Hello,

In my reference laboratory, we have a renal transplant patient with multiple antibodies; anti-D, anti-K and anti-Fya.  The patient had always been DAT positive and we had been unable to type for Fya.  Finally got around to genotyping, and were surprised to find that the patient is Fya positive.  A quick read up suggested that Fya can be involved in renal allograft rejection.  If the patient received a Fy(a-) kidney, could the auto-Fya have originated from that? Not ever seen an auto-Fya before, and wondered if it was more common in renal transplant, or purely coincidental?

 

Kind regards

Alison

1 hour ago, Alisun said:

In my reference laboratory, we have a renal transplant patient with multiple antibodies; anti-D, anti-K and anti-Fya.  The patient had always been DAT positive and we had been unable to type for Fya.  Finally got around to genotyping, and were surprised to find that the patient is Fya positive.  A quick read up suggested that Fya can be involved in renal allograft rejection.  If the patient received a Fy(a-) kidney, could the auto-Fya have originated from that? Not ever seen an auto-Fya before, and wondered if it was more common in renal transplant, or purely coincidental?

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-Fy^a (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-Fy^a, and then when the kidney was transplanted a clone of B-Lymphocytes producing the anti-Fy^a 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-Fy^a 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).