Organ transplantation is the treatment of choice for end stage organ failure, and in recent decades
one year results have greatly improved. Two major problems facing the transplant community
remain; long-term survival of organ grafts has still not reached its full potential, and the shortage
of suitable donor organs is still increasing.
Long-term graft survival is significantly hampered by chronic transplant dysfunction (CTD). This
still poorly defined process of untreatable functional deterioration of an organ following transplantation
accounts for approximately 30 percent of graft loss in the first 5 years after transplantation.
In the kidney CTD, also known as chronic allograft nephropathy (CAN), is clinically
characterized by progressive renal dysfunction, associated with hypertension and proteinuria.
Renal biopsies show characteristic but nonspecific histopathological changes in the vascular, glomerular
and tubulointerstitial compartments of the kidney, which overlap with the histology of
normally aging kidneys. Although the term CAN has been recently replaced by “interstitial fibrosis
and tubular atrophy without evidence of any specific etiology” [3], we continue to use CAN in this
thesis, as this is the terminology used in the majority of the literature available to date.
Increasing evidence suggests that the development of CAN is multifactorial in origin, with alloantigen
dependent and allo-antigen independent factors contributing to the decline of renal
graft function. Of the allo-antigen independent factors, donor age and cold ischemia time
seem to be the major correlate to transplant survival. Clinical observations suggest an inverse
relationship between both donor age and ischemia time and long-term graft survival.
The mechanisms by which donor age or ischemia lead to reduced functional life span are currently
unknown.
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