Matthew Kim

Today, We performed Kell antigen phenotyping, revealing k-, Kpb-, Jsb- (genotypically predicted as positive using SNP typing). Now, I believed his phenotype is Ko. I consider further genotyping using Sanger sequencing. Thank you for your help. Matthew Kim

Thank you for Malcom. Your explanation greatly helps as always. Unfortunately, we don't have reagents such as anti-k, -Kpb, and -Jsb. We are thinking about purchasing them from commercial companies. You recommend using anti-K from different clones, but is it okay to use polyclonal anti-k from Grifols? Otherwise, we will purchase a monoclonal anti-k from a different clone. Secondly, is it okay to purchase polyclonal anti-kpa, -kpb, and-Jsb from Grifols? I am not relevant to Grifols, but I just wonder if I should go with a monoclonal reagent or a polyclonal reagent for Kell antigen typing. Once again, I appreciate your insightful explanation. Now I am staying in Liverpool for travel, so we are not far way right now.

Dear fellow blood bankers, A 50-year old patient presented with an early gastric cancer to a korean university hospital. He underwent pre-transfusion testing for pre-op work-up and the antibody identification revealed that anti-K(KEL1) was identified. The Korean population is known to have only K-k+ phenotype (100% KEL1 negative in several donor cohort studies. I thought that the patient might have been immunized to the previous transfusion from foreign donors. Suprisingly, his phenotype was K-k-. We repeated the testing, revealing the same result. We genotyped Kell groups (targeting biallelic SNPs) and his predicted phenotype was K-k+, Kpa-Kpb+, Jsa-Jsb+ compatible with that of typical Koreans. Considering anti-ku was not identified in this patient, do you think his phenotype might be a Kell null phenotype? It is my first time or my country's first time to encounter K-k- phenotype with anti-K. Could you explain this case and teach me what I can do for solving the mystery? I need your help.

Hello, fellow blood bankers. I recently got a DAT positive result; poly 4+ IgG 4+ IgA 2+ IgM1+ C3c 1+ C3d 2+ control 1+ using Bio-rad DAT card. Antibody identification revealed pan-reactivity at the IAT. I thought this result might be caused by spontaneous agglutination of heavily IgG-coated patient's red cells. According to AABB technical manual 18th ed, removing autoantibody by warm saline wash (method 2-17) is recommended for ABO, RhD cell typing. I guess warm saline washing is done to remove cold agglutinins, not IgG antibody. Is there an appropriate method to have a valid DAT result in this case? Please help me. Forgive my ignorance.

Thank you very much. Now I understand why. Your comment helps me a lot.

Wow. Now I understand the cause of C-negative phenotype. Malcolm, I am sorry for my mistake about Dw. I meant that the patient has the weak D phenotype. However, there is one thing I cannot fully understand. CdeS type has (RHD-CE(3-7)-D) on his RHD gene capable of causing altered C antigen. You previously mentioned that Trp16Cys is a source of weakened C antigen expression. Do you think that both mutated RHD and RHCE genes affect altered C antigen expression? Thank you for such a great answer.

Hello. I've tried to come up with an answer over and over, but I've failed so far. Can I ask a question here? Our patient was identified to harbor DAR/Cdes (compound heterozygote) in our commercial kit. His Rh phenotype is Dwce. (c,e antigens are strongly positive) If his Cdes (RHD-CE(3-7)-D) allele is true, the patient's phenotype should Cces. But why ce? I am looking at blood group antigen factsbook and other papers, but I cannot find an answer. Any help would be appreciated.

Thank you, Malcolm I admire you clear answer. I also appreciate your recommendation on the book, Immune Hemolytic Anemias. I will definitely read it.

Anti-C and anti-e were identified in our patient and his DAT was 3+positive for IgG without previous transfusion history. His RBCs were typed as R1R2. Therefore, we suspect that auto-anti-C+e were present in his blood. I heard his antibodies could be autoantibodies mimicking anti-C and anti-e. Does anyone know the concept of autoantibodies mimicking specificity and the effective method to differentiate from just autoantibodies in detail? Any help would be appreciated. Thanks