PubMed · 118531
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D Chandanayingyong. 1979. Common problems in routine pre-transfusion testing.. https://pubmed.ncbi.nlm.nih.gov/118531/
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We report a case of accelerated acute rejection of a renal allograft from a presumed ABO histo-blood group A2 donor in an O recipient, in which all of the published criteria for compatibility had been met. Flow cytometric analysis of the A and H antigen expression on the kidney donor's erythrocytes suggested that this donor did not have an A2 phenotype, but rather another subgroup of A. Some of the reported cases of accelerated acute rejection of A2 renal allografts in O recipients may have resulted from misapplication of the results of standard lectin agglutination to the transplant setting. The current case suggests that a more sophisticated method of ABO phenotyping, such as erythrocyte flow cytometric analysis, may be necessary in the transplant setting.
Defect in degradation of blood group B-immunoactive glycosphingolipids in Fabry disease (deficiency of lysosomal alpha-galactosidase EC 3.2.1.22) has been studied using highly sensitive and specific TLC-immunostaining analysis of urinary sediments and tonsillar tissues of blood group B patients and healthy controls, secretors and nonsecretors. The B glycolipid antigens with hexasaccharide chains were consistently found increased (25- to 100-fold) in the urinary sediments of three Fabry patients, blood group B or AB secretors. Conversely, they were absent in the urinary sediment of one blood group B nonsecretor patient. In normal secretors, B glycosphingolipids were present only in traces. Moreover, significant increase in B glycolipid antigens (8-fold) was found in the tonsillar tissue of a Fabry patient blood group B secretor. We conclude that the secretor status is responsible for increased concentration of blood group B glycosphingolipids in both urinary cells and tonsils in alpha-galactosidase deficiency. The quantity of stored B-immunoactive glycosphingolipids, however, is much lower than that of the mainly accumulated glycosphingolipid Gb(3)Cer. The results clearly indicate that active or silent Se gene, which controls synthesis of B-antigen precursors, is responsible for notable difference in B-glycosphingolipids expression in Fabry patients - secretors and nonsecretors. Whether this novel aspect may be of prognostic significance, remains to be established.
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