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Objective To investigate the relationship between the interleukin (IL)-35 and the recovery of renal graft function. Methods Clinical data of 45 recipients receiving renal transplantation from donation after cardiac death (DCD) were retrospectively analyzed. According to the presence of delayed graft function (DGF) after renal transplantation, all recipients were divided into the immediate graft function (IGF) group (n=32) and DGF group (n=13). The serum creatinine (Scr) level and estimated glomerular filtration rate (eGFR) in the recipients were statistically compared between two groups at 1, 2, 3, 7, 14, 28 d and 3, 6 and 12 months after renal transplantation. The IL-35 levels in the serum and urine samples of the recipients were statistically compared between two groups at 1, 2, 3, 7, 14, 28 d following renal transplantation. Results In the DGF group, the renal function was restored slowly. Compared with the IGF group, the Scr level was significantly higher, whereas the eGFR was considerably lower in the DGF group at postoperative 7 d (both P < 0.05). At 1 year after surgery, there was no significant difference in the Scr level between two groups. Compared with the IGF group, the eGFR in the DGF group was significantly lower at postoperative 1 year (P < 0.05). At 1, 2, 3, 7, 14 d after operation, the serum levels of IL-35 in the DGF group were evidently lower than those in the IGF group (all P < 0.05). Compared with the IGF group, the serum level of IL-35 in the DGF group was significantly increased at postoperative 28 d (P < 0.05). At postoperative 1, 2, 3, 7 d, the IL-35 levels in the urine samples in the DGF group were significantly lower than those in the IGF group (all P < 0.05). At postoperative 14 and 28 d, the IL-35 levels in the urine samples did not significantly differ between two groups (both P > 0.05). Conclusions The low levels of IL-35 in the serum and urine of recipients after renal transplantation are associated with the incidence of DGF to certain extent, prompting that excessively weak systemic and local anti-inflammatory responses early after renal transplantation and uncontrolled excessive inflammatory response are probably the pivotal causes of DGF.