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Objective: We aimed to evaluate the effect of prolonged recovery from DGF on outcomes, using a new definition of DGF recovery time, among deceased donor kidney transplant recipients with DGF, and to examine the risk factors for prolonged recovery. Methods: From 2007 to 2016, 91 deceased donor kidney transplant recipients with DGF were retrospectively analyzed. DGF recovery time was defined as the time from transplantation to achieve a stable estimated glomerular filtration rate (eGFR). Recipients with a DGF recovery time greater than or equal to the median were assigned to the prolonged recovery group, while the others were assigned to the rapid recovery group. Result: The median DGF recovery time was 27 days. Donor terminal eGFR was significantly lower in the prolonged recovery group (n ¼ 46) compared with the rapid recovery group (n ¼ 45) (median 24.9 vs. 65.4 ml/min/1.73m 2 , p ¼ 0.004). The eGFR at 1 year post-transplant in the prolonged recovery group was significantly lower than that in the rapid recovery group (50.6 ± 20.0 vs. 63.5 ± 21.4 ml/min/1.73m 2 , p ¼ 0.005). The risk of adverse outcomes (acute rejection, pneumonia, graft failure, and death) was significantly greater in the prolonged recovery group (hazard ratio 2.604, 95% confidence interval 1.102-6.150, p ¼ 0.029) compared with the rapid recovery group. Conclusion: Decreased donor terminal eGFR is a risk factor for prolonged recovery from DGF after deceased kidney transplantation. Prolonged DGF recovery time is associated with reduced graft function at 1-year post-transplant, and poor transplant outcome.

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Background: Donor-derived cell-free DNA (ddcfDNA) has been suggested as an indicator of allograft injury in adult and pediatric kidney transplantation (KTx). However, the dynamics of ddcfDNA in pediatric KTx have not been investigated. In addition, it has not been demonstrated whether donor-recipient (D/R) size mismatch affect ddcfDNA level.Methods: Pediatric KTx recipients with a single donor kidney were enrolled and followed up for 1 year. ddcfDNA, calculated as a fraction (%) in the recipient plasma, was examined longitudinally within 3 months post-transplant. D/R size mismatch degree was described as D/R height ratio. The 33rd percentile of D/R height ratio (0.70) was used as the cut-off to divide the patients into low donor-recipient height ratio group (<0.70) and high donor-recipient height ratio group (≥0.70). The dynamics of ddcfDNA were analyzed and the impact factors were explored. Stable ddcfDNA was defined as the first lowest ddcfDNA. ddcfDNA flare-up was defined as a remarkable elevation by a proportion of >30% from stable value with a peak value >1% during elevation.Results: Twenty-one clinically stable recipients were enrolled. The median D/R height ratio was 0.83 (0.62–0.88). It took a median of 8 days for ddcfDNA to drop from day 1 and reach a stable value of 0.67% (0.46–0.73%). Nevertheless, 61.5% patients presented ddcfDNA>1% at day 30. Besides, 81.0% (17/21) of patients experienced elevated ddcfDNA and 47.6% (10/21) met the standard of ddcfDNA flare-up. Donor-recipient height ratio was an independent risk factor for ddcfDNA flare-up (odds ratio = 0.469 per 0.1, 95% CI 0.237–0.925, p = 0.029) and low donor-recipient height ratio (<0.70) was found to increase the risk of flare-up occurrence (odds ratio = 15.00, 95% CI 1.342–167.638, p = 0.028).Conclusions: ddcfDNA rebounds in many stable pediatric KTx recipients without rejection. This may be induced by significant D/R size mismatch and may affect its diagnostic performance at the early phase after pediatric KTx in children.

Antibody-mediated rejection (AMR) induced by donor-specific anti-HLA antibodies (DSA) remains a major cause of long-term graft loss after kidney transplantation. Currently, the presence of DSA cannot always be determined at a specific allele level, because existing donor HLA typing is low resolution and often incomplete, lacking HLA-DP, and occasionally HLA-C and HLA-DQ information and historical donor DNA samples are not available for HLA retyping. Here we present a novel, non-invasive technique for obtaining donor DNA from selectively expanded donor cells from urine of renal transplant recipients. Urine-derived cells were successfully expanded ex vivo from 31 of 32 enrolled renal transplant recipients, and with DNA obtained from these cells, donor HLA typing was unambiguously determined for HLA-A, -B, -C, -DRB1, -DQA1, -DQB1, -DPA1 and -DPB1 loci by next-generation sequencing.Our results showed 100% concordance of HLA typing data between donor peripheral blood and recipient urine-derived cells. In comparison, HLA typing showed that DNA derived from urine sediments mainly contained recipientderived DNA. We also present the successful application of our novel technique in a clinical case of AMR in a renal transplant recipient. Urine-derived donor cells can be isolated from kidney transplant recipients and serve as a suitable source of donor material for reliable high-resolution HLA genotyping.Thus, this approach can aid the assessment of DSA specificity to support the diagnosis of AMR as well as the evaluation of treatment efficacy in kidney transplant recipients when complete donor HLA information and donor DNA are unavailable.