Klinisch II - P22 - Development of donor specific antibodies after islet-after-kidney transplantation

M.F. Nijhoff, H. Bouwsma, H.J.W. de Fijter, T.A. Rabelink, D.L. Roelen, E.J.P de Koning

Chair(s): drs. Christina Krikke, chirurg, UMC Groningen

Thursday 10 march 2016

13:00 - 13:30h at Foyer

Categories: Postersessie

Parallel session: Postersessies XI - Opgesplitst in 3 tijdblokken en 3 categoriëen (klinisch, basaal, donatie)

Islet transplantation is performed in a small group of patients with complicated type 1 diabetes mellitus. Often, multiple donor pancreata are used to achieve a satisfying clinical result, thereby exposing recipients to a large pool of HLA antigens and potential risk of allo-immunization. We studied the development of donor specific HLA antibodies (DSA) in islet-after-kidney (IAK) transplantation recipients and furthermore aimed to assess the relation with the amount of donor pancreata utilized. Methods: Patients receiving an IAK transplantation with alemtuzumab induction therapy for a first transplant, basiliximab for subsequent transplants, and tacrolimus/MMF/prednisolone maintenance therapy were followed. Recipients were screened after 3 months and then yearly for donor specific HLA antibodies using a Luminex assay. Patients were also assessed for islet function using insulin independence and beta score (from 0 to 8 points): a combined measure of insulin secretion and clinical outcome. Results: 18 IAK patients were assessed (13M/5F, age 50.8±9.3 years). Previous solitary kidney transplantation was present in 12/18 recipients (one patient had received 3 kidney transplantations) and simultaneous pancreas-kidney transplantation in 6/18 recipients (two patients had received two pancreas transplantations). DSA were present in 10/18 (67%) recipients before islet transplantation. Follow up after IAK was 47.4±23.5 (range 22–97) months. Patients underwent 1.9±0.5 (range 1–3) islet transplantation procedures using 2.8 ±1.1 (range 1–5) pancreata. Insulin independence was achieved by 72%. At the last follow up 6/15 (40%) recipients were insulin independent and the median beta score was 5 (range 0–8). HbA1c decreased from 63.6±16.5 to 50.5±11.9 mmol/mol (-21%, p=0.009). One patient had graft failure. Four patients (22%) developed DSA against islet donor HLA antigens (both type I and type II). The number of donor pancreata used was similar for both groups (2.8±1.7 pancreata (DSA+) versus 2.8±0.9 pancreata (DSA-); p=0.96). Development of DSA was not associated with a lower beta score (median 3.5 (DSA+) versus 5 (DSA-), p=0.44). Conclusion: 22% of IAK recipients developed DSA, as compared to 67% after previous solid organ transplantation. There was no association between the number of pancreata used for islet transplantation and development of DSA against donor islet HLA antigens. Development of DSA was not associated with a decline in islet transplant function.