AB0461 BELATACEPT IN SLE KIDNEY TRANSPLANT PATIENTS
Authors: Irene Carrión Barberà, Melissa Fajardo, Demetra Tsapepas, Hilda Fernandez, Anca Askanase
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background:</h3> Lupus nephritis (LN) results in the need for renal replacement therapy (RRT) in 10-30% of LN pts; of these 30% receive a kidney transplant (KT). Belatacept (bela) is a second-generation selective T-cell co-stimulator blocker (inhibits CTLA-4) used as an alternative to calcineurin inhibitors (CNI) for maintenance regimens after KT. The pathogenic relevance of CTLA-4 inhibition and the favorable cardiovascular profile of bela make it an attractive therapeutic option in SLE. Additionally, bela IV ensures therapeutic adherence. <h3>Objectives:</h3> The current study was initiated to evaluate the effect of bela on graft function and extrarenal SLE. <h3>Methods:</h3> This retrospective single-center study evaluates the outcomes of LN KT recipients treated with bela from 2006–2018 at the Columbia University Lupus and Renal Transplant Cohorts. The bela regimen was 5mg/kg every 2 weeks x 5 doses, then monthly. CNI weaning among the bela group was not standardized. Immunosuppressive regimen, kidney allograft function, and SLE activity were examined. <h3>Results:</h3> 48 pts with LN had undergone KT between 2006–2018 with follow-up time of 72.2 ± 74.6 months. Bela was started in 7 pts on CNI regimens (TAC N=6, cyclosporine N=1) at 15.5 ± 17.1 months after KT. All pts were female, age at SLE diagnosis 21.1 ± 4.9 yrs; 5 had undergone RRT prior to KT (4 hemodialysis, 1 peritoneal dialysis) for 38.7 ± 37.8 months. The interval between SLE diagnosis and KT was 13.1 ± 8.3 yrs. At the time of bela initiation, all pts were also treated with prednisone (7.1 ± 2.7 mg/day), 6 with mycophenolate (1123 ± 625 mg/day), and 1 azathioprine (25mg/day). CNIs were continued in 5/7 patients at 6 months after bela. 2 pts were on hydroxychloroquine, 2 took it only prior to KT. In 5 patients, creatinine stabilized 6 months after bela, 1 returned to HD due to CNI-toxicity and pyelonephritis and 1 is relisted for KT due to ACR and cortical necrosis (Fig. 1). No allograft failure due to recurrent LN was noted in any of the 7 pts. 5 pts are followed by Rheumatology for extrarenal SLE; no extrarenal manifestations are documented in the other 2. Data on SLE Disease Activity pre and post bela were available and scored in 3/5 pts using the SLEDAI-2KG which accounts for clinical and laboratory manifestations, as well as steroid use (Fig. 2). Mean ds-DNA pre and post bela was 133 ± 178 UI/mL and 58 ± 72 UI/mL; C3 89 ± 31mg/dL pre and 91 ± 21 mg/dL post; C4 35 ± 15 mg/dL pre and 38 ± 7 mg/dL post. <h3>Conclusion:</h3> Bela in LN KT recipients may decrease extrarenal manifestations, attenuate CNI toxicity and stabilize allograft function, providing a better alternative to CNI regimens. Furthermore, these data suggest that bela may be a therapeutic option in SLE. <h3>References</h3> [1] Almaani, Salem, Alexa Meara, and Brad H. Rovin. Update on lupus nephritis. Clinical Journal of the American Society of Nephrology 12.5 (2017):825–835. [2] Ortega, L. M., et al. Lupus nephritis: pathologic features, epidemiology and a guide to therapeutic decisions. Lupus 19.5 (2010):557-574. [3] Sexton, Donal J., et al. ESRD from lupus nephritis in the United States, 1995–2010. Clinical Journal of the American Society of Nephrology 10.2 (2015):251-259. <h3>Acknowledgement:</h3> We would like to thank KERN PHARMA laboratories for their support through "Becas FER-KERN PHARMA". <h3>Disclosure of Interests:</h3> None declared