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

*Methods: We report 22 ABO-incompatible A₂/A₂B to B/O transplants at a single center with pre-transplant anti-A gel titers ≤64 who underwent prospective post-transplant titer monitoring. Immunosuppression consisted of anti-thymocyte globulin induction, tacrolimus, mycophenolate mofetil and prednisone. No patients received pre-transplant conditioning regimen with therapeutic plasma exchange (TPE). Anti-A titers were measured at baseline and daily for 14 days post-operatively. Biopsy was performed if anti-A titers rebounded above pre-transplant levels.

*Results: Recipients were predominantly blood type B (B:59%; O:41%), male (64%), black (55%), and received deceased donor kidneys (55%). Median pre-transplant gel titers were ≤64 (range 2-64) and declined in all patients immediately after transplantation. Median time to onset of rebound was 5 days (range 4-6). Median time to peak rebound was 10 days (range 9-12 days). Three/22 (13%) patients had biopsy-proven Banff AbMR (>1: thrombotic microangiopathy, glomerulities and peritubular capillaritis), no graft dysfunction at the time of rise in titer, but mild graft dysfunction at biopsy. Baseline pre-transplant titers did not correlate with AbMR but post-transplant titers did (Figs. 1&2). Three patients with AbMR were treated with TPE, low-dose IVIg, and anti-C5 antibody with excellent clinical response; follow up allograft biopsy at 3 months showed complete morphologic resolution and no allografts were lost to AbMR.

*Conclusions: Pre-transplant anti A titers do not tell the full story regarding AbMR. Until further pathophysiology of the AbMR is defined, it is essential to continue monitoring anti A titers immediately following transplant as it appears to herald AbMR. Furthe more with prompt and aggressive treatment, AbMR in this setting appears to resolve completely .

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