one of the major threats of graft function on a long-term basis in heart and kidney transplantation.During the last decades, the results of organ transplantation have improved steadily, whereas the annual rate of graft loss after the first post-transplantation year has not changed significantly (Cook and Terasaki, 1989; Thorogood et al., 1992). The diagnosis of chronic rejection is based on a combination of clinical, morphological and angiographic findings. The histopathology of chronic renal transplant rejection is charactenzed by various degrees of narrowing of the graft arteries and arterioles, interstitial cellular infiltration and fibrosis, tubular atrophy and variable glomerular changes (Maryniak et al., 1985; Kasiske et al., 1991; Paul et al.,1992). The vascular narrowing results from infiltration of the intima by mononuclear cells, migration and proliferation of vascular smooth muscle cells and fibroblasts from the media into the intima and subsequent deposition of extracellular matrix material. The histopathological picture of chronic heart graft rejection is characterized by atherosclerotic vascular changes in combination with variable degrees of interstitial fibrosis (Gao et al., 1987; Cary, 1992). The atherosclerotic vessel wall lesions are important features of chronic rejection in hearts and kidneys, but not specific, since they may also be observed in other vascularized organ allografts.
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Fellström, B., Larsson, E. (1993). Modulators of Chronic Rejection. In: Catravas, J.D., Callow, A.D., Ryan, U.S. (eds) Vascular Endothelium. NATO ASI Series, vol 257. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2437-3_13
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