BACKGROUND: The detection of anti-D in a D-positive renal transplant recipient is unusual and may arise by several potential mechanisms. These include passive transfer of alloantibody and the presence of autoanti-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 transplant 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 A1, A2; B8, B44; DR3, DR6, DR52; DQ1, DQ2, underwent the transplantation of a kidney from a cadaveric donor who was serologically HLA type A1, A2; B8, B44; DR13, DR17, DR52; DQ1, DQ2. The donor was known to be D-negative and immunized to D. No blood components or derivatives were administered at the time of organ graft. Ten weeks after the transplant, the direct antiglobulin test was positive in the recipient, and anti-D was eluted. Polymerase chain reaction amplification using primers to distinguish DR13 (donor) from DR14 alleles (recipient split of DR6) in the peripheral blood showed the recipient to be DR14. No DR13 could be detected, and thus microchimerism could not be confirmed. However, in the peripheral blood, 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 with an alloantibody. Eleven months after transplantation, the graft continued to function; the direct antiglobulin test was still positive, and elution of anti-D persisted. CONCLUSION: This case of anti-D in a D-positive renal transplant recipient is attributed to microchimerism, despite the lack of confirmation by genotypic analysis of the peripheral blood. It raises the possibility that microchimerism may be a more common phenomenon in solid allograft recipients than is realized.
BACKGROUND: The detection of anti-D in a D-positive renal transplant recipient is unusual and may arise by several potential mechanisms. These include passive transfer of alloantibody and the presence of autoanti-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 transplant 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 A1, A2; B8, B44; DR3, DR6, DR52; DQ1, DQ2, underwent the transplantation of a kidney from a cadaveric donor who was serologically HLA type A1, A2; B8, B44; DR13, DR17, DR52; DQ1, DQ2. The donor was known to be D-negative and immunized to D. No blood components or derivatives were administered at the time of organ graft. Ten weeks after the transplant, the direct antiglobulin test was positive in the recipient, and anti-D was eluted. Polymerase chain reaction amplification using primers to distinguish DR13 (donor) from DR14 alleles (recipient split of DR6) in the peripheral blood showed the recipient to be DR14. No DR13 could be detected, and thus microchimerism could not be confirmed. However, in the peripheral blood, 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 with an alloantibody. Eleven months after transplantation, the graft continued to function; the direct antiglobulin test was still positive, and elution of anti-D persisted. CONCLUSION: This case of anti-D in a D-positive renal transplant recipient is attributed to microchimerism, despite the lack of confirmation by genotypic analysis of the peripheral blood. It raises the possibility that microchimerism may be a more common phenomenon in solid allograft recipients than is realized.