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P12.04 Switch from Calcineurin Inhibitor to Belatacept in kidney-pancreas transplant recipients. Single-center retrospective study from Argentina

Sebastián Jaurretche Sr., Argentina

Renal Transplant
Sanatorio Parque de Rosario


Switch from calcineurin inhibitor to belatacept in kidney-pancreas transplant recipients: single-center retrospective study from Argentina

Maira M Escobar E1, Sebastian S Rodriguez R1, Sebastián S Jaurretche J1, Vanina V Barranco B1, Elisa E Cerri C1, Martin M Rodenas R1, Ivan I Bertolin B1, Ricardo R Pereyra P1, Alfredo A Buschemi B1, Jose Luis JL Sgrosso S1.

1Renal, pancreas and heart transplant, Sanatorio Parque de Rosario, Rosario, Argentina

Introduction: High levels of calcineurin inhibitors (CNI) have been identified as risk factors for decline in kidney function and progression to end-stage renal disease. Belatacept‐treated kidney transplant recipients were less likely to have chronic kidney scarring and also had better graft function. In pancreatic transplantation, the evidence for immunosuppression regimens including Belatacept is scarce. The purpose of this study is to report the results of renal and pancreatic grafts evolution in 4 kidney-pancreatic transplant recipients who switched from CNI to Belatacept.

Method: Kidney-pancreas transplant recipient who switched from CNI to Belatacept due to renal fibrosis in graft biopsy were included. Due to the small sample size, Fisher's Test was used to evaluate the statistical significance of the results.

Results: Four males were studied (mean age 38.25±8.64 ys). All patients received thymoglobulin induction therapy and initially maintained on steroids, tacrolimus and mycophenolate. Renal biopsy was indicated due to increased serum creatinine in 100% of population included; 1 patient also presented increased serum amylase and hyperglycemia. Three patients (75%) presented only renal fibrosis at time of the switch and the remaining patient (25%) also presented acute pancreatic rejection 1A concomitant with renal graft fibrosis. During the follow-up period after the switch (3.6±1.47 ys): 3 patients who presented isolated renal graft fibrosis maintained stable serum creatinine and adequate pancreatic graft function (p<0.05), while the patient with acute concomitant pancreatic graft rejection presented stable serum creatinine during the follow-up period but pancreatic graft loss function 28 months after the switch (p<0.05).

Conclusion: In our experience, switch from CNI to Belatacept in renal-pancreatic transplant recipients when they present renal fibrosis without pancreatic graft pathology is adequate to prevent worsening renal and pancreatic graft function. Belatacept was not an adequate maintenance immunosuppressive therapy to preserve pancreatic graft function when acute pancreatic graft rejection was present at the time of switching from CNI to Belatacept.

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