BACKGROUND: The detection of anti-D in a D-positive renal transplant r
ecipient is unusual and may arise by several potential mechanisms. The
se include passive transfer of alloantibody and the presence of autoan
ti-D or alloanti-D that is due to microchimerism when the allograft is
from a D-negative donor. In the latter case, overt hemolysis has been
seen or suspected. The occurrence of anti-D in a D-positive renal tra
nsplant recipient without hemolysis, which is most likely attributable
to microchimerism, is reported. CASE REPORT: A 51-year-old group O, D
-positive woman, who was serologically HLA type Al, A2; BE, B44; DR3,
DR6, DR52; DQ1, DQ2, underwent the transplantation of a kidney from a
cadaveric donor who was serologically HLA type Al, A2; B8, B44; DR13,
DR17, DR52; DQ1, DQ2. The donor was known to be D-negative and immuniz
ed to D. No blood components or derivatives were administered at the t
ime of organ graft. Ten weeks after the transplant, the direct antiglo
bulin test was positive in the recipient, and anti-D was eluted. Polym
erase chain reaction amplification using primers to distinguish DR13 (
donor) from DR14 alleles (recipient split of DR6) in the peripheral bl
ood showed the recipient to be DR14. No DR13 could be detected, and th
us microchimerism could not be confirmed. However, in the peripheral b
lood, GM and KM allotyping of the serum (GM A,F;X B,G and KM 1,3) and
eluate (G1M F, KM 3) showed a pattern of allotypes most consistent wit
h an alloantibody. Eleven months after transplantation, the graft cont
inued to function; the direct antiglobulin test was still positive, an
d elution of anti-D persisted. CONCLUSION: This case of anti-D in a D-
positive renal transplant recipient is attributed to microchimerism, d
espite the lack of confirmation by genotypic analysis of the periphera
l blood. It raises the possibility that microchimerism may be a more c
ommon phenomenon in solid allograft recipients than is realized.