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Acquired hemolytic anemia due to “auto”‐anti‐A or “auto”‐anti‐B induced by group O homograft in renal transplant recipients
Author(s) -
Mangal A.K.,
Growe G.H.,
Sinclair M.,
Stillwell G.F.,
Reeve C.E.,
Naiman S.C.
Publication year - 1984
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.1984.24384225021.x
Subject(s) - medicine , azathioprine , immunosuppression , prednisone , gastroenterology , hemolysis , transplantation , group b , autoantibody , kidney transplantation , kidney , anemia , abo blood group system , hemolytic anemia , plasmapheresis , autoimmune hemolytic anemia , immunology , serology , antibody , disease
Three patients developed severe but self‐limited hemolytic anemia within 2 weeks of renal transplantation. All three had received kidneys from cadaver donors who were blood group O. Two of the recipients were blood group B while the third was blood group A. There was no pretransplant preparation of the donors or the recipients. Preoperative crossmatch and antibody screen were negative; however, subsequent to the hemolytic episodes, group‐specific blood was incompatible and the patients were transfused with group O crossmatch‐compatible blood. Blood bank serological tests showed a positive direct antiglobulin test (DAT), and anti‐A and anti‐B were eluted from group A and B patients, respectively. There was no evidence of hemolysis despite the positive DAT at 37 days following transplantation in two of the three patients who were maintained on cyclosporine immunosuppression. Retrospective analysis of renal transplant records showed that these “autoantibodies” appeared in three of the four renal transplant recipients who were on an immunosuppressive regimen of cyclosporine, with or without prednisone, but not in the 21 recipients who received radiotherapy to the donor kidney in addition to cyclosporine or azathioprine (p = less than 0.001). The possible pathogenetic mechanism for “autoantibody” formation by donor kidney and the role of immunosuppressive agents are discussed.