P084 Post transplant DSA in a cohort of kidney recipients 8 to 16 years after transplantation

Abstract

Aim We previously published a study (1998–2008) of 624 patients showing the association of pre-transplant DSA with poor kidney allograft survival. The aim of the current study was to assess development of post-transplant DSA in patients with well-functioning grafts >8 years after transplantation in comparison to patients with failed grafts. Methods HLA typing (A, B, C, DR, DQ) of recipients and donors was performed by standard serologic and/or DNA (SSP or SSO) methods. Anti-HLA antibody specificity was determined by single antigen beads (Lifecodes) on a Luminex platform. Though donors were not typed for DPB1 or DPA1 the de novo development of antibodies to DP alleles was presumed to be donor specific. Results Of 624 patients that were originally enrolled 131 were available for evaluation. 67 recipients had functioning kidney allografts 8 to 18 years after transplantation with >10 years follow up in 50% of these patients. The remaining 64 patients had graft failure (return to dialysis) with a median survival of 7.5 years. Of these patients, 44 (68%) had evidence of post-transplant DSA to HLA class 1 and/or class 2 as detected 0.1 to 5 years prior to graft failure. Most DSA positive recipients had antibodies to both Class 1 and 2 (32, 50%), whereas only 3 patients had DSA to Class 1 and only 9 patients had DSA to Class 2. Of patients with functioning grafts only 32% had evidence of DSA. In a new cohort transplanted in 2012–2015, that received identical induction and maintenance immunosuppression as the earlier cohort, similar DSA results were observed. Approximately, 33% of recipients with functioning kidney allografts had evidence of DSA whereas 65% of patients with failed grafts had DSA. In many cases, in both cohorts, the detection of a relatively low level of DSA occurred without concomitant clinical signs of rejection (e.g., a rise in creatinine). Conclusion As demonstrated in many studies of shorter duration the development of DSA was associated in this 18 year study with kidney allograft failure long after antibody has been detected and in the absence of standard clinical markers of rejection. Patients that exhibit persistent levels of DSA without clinical signs of rejection may benefit from enhanced immunosuppressive therapy to prevent damage to the kidney tubules and glomeruli that eventually lead to graft failure.