Leaderboard

Many years ago when working at ARC, I asked Dr. Garratty with some assistance with a patient who had a Warm Auto-e and was hemolyzing. So we were giving e NEG RBCs, but the patient was still hemolyzing. He spoke with the physician and suggested he stop transfusing (the guy was down to like a 4 Hgb at that point and probably would have died had we kept transfusing him). Plus, that then sets them up for making the alloantibody. I have always been taught that as a general rule, you do not honor a warm autoantibody with specificity unless there is evidence of hemolysis due to that antibody.....but still, transfusing these patients "at all" then, seems to make the situation worse. Plus donor facilities do not tend to want to let their e NEG units go for a warm autoantibody; they need them for the patients with allo anti-e. On another note, our protocol for patients with Warm Autos is that if we can get them in an untransfused state (last 3 months), we do a complete phenotype (major antigens only; do not include M) and then going forward, give them matched units as long as the warm autoantibody is demonstrable. That is for no other reasons than turnaround time (our Reference Lab is about 5 hours away) and cost of a work-up (though depending on their type, getting matched RBCs can be the more expensive option). We also started doing that on patients with Darzalex (which at any given time, we have about 3 patients). If a patient's phenotype is too difficult for ARC to supply just based on us not wanting to send a work-up, they will tell us they cannot provide that and we will then submit them for work-ups when necessary...but for the most part, they have been able to. Brenda Hutson, MT(ASCP)SBB

I think it is purely coincidental. As far as I know, there have only ever been one or two papers published that suggested that Duffy antibodies have anything to do with renal transplant rejection (but I could be wrong about this, because I don't read every paper that is ever published!). There are two alternative things that spring to mind (neither of which may actually be the right answer, of course). The first is that it is an auto-antibody that has a specificity that mimics anti-Fya (see also the recent thread talking about auto-anti-K-like specificities in K Negative patients). The second is that the transplanted kidney came from a donor who was Fy(a-) and who had already produced an anti-Fya, and then when the kidney was transplanted a clone of B-Lymphocytes producing the anti-Fya was transplanted at the same time (rather in the manner of passenger lymphocyte syndrome, but not as clinically significant). The clones could then set up as a sort of micro-chimera, and the anti-Fya would continue to be produced. I should warn you that this second alternative is rare in the extreme, and may actually have never been proven (it may remain a theory).

Still doing IgG crossmatches but they are on an analyzer so that helps.

see attached Blood returned unused.pdf

I am at the mercy of the blood supplier for plts. Usually all they have are A+ with an occasional O+. I can get Rh= products if I know in advance and request them (usually). All the products I get are apheresis derived - we do not consider giving RhIg to Rh= recipients (maybe if they were randoms and bloody). We are unconcerned with the K typing of the donor.