Decreased expression of sirtuin 3 protein correlates with early stage chronic renal allograft dysfunction in a rat kidney model.

Chronic renal allograft dysfunction (CRAD) is the primary factor affecting the long-term survival of patients who have undergone renal transplantation. Oxidative stress and inflammation serve an important role in the pathological damage caused by CRAD in the early post-transplantation phase. Previous studies have demonstrated that sirtuin 3 (sirt3) protects cells from oxidative stress and inflammation. A model of renal orthotopic transplantation was established in the current study and kidney samples were harvested from the rats 12 weeks following surgery. Compared with the control groups, there were significantly increased levels of serum creatinine, blood urea nitrogen and 24 h urinary protein in the allograft group (P<0.05). Pathological examinations indicated mononuclear cell infiltration and intimal proliferation in the allograft group, which had a higher Banff score compared with the control groups. There were increased levels of malondialdehyde, decreased sirt3 protein expression and decreased superoxide dismutase enzyme activity in the allograft group compared with the control groups (P<0.05). In addition, there was a negative correlation between the expression of sirt3 and 24 h urinary protein excretion, serum creatinine levels, tubulointerstitial mononuclear cell infiltration, smooth muscle cell migration in the vascular wall and Banff scores. Thus, sirt3 may serve an important protective role in the early stage of CRAD.