MO954DONOR TYPE INFLUENCE IN EARLY POST KIDNEY TRASPLANTATION HYPERTRANSAMINASEMIA

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Eulàlia Solà-Porta ◽  
Dolores Redondo Pachon ◽  
Sara Núñez-Delgado ◽  
Carlos Arias-Cabrales ◽  
Marisa Mir ◽  
...  

Abstract Background and Aims The early increase in transaminases after kidney transplant (KT) is a frequent finding. It has been associated with the cross-talk produced between liver and kidney in ischemia-reperfusion situations. However, the influence of the donor type has not been evaluated. We analyze the incidence, relevance and possible correlations of postKT hypertransaminasemia. Method Retrospective study (2004-2018) to analyze the increase in serum AST/ALT during the first 3 months after KT in 119 KT recipients of deceased donors, either brain death (DBD n=59), controlled after cardiac death (cDCD n=21) or uncontrolled after cardiac death (uDCD n=39). All recipients received induction with thymoglobulin and maintenance immunosuppression with tacrolimus and mycophenolate. Results Recipients of uDCD group were younger, with a higher proportion of men and lower percentage of diabetics and retransplants. Delayed graft function duration was longer, although serum creatinine was similar at 3 months between groups. There were no differences between recipients in terms of past medical liver disease, postKT transfusion requirement or vasoactive drug use. There were also no differences in cumulative thymoglobulin dose, and uDCD recipients presented, as expected, lower levels of tacrolimus at one week postKT (Table). From all KT recipients, 37.3/45.3% presented with an increase in AST/ALT at 72 hours postKT. Regarding donor type, the percentage of recipients who experienced 72 hours postKT hypertransaminasemia was higher (69.2/82.1% in uDCD group vs 22/29.3% in DBD and 21.1/21.1% in cDCD, p<0.001). This liver function alteration resolved early, and one month after transplant, AST/ALT values in all groups returned to baseline (Figure). The multivariate analysis showed that uDCD recipients had x10 higher risk of developing early post-KT hypertransaminasemia than the other groups (for AST, OR 10.85 [2.463-47.826] and for ALT OR 11.15 [2.627-47.294]). However, when we tried to correlate this hypertransaminasemia with a prolonged delayed graft function (creatinine decrease> 14 days postKT) we did not find any association. Conclusion Early postKT hypertransaminasemia is a frequent and transient event that is related to the kidney donor type, being more frequent in recipients of donors in uncontrolled cardiac death.

2019 ◽  
Vol 15 (1) ◽  
pp. 109-116 ◽  
Author(s):  
Edmund Huang ◽  
Ashley Vo ◽  
Jua Choi ◽  
Noriko Ammerman ◽  
Kathlyn Lim ◽  
...  

Background and objectivesDelayed graft function is related to ischemia-reperfusion injury and may be complement dependent. We previously reported from a randomized, placebo-controlled trial that treatment with C1 esterase inhibitor was associated with a shorter duration of delayed graft function and higher eGFR at 1 year. Here, we report longer-term outcomes from this trial.Design, setting, participants, & measurementsThis is a post hoc analysis of a phase 1/2, randomized, controlled trial enrolling 70 recipients of deceased donor kidney transplants at risk for delayed graft function (NCT02134314). Subjects were randomized to receive C1 esterase inhibitor 50 U/kg (n=35) or placebo (n=35) intraoperatively and at 24 hours. The cumulative incidence functions method was used to compare graft failure and death over 3.5 years. eGFR slopes were compared using a linear mixed effects model.ResultsThree deaths occurred among C1 esterase inhibitor–treated patients compared with none receiving placebo. Seven graft failures developed in the placebo group compared with one among C1 esterase inhibitor–treated recipients; the cumulative incidence of graft failure was lower over 3.5 years among C1 esterase inhibitor–treated recipients compared with placebo (P=0.03). Although no difference in eGFR slopes was observed between groups (P for group-time interaction =0.12), eGFR declined in placebo-treated recipients (−4 ml/min per 1.73 m2 per year; 95% confidence interval, −8 to −0.1) but was stable in C1 esterase inhibitor–treated patients (eGFR slope: 0.5 ml/min per 1.73 m2 per year; 95% confidence interval, −4 to 5). At 3.5 years, eGFR was 56 ml/min per 1.73 m2 (95% confidence interval, 42 to 70) in the C1 esterase inhibitor group versus 35 ml/min per 1.73 m2 (95% confidence interval, 21 to 48) in the placebo group, with an estimated mean eGFR difference of 21 ml/min per 1.73 m2 (95% confidence interval, 2 to 41 ml/min per 1.73 m2).ConclusionsTreatment of patients at risk for ischemia-reperfusion injury and delayed graft function with C1 esterase inhibitor was associated with a lower incidence of graft failure.


2020 ◽  
Vol 98 (6) ◽  
pp. 1489-1501
Author(s):  
Longhui Qiu ◽  
Xingqiang Lai ◽  
Jiao-jing Wang ◽  
Xin Yi Yeap ◽  
Shulin Han ◽  
...  

2014 ◽  
Vol 98 ◽  
pp. 99
Author(s):  
Sanchez B. Sobrino ◽  
Karsten S. Alvarez ◽  
Lafuente O. Covarrubias ◽  
Zalamea F. Jarrin ◽  
Rubio E. Gonzalez ◽  
...  

2020 ◽  
Vol 30 (4) ◽  
pp. 342-348
Author(s):  
Fahad Aziz ◽  
Ali Gardezi ◽  
Brenda Muth ◽  
Justin Blazel ◽  
Neetika Garg ◽  
...  

Background: The effects of delayed graft function on long-term kidney allograft outcomes are poorly defined among simultaneous liver and kidney transplant recipients. Methods: We analyzed data of all simultaneous liver and kidney recipients transplanted at the University of Wisconsin between 2010 and 2017. Risk factors for the development of delayed graft function, kidney graft failure, and patient mortality were outcomes of interest. Results: There were a total of 60 simultaneous liver and kidney recipients; 28 (47%) had delayed graft function. After adjustment for multiple variables, we found that pretransplant dialysis >6 weeks (hazard ratio [HR] = 5.6, 95% CI: 1.23-25.59, P = .02), pretransplant albumin <3 g/dL (HR = 5.75, 95% CI: 1.76-16.94, P = .003), and presence of pretransplant diabetes (HR = 2.5, 95% CI: 0.97-4.77, P = .05) were significantly associated with delayed graft function. Multivariate analysis showed that pretransplant albumin <3 (HR = 4.86, 95% CI: 1.07-22.02, P = .02) was associated with a higher risk of all-cause kidney allograft failure, whereas the duration of delayed graft function (HR = 1.07 per day, 95% CI: 1.01-1.14, P = .01) was associated with a higher risk of death-censored kidney allograft failure. The presence of delayed graft function was not associated with all-cause or death-censored kidney or liver allograft failure. Similarly, the presence of delayed graft function was not associated with patient mortality. Conclusion: The incidence of delayed graft function was high in simultaneous liver and kidney recipients. However, with appropriate management, delayed graft function may not have a negative impact on patient or kidney allograft survival.


2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Xinyi Hu ◽  
Ming Su ◽  
Jun Lin ◽  
Lei Zhang ◽  
Wen Sun ◽  
...  

Renal ischemia/reperfusion (IR) injury is one of the most important risk factors for the occurrence of delayed graft function (DGF) after kidney transplantation; however, its mechanism remains not fully understood. In the present study, we screened differentially expressed genes in a murine model of renal IR injury by using high-throughput assays. We identified Corin as one of the most significantly downregulated genes among 2218 differentially expressed genes (≥2-fold, P<0.05). By using a real-time qPCR assay, we observed that the expression of renal Corin in IR-injured mice was reduced to 11.5% of the sham-operated mice and that the protein level of renal Corin in IR-injured mice was also downregulated. Interestingly, renal IR injury in mice induced the downregulation of Corin in heart tissues, suggesting that the overall synthesis of Corin may be suppressed. We recruited 11 recipients complicated with DGF and 16 without DGF, and plasma Corin concentrations were determined by ELISA. We observed that the plasma Corin levels were indeed reduced in recipients complicated with DGF (0.98 vs. 1.95 ng/ml, P<0.05). These findings demonstrate that Corin may be a potential biomarker of DGF after kidney transplantation and may participate in the regulation of renal IR injury.


2012 ◽  
Vol 94 (12) ◽  
pp. 1218-1223 ◽  
Author(s):  
Pramod Nagaraja ◽  
Gareth W. Roberts ◽  
Michael Stephens ◽  
Szabolcs Horvath ◽  
Jana Fialova ◽  
...  

2012 ◽  
Vol 12 (10) ◽  
pp. 2774-2780 ◽  
Author(s):  
S. A. Lodhi ◽  
K. E. Lamb ◽  
I. Uddin ◽  
H. U. Meier-Kriesche

Sign in / Sign up

Export Citation Format

Share Document