2016, Number 2
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ABSTRACTThere are several immunological and non-immunological factors related to renal graft deterioration, and histological lesions such as interstitial fibrosis and tubular atrophy overlap with those observed in aging kidneys. Consequently, it has been proposed that kidney transplant senescence could contribute to graft loss. The process of cell senescence displays characteristics such as an increased expression of specific aging suppressor genes, shortened telomeres, mitochondrial changes, increased expression of negative regulators of the cell cycle, and immunological senescence. Additionally, tubular frailty characterizes the aged kidney, making it more susceptible to ischemia, reperfusion, toxic injury, and consequently, to inflammation. Moreover, renal tissue injury predisposes the older graft not only to progressive deterioration due to glomerular hyperfiltration, but also triggers acute rejection due to increased immunogenicity. In conclusion, renal graft senescence is a complex process, and its better understanding will help the nephrologist in its management in order to achieve a longer graft survival.
Furuzawa-Carballeda J, Lima G, Alberú J, et al. Infiltrating cellular pattern in kidney graft biopsies translates into forkhead box protein 3 up-regulation and p16INK4α senescence protein down-regulation in patients treated with belatacept compared to cyclosporin A. Clin Exp Immunol. 2012;167:330-7.