TRANSPLANTATION OF ABO-A2 KIDNEYS TO BLOOD GROUP B OR O RECIPIENTS???TOO MANY UNANSWERED QUESTIONS

Abstract

The recent article by Alkhunaizi et al. (1) describes additional cases supporting the practice of transplanting ABO-A2 kidneys to blood group B or O recipients and provides interesting data on changes in anti-A isoagglutinin titers measured after transplantation. A number of questions remain concerning the criteria used to identify the optimal recipients for such transplants, and whether there is any need for plasmapheresis or increased immunosuppressive therapy. Unfortunately, the current article falls short of answering these questions. One important question is whether there is a maximum titer of anti-A isoagglutinins in recipients that can predict poor graft survival of ABO-A2 kidneys. A number of investigators (1–6) have attempted to correlate pretransplant ABO titers with outcome. Unfortunately, the immunoglobulin (Ig) class of the antibodies studied (i.e., IgG vs. IgM), the ABO group of the target cells used to determine titer (i.e., A1 vs. A2), and the techniques used to detect the antibody (direct agglutination vs. Coombs test) have varied, making it nearly impossible to compare one study with another. One of the largest series published is by Nelson et al. (5), who show a 1-month kidney function rate of 94% in patients whose IgG anti-A titer is ≤1:4, versus 68% in patients with IgG titers >1:4, but they state that IgM titers did not predict graft function. Alkhunaizi et al. report IgG and IgM titers in their patients against both A1 and A2 cells. They decided which patients were eligible for transplantation and based the decision to treat with perioperative plasmapheresis only on IgM anti-A titers. The IgG titers were ≤1:4 in 14 of 15 patients, so they would be predicted to do well according to Nelson’s criteria. However, because patients with IgM titers ≥1:8 were treated with plasmapheresis, the significance of a high IgM titer remains unclear. Another question is whether plasmapheresis is necessary or beneficial in this type of transplantation. Again the question is not addressed appropriately in the Alkhunaizi article. They attribute their success (93% 1-year graft survival) in part to the use of plasmapheresis in patients with high IgM titers. They point out that the only patient whose graft failed was the only patient with a high IgM titer who did not receive plasmapheresis. However, she was also the only patient with an IgG titer >1:4. Nelson et al. (7) report 2-year graft survivals of 94% in patients with low IgG titers without plasmapheresis or additional immunosuppressive therapy. Therefore, the graft failure in Alkhunaizi’s patient may be caused by the IgG titer as much as by the lack of plasmapheresis. If the authors had done a trial in which the patients were randomized into plasmapheresis and no plasmapheresis treatment groups, they may have been able to provide an answer to this important question. Susan L. Saidman1