Severe Intravascular Haemolysis in a Renal Transplant Recipient due to Anti‐B of Donor Origin

Abstract

A group B recipient of a group 0 kidney developed severe intravascular haemolysis due to the formation of anti-B. Immunoglobulin allotyping of donor serum, recipient serum and 'unexpected' anti-B antibody showed the antibody to be of donor origin. The patient and donor genotypes were Gm 3;5/3;5 and Gm 1,2;21/1;21, respectively, and the anti-B antibody allotype was Gm 1;21. The group B recipient of the other donor kidney showed no evidence of haemolysis. Possible factors influencing the occurrence and severity of post-transplantation haemolysis are discussed. The production of anti-A or anti-B antibodies in non-group 0 patients who receive group 0 organ transplants is well described [1-8]. We report a case of severe intravascular haemolysis in a group B patient who received a group 0 kidney, together with immunoglobulin allotyping studies which show conclusively that the antibody responsible for the haemolysis was of donor origin.

Alloimmune Hemolysis after Renal Transplantation

“…Severe intravascular hemolysis has been reported in renal transplant recipients due to alloantibodies of donor origin [1,2]. Using immunoglobulin allotyping, it was confirmed that the antibodies were derived from donor lymphocytes [1,3].…”

“…Using immunoglobulin allotyping, it was confirmed that the antibodies were derived from donor lymphocytes [1,3]. Alloimmune hemolysis has also been reported in other solid-organ transplantations, including liver [4,5], lung [6,7], heart-lung [7,8], spleen [9] and pancreas [10], when there is a minor ABO mismatch between donor and recipient [4,8,10,11].…”

Allogeneic peripheral blood hematopoietic stem cell transplantation: guidelines for red blood cell immuno-hematological assessment and transfusion practice

“…Interestingly, hemolysis with a similar mechanism has been described after organ transplantation using CsA for the prevention of graft rejection. [26][27][28][29][30][31] Several quantitative and qualititative differences in a PBSC graft vs a marrow graft could contribute to enhancing the risk for acute immune-mediated hemolysis after PBSCT. An increased number of B cells, T cells and CD34 + present in a PBSC graft could result in an accelerated immune reconstitution with production of anti-recipient Ab early after transplantation at a time when significant numbers of recipient RBC are present.…”

Transfer of HLA-Specific Allosensitization From a Highly Sensitized Deceased Organ Donor to the Recipients of Each Kidney

“…A previously unexplored possibility is that de novo HLA-specific antibodies may also result from alloantibody producing passenger B lymphocytes/plasma cells present within the donor organ at the time of transplantation that after transfer into the immunosuppressed recipient continue to produce alloantibody. This situation would be analogous to the transfer of immune competent B cells in an ABO compatible donor organ that produce antibodies to recipient ABO blood group antigens and cause transplant associated hemolytic anemia (7,8). We describe herein, for the first time, the appearance of high level de novo IgG HLA class I-and class II-specific allosensitization in two nonsensitized recipients of a primary kidney transplant that we attribute to the transfer of donor passenger leukocytes from the same HLA highly sensitized donor.…”

“…It occurs when primed immunecompetent donor cells present within the graft are transferred into an immune compromised recipient. The most common manifestation is the antibody-mediated hemolytic anemia that follows ABO-compatible but nonidentical transplantation mediated by donor-derived B cells/ plasma cells primed to host allogeneic red blood cell antigens (7,8,10,11). Other manifestations may include acute graftversus-host disease mediated by donor-derived alloreactive cytotoxic T cells that attack host gut, skin, bone marrow, liver, and lungs (12).…”