*Purpose: Decreased antigen expression among blood group A, subtype 2 (A2), donor kidneys allows these kidneys to be considered as universal donor kidneys and under the new Kidney Allocation System to be preferentially transplanted into blood group B recipients. Blood group B and O recipients with low titer pre-transplant anti-A antibodies have been shown to have excellent outcomes after A2-incompatible transplantation. However, post-transplant rebound is common, and to date, no study has examined the correlation between this rebound and likelihood of subclinical antibody mediated rejection (AMR).

*Methods: We report 22 ABO incompatible A2/A2B to B/O transplantations with pre transplant anti-A gel titers ≤ 1:64 and daily post-transplant anti-A gel titer monitoring. Immunosuppression consisted of anti-thymocyte globulin induction, tacrolimus, mycophenolate mofetil and prednisone. No patients received pre-transplant conditioning regimen with plasmapheresis. Anti-A titers were measured at baseline and then daily for 14 days after transplantation.

*Results: Median age at transplantation was 50 years. Pre transplant titers were ≤ 1:64 (range 1:2- 1:64). Recipients were predominantly blood type B (B: 59%; O: 41%), male (64%), black race (55%), and received deceased donor kidneys (55%). Titers declined in all patients immediately after transplant and gradually increased during the first post-transplant week. Median time to rebound was 5 days (range 4-6). Median time to peak in gel titers was 10 days (range 9-12 days). There were 3 patients with biopsy proven Banff AMR (>1: thrombotic microangiopathy, glomerulities, and peritubular capillaritis), and none had graft dysfunction at the time of biopsy. Baseline pre-transplant titers did not correlate with AMR; no patients with a rebound titer < 1:128 developed AMR; and 3 out of 6 patients (50%) with anti-A gel titer rebound to > 1:128 developed AMR (Table 1). All 3 patients with biopsy proven subclinical AMR were treated with plasmapheresis, low-dose IVIg, and anti-C5 antibody. No allografts were lost secondary to AMR.

*Conclusions: Rebound in anti-A gel titer to > 1:128 after an A2-incompatible kidney transplantation should prompt a kidney biopsy even in the absence of graft dysfunction to evaluate for subclinical acute AMR. Prompt and aggressive treatment of subclinical AMR should be considered.

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