Prolonged cold storage leads to renal allograft injury lowering the allograft and, possibly, the recipient survival. The cold ischemia time (CIT) of the deceased donor kidney transplants inversely correlated with the transplant years (UNOS, 87-03, n = 116,638; r = −.22, p < .001). The CIT from 96-00 was lower than 90-95 (average 20 vs 23 hours; p < .05) despite higher ECD and DCD kidneys in the second half. In the first 6 months, rejection treatment was also lower for the second half (29% vs 19%, p < .05). HLA mismatch and PRA > 30% did not differ. The wait on dialysis, the recipient age, percentage of head trauma, and the kidneys' travel distance were higher in the second half. The use of newer immunosuppressants such as IL-2 receptor antagonists, tacrolimus, and mycophenolate were higher for the second half. The recipient survival, which was close to 90% at 3 years, did not differ between the periods. However, in the Cox model, after adjusting for age, gender, race, diabetes, and wait on dialysis, the CIT had a significant negative impact on recipient survival (RR for each 10-hour increase in CIT: 1.04; 1.01-1.07, 95% CI; p < .05), and the impact was more pronounced when the donor kidneys had > 30-hour CIT. Likewise, CIT had a significant negative impact on graft survival, particularly so for CIT > 20 hours. Unlike the recipient survival, the allograft survival was significantly higher in the second half than in the first half (79% vs 73%). Despite the higher survival, CIT continued to exert a graft-losing effect on the second half as analyzed in the multivariate model adjusting for recipient and donor age, recipients' race, HLA mismatch, PRA levels, rejection treatments, wait on dialysis, and presence of diabetes and donor's head trauma. Moreover, the % DGF between the two periods did not differ, indicating the persistence of cold ischemic injury in the second half of the last decade. Thus, this detailed analysis of the CIT and its effect on graft and patient survival over the last decade demonstrates (1) a modest reduction in CIT, mostly due to shifting of CIT from > 30 hours to 20 to 30 hours and (2) a change in immunosuppression in the second half, with lower rejection and graft loss but (3) no change in DGF and in the influence of CIT on graft survival, and (4) CIT as an independent risk factor for recipient survival.