Chronic rejection is the most common cause of the long term renal graft loss. It is characterized by luminal
thickening and obliteration, interstitial sclerosis, glomerulosclerosis and tubular atrophy development. The pathology
is still unclear.
Alloantigen-dependent factors (acute rejection, HLA mismatch) and allograft-independent factors (ischaemia-re-
perfusion, hyperlipidaemia, hypertension, infection, nephrotoxicity, reduced nephron dose) have been implicated in
the etiology of chronic rejection. As a result of these factors, endothelial cells are activated and express a variety of
adhesion molecules, cytokines and growth factors. Lymphocytes and macrophages infiltrate the areas of local damage
and express other cytokines and growth factors (TGF, bFGF, PDGF). In the next step, vascular smooth muscle cells
proliferate and migrate from the media into the vascular intima and produce local extracellular matrix.
Which factors are the most important and which mechanisms are the key for the development of chronic rejection
are in the focus of ongoing research.
renal transplantation, chronic rejection