scholarly journals Creatinine Reduction Ratio on Post-Transplant Day Two as Criterion in Defining Delayed Graft Function

2004 ◽  
Vol 4 (7) ◽  
pp. 1163-1169 ◽  
Author(s):  
Emilio Rodrigo ◽  
Juan C. Ruiz ◽  
Celestino Pinera ◽  
Gema Fernandez-Fresnedo ◽  
Rafael Escallada ◽  
...  
2012 ◽  
Vol 26 (5) ◽  
pp. 782-791 ◽  
Author(s):  
Miklos Z. Molnar ◽  
Csaba P. Kovesdy ◽  
Laszlo Rosivall ◽  
Suphamai Bunnapradist ◽  
Junichi Hoshino ◽  
...  

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Clara Pardinhas ◽  
Rita Leal ◽  
Francisco Caramelo ◽  
Teofilo Yan ◽  
Carolina Figueiredo ◽  
...  

Abstract Background and Aims As kidney transplants are growing in absolute numbers, so are patients with failed allografts and thus potential candidates for re-transplantation. Re-transplantation is challenging due to immunological barriers, surgical difficulties and clinical complexities but it has been proven that successful second transplantation improves life expectancy over dialysis. It is important to evaluate re-transplantation outcomes since 20% of patients on the waiting list are waiting for a second graft. Our aim was to compare major clinical outcomes such as acute rejection, graft and patient survival, between patients receiving a first or a second kidney transplant. Method We performed a retrospective study, that included 1552 patients submitted to a first (N=1443, 93%) or a second kidney transplant (N=109, 7%), between January 2008 and December 2018. Patients with more than 2 grafts or multi-organ transplant were excluded. Demographic, clinical and histocompatibility characteristics of both groups were registered from our unit database and compared. Delayed graft function was defined has the need of dialysis in the first week post-transplant. All acute rejection episodes were biopsy proven, according to Banff 2017 criteria. Follow-up time was defined at 1st June 2020 for functioning grafts or at graft failure (including death with a functioning graft). Results Recipients of a second graft were significantly younger (43 ±12 vs 50 ± 13 years old, p<0.001) and there were significantly fewer expanded-criteria donors in the second transplant group (31.5% vs 57.5%, p<0.001). The waiting time for a second graft was longer (63±50 vs 48±29 months, p=0.011). HLA mismatch was similar for both groups but PRA was significantly higher for second KT patients (21.6±25% versus 3±9%; p<0.001). All patients submitted to a second KT had thymoglobulin as induction therapy compared to 16% of the first KT group (p<0.001). We found no difference in primary dysfunction or delayed graft function between groups. Acute rejection was significantly more frequent in second kidney transplant recipients (19% vs 5%, p<0.001), being 10 acute cellular rejections, 7 were antibody mediated and 3 were borderline changes. For the majority of the patients (85%), acute rejection occurred in the first-year post-transplant. Death censored graft failure occurred in 236 (16.4%) patients with first kidney transplant and 25 (23%) patients with a second graft, p=0.08. Survival analysis showed similar graft survival for both groups (log-rank p=0.392). We found no difference in patients’ mortality at follow up for both groups. Conclusion Although second graft patients presented more episodes of biopsy proven acute rejection, especially at the first-year post-transplant, we found no differences in death censored graft survival or patients’ mortality for patients with a second kidney transplant. Second transplants should be offered to patients whenever feasible.


2021 ◽  
Vol 8 ◽  
Author(s):  
Yongrong Ye ◽  
Fei Han ◽  
Maolin Ma ◽  
Qipeng Sun ◽  
Zhengyu Huang ◽  
...  

Background: Delayed graft function (DGF) is a common complication after kidney transplantation (KT) with a poor clinical outcome. There are no accurate biomarkers for the early prediction of DGF. Macrophage migration inhibitory factor (MIF) release during surgery plays a key role in protecting the kidney, and may be a potential biomarker for predicting post-transplant renal allograft recovery.Methods: Recipients who underwent KT between July 2020 and December 2020 were enrolled in the study. Plasma MIF levels were tested in recipients at different time points, and the correlation between plasma MIF and DGF in recipients was evaluated. This study was registered in the Chinese Clinical Trial Registry (ChiCTR2000035596).Results: Intraoperative MIF levels were different between immediate, slowed, and delayed graft function groups (7.26 vs. 6.49 and 5.59, P < 0.001). Plasma MIF was an independent protective factor of DGF (odds ratio = 0.447, 95% confidence interval [CI] 0.264–0.754, P = 0.003). Combining plasma MIF level and donor terminal serum creatinine provided the best predictive power for DGF (0.872; 95%CI 0.795–0.949). Furthermore, plasma MIF was significantly associated with allograft function at 1-month post-transplant (R2 = 0.42, P < 0.001).Conclusion: Intraoperative MIF, as an independent protective factor for DGF, has excellent diagnostic performance for predicting DGF and is worthy of further exploration.


2021 ◽  
Vol 156 (Supplement_1) ◽  
pp. S159-S160
Author(s):  
E S Lee ◽  
A McHenry ◽  
A Siddon ◽  
C Tormey

Abstract Introduction/Objective The Kidd blood group antigens are urea transporters found on the surface of red blood cells, renal tubular epithelial cells, and endothelial cells in the renal medulla and vasa recta. While controversial, some reports have described an association between Kidd antigen donor/recipient mismatches and kidney transplant rejection when recipients possess or form anti-Kidd alloantibodies. To date, none of these reports have described development of a thrombotic microangiopathy (TMA) in the renal graft associated with these antibodies. We describe a case of fulminant renal transplant rejection associated with TMA in a patient with anti-Jk(a) alloantibodies who received a deceased-donor kidney transplant (DDKT). Methods/Case Report A 64-year-old woman with end-stage renal disease secondary to AL amyloidosis caused by plasma cell neoplasm received a DDKT associated with delayed graft function. No pre- or post-transplant donor specific antibodies (DSA) were detected, the flow crossmatch testing was negative, and a pre-operative type and screen identified anti-Jk(a) alloantibodies. On post-transplant day 5, her creatinine remained elevated at 6 mg/dL (ref range: 0.4–1.3 mg/dL) with an acute drop in platelets and undetectable haptoglobin. Allograft biopsy showed a combination of TMA with some additional evidence of acute cellular rejection. Tacrolimus was stopped to rule out drug-induced TMA, and the workup showed negative Shiga toxin, normal ADAMTS13 activity, negative atypical HUS genetic testing, and negative antiphospholipid syndrome testing. Genotyping of the donor kidney was positive for the Jk(a) antigen. Eculizumab, IVIG, and a trial of 8 sessions of therapeutic plasma exchange (TPE) were administered. Her creatinine improved (1.93–2.05 mg/dL), indicating a significant antibody-mediated etiology to her delayed graft function. About one month later, her creatinine worsened, and she received another trial of TPE with IVIG and eculizumab. Despite a mild decrease in her creatinine, repeat biopsies showed acute cellular rejection, persistent TMA, and chronic allograft injury. No DSAs were ever detected. Her creatinine never recovered, and she is now dialysis-dependent. Results (if a Case Study enter NA) NA Conclusion We speculate that anti-Jk(a) antibodies interacting with a Jk(a)-positive donor kidney account for graft TMA. This case underscores the potential importance of matching Kidd antigens in kidney transplantation.


Sign in / Sign up

Export Citation Format

Share Document