Abstract: SA-PO469
The Natural History of De Novo Donor Specific Antibody (dn DSA): Results from Systemic Monitoring of DSA at ECMC
Session Information
- Transplantation: Balancing Rejection and Infection
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Transplantation
- 1702 Transplantation: Clinical and Translational
Authors
- Chang, Shirley Shwu-Shiow, SUNY Buffalo, Buffalo, New York, United States
- Yip, Cindy S, SUNY Buffalo, Buffalo, New York, United States
- Patel, Sunil, SUNY Buffalo, Buffalo, New York, United States
- Gundroo, Aijaz A., SUNY Buffalo, Buffalo, New York, United States
- Zachariah, Mareena Susan, SUNY Buffalo, Buffalo, New York, United States
Background
Dn DSA development has shown to adversely affect long-term allograft survival, but it’s natural history is not well studied.
Methods
Systemic screening DSA post-transplant at ECMC prospectively was performed from Jan 2012 to Sept 2016 on kidney (K) transplant (tx) recipients at 1 month (m), 2 m, 3 m, 6 m, & yearly interval, more frequently if DSA+. Management of dn DSA+ includes Tx K Bx if MFI>3000, and treatment depends on the bx findings. ACR is treated with steroid bolus, acute AMR with steroid bolus±Thymo & Plasmapheresis/IVIG, and those without rejection were treated with IVIG until MFI<1500 (negative).
Results
49 recipients developed DSA, & 330 did not. Of those with dn DSA, 27% developed HLA I DSA (median onset 40 days post-tx), 88% HLA II DSA (median onset 180 days, p<0.05), 12% had HLA I & II DSA. Causes of dn DSA were due to infection [N=12 (8 had BKN, 1 BK viremia, 1 BK viremia & CMV viremia, 1 recurrent UTI, 1 Hep C], rejection [N=11 (3 with prior ACR, 3 prior AMR, 1 prior ACR+AMR; 4 with current ACR, 1 with current AMR], elevated cPRA/prior Tx [N=9 (4 due to cPRA>80%, 5 with prior K Tx with elevated cPRA), nonadherence (N=8), unknown etiology (N=7), and long CIT >39 hours with DGF (N=2). Patient with dn DSA were grouped into Transient DSA (N=19, with 10 had minimal intervention, & 9 had intervention such as PE+IVIG or Rituximab or IVIG alone), Persistent DSA (N=30, 7 had MFI<3000, 8 had MFI between 3000-6000, and 15 had MFI>6000). Of those dn DSA who had K Bx (N=48), 36% developed concomitant rejections at initial dn DSA presence; 3 with borderline, 4 Banff 1A, 3 Banff 1B, 3 Banff 2B, and 3 with acute AMR rejections. None of the recipients with transient DSA lost their graft. There was one graft failure in the persistent dn DSA with MFI<3000, 3 graft failure in the MFI 3000-6000 range, & 5 graft failures including 2 patient death in the MFI>6000 group.
Conclusion
12.9 % K Tx recipients develop dn DSA, with HLA I occurs earlier than HLA II. Causes for dn DSA include infection (25%), rejection (22 %, with 12% occurs after prior rejection episodes, & 10% with active rejection concomitantly), highly sensitization (18%), nonadherence (16%), unknown cause (14%), & prolonged CIT/DGF (4%). Recipients with persistent DSA especially Class II and higher MFI levels are risk factors for graft failure.
Funding
- Clinical Revenue Support