Peri−Transplant Apoptosis in Renal Allografts*

Background. Apoptosis is one of the central mechanisms leading to organ damage in the course of renal ischemia− reperfusion. Objectives. The aim of the study was to investigate the extent of apoptosis in 53 renal allograft biopsies. Material and Methods. Twenty−two specimens were taken from deceased donors during organ procurement, 18 were taken after cold ischemia, and 13 were obtained 30 minutes after reperfusion. Apoptosis in kidney tissue was examined by TUNEL staining. Expression of the apoptotic mediator genes for Bcl−2 and iNOS were assessed using semiquantitative evaluation of the RT−PCR in situ. Results. Intense TUNEL staining as well as bcl−2 and iNOS gene expressions were found in the specimens taken from the deceased donors compared with those of a living donor. No significant differences between the three examined groups were noted. There was no effect of duration of brain death on gene expression and TUNEL stain− ing. Cold ischemia time influenced the expression of the gene for tubular iNOS analyzed after cold ischemia (r = 0.98, p < 0.0001). There was no significant correlation between the level of apoptosis and the extent of delayed graft function. Early allograft function (at days 14 and 30) positively correlated with the expression of bcl−2 as well as TUNEL staining in tubules after cold ischemia and negatively correlated with tubular TUNEL staining and expression of bcl−2 and iNOS in biopsies obtained during procurement (p < 0.05). Conclusions. Extensive apoptotic cell death was observed in the specimens taken directly after brain death with− out a further increase during cold ischemia and reperfusion. Surprisingly, only the presence of the apoptotic process in tubular cells exerted a negative effect on early allograft function (Adv Clin Exp Med 2008, 17, 2, 197–200).