ANTI-CELLANO MISTAKEN FOR AUTOANTIBODY DUE TO ABSENCE OF K-NEGATIVE RED CELLS IN A COMMERCIAL PANEL: LABORATORY RESOLUTION AND TRANSFUSION SUPPORT
- 1Hospital das Clínicas da Universidade Federal de Goiás (UFG), EBSERH, Goiânia, Brazil
- 2Instituto de Patologia Tropical e Saúde Pública (IPTSP), Universidade Federal de Goiás (UFG), Goiânia, Brazil
- 3Hospital da Região Leste, Paranoá, Brazil
Abstract
Introduction: The k antigen (Cellano, KEL2) is present in more than 99.8% of the population. While the K+k- phenotype, which requires homozygosity for KEL1, is rare in Brazil, where the prevalence of K is 4% to 5% and only 1.47% of K+ samples are k-negative, bringing it close to the international rare blood threshold (less than 1:1,000). Since no commercial panel contains k-negative red cells, anti-k reacts with the entire panel and simulates an autoantibody, making identification and transfusion support difficult. Case description: Female patient, 59 years old, with metastatic clear cell renal carcinoma, two pregnancies, and previous transfusions, presenting with severe hyporegenerative anemia (hemoglobin 6.0 g/dL). Extended red cell phenotyping, irregular antibody screening, direct antiglobulin test, acid elution, score-based titration, and, at a reference laboratory, serum testing against a panel treated with 0.2 M dithiothreitol and k-negative red cells were performed. Blood typing result: group A, RhD positive; phenotype C+c-E-e+ K+k-. In November 2025, six weeks after transfusion, a 2+ direct antiglobulin test (IgG) and reactivity against the entire panel were obtained. Serum treatment with 0.01 M dithiothreitol, which inactivates IgM without altering Kell antigens on test red cells, was ineffective. At the reference laboratory, the direct antiglobulin test was confirmed, autocontrol and eluate were negative, and the serum lost reactivity against the panel treated with 0.2 M dithiothreitol, which denatures Kell antigens and other disulfide-dependent systems. In addition, there was no reactivity against three untreated k-negative red cells, which, together with the K+k- phenotype, defined anti-k (titer 2, score 16). In March 2026, nivolumab was started; the following month, positive autocontrol and eluate reactive with the entire panel appeared, findings of limited interpretation due to transfusion in the interval and absence of testing against k-negative red cells. Indirect bilirubin remained normal, with no other markers of hemolysis. After ruling out autologous donation due to severe anemia and erythropoietin refractoriness, the National Rare Blood Registry was activated, obtaining k-negative units from the state inventory and, by air transport, from a blood center in another federal unit, which were transfused without adverse reactions. However, the patient died due to progression of the neoplasm. Discussion: The concentration of dithiothreitol determined the course of the investigation: 0.01 M in serum inactivates IgM, whereas abolishing Kell antigens requires 0.2 M in test red cells. Another important issue is the habit of attributing any panagglutinating reactivity to an autoantibody, which, in the context of a k-negative phenotype, may be entirely due to the alloantibody. Without testing the eluate against k-negative red cells, one cannot assert overlapping autoimmunity, and the association with immunotherapy remains a hypothesis. Conclusion: In the presence of generalized agglutination in a patient with a rare phenotype, extended phenotyping combined with a panel treated with 0.2 M dithiothreitol and k-negative red cells resolves specificity without the need for adsorption. This case also reinforces the role of the National Rare Blood Registry in supporting patients alloimmunized against high-frequency antigens.
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BibTeX
@article{silva2026anticellano,
title = {{ANTI-CELLANO MISTAKEN FOR AUTOANTIBODY DUE TO ABSENCE OF K-NEGATIVE RED CELLS IN A COMMERCIAL PANEL: LABORATORY RESOLUTION AND TRANSFUSION SUPPORT}},
author = {Jefferson Vinicius DA SILVA and Fátima Ribeiro DIAS and Rodrigo Saar GOMES and Muriel Vilela Teodoro SILVA and Amanda Souza ROSA and Larissa Martins Helcias TORRES},
journal = {Hematology, Transfusion and Cell Therapy},
year = {2026},
month = oct,
doi = {10.1016/j.htct.2026.107263},
url = {https://doi.org/10.1016/j.htct.2026.107263},
note = {CC BY},
}
RIS
TY - JOUR
TI - ANTI-CELLANO MISTAKEN FOR AUTOANTIBODY DUE TO ABSENCE OF K-NEGATIVE RED CELLS IN A COMMERCIAL PANEL: LABORATORY RESOLUTION AND TRANSFUSION SUPPORT
AU - Jefferson Vinicius DA SILVA
AU - Fátima Ribeiro DIAS
AU - Rodrigo Saar GOMES
AU - Muriel Vilela Teodoro SILVA
AU - Amanda Souza ROSA
AU - Larissa Martins Helcias TORRES
PY - 2026
DA - 2026/10/23
JO - Hematology, Transfusion and Cell Therapy
DO - 10.1016/j.htct.2026.107263
UR - https://doi.org/10.1016/j.htct.2026.107263
AB - Introduction: The k antigen (Cellano, KEL2) is present in more than 99.8% of the population. While the K+k- phenotype, which requires homozygosity for KEL1, is rare in Brazil, where the prevalence of K is 4% to 5% and only 1.47% of K+ samples are k-negative, bringing it close to the international rare blood threshold (less than 1:1,000). Since no commercial panel contains k-negative red cells, anti-k reacts with the entire panel and simulates an autoantibody, making identification and transfusion support difficult. Case description: Female patient, 59 years old, with metastatic clear cell renal carcinoma, two pregnancies, and previous transfusions, presenting with severe hyporegenerative anemia (hemoglobin 6.0 g/dL). Extended red cell phenotyping, irregular antibody screening, direct antiglobulin test, acid elution, score-based titration, and, at a reference laboratory, serum testing against a panel treated with 0.2 M dithiothreitol and k-negative red cells were performed. Blood typing result: group A, RhD positive; phenotype C+c-E-e+ K+k-. In November 2025, six weeks after transfusion, a 2+ direct antiglobulin test (IgG) and reactivity against the entire panel were obtained. Serum treatment with 0.01 M dithiothreitol, which inactivates IgM without altering Kell antigens on test red cells, was ineffective. At the reference laboratory, the direct antiglobulin test was confirmed, autocontrol and eluate were negative, and the serum lost reactivity against the panel treated with 0.2 M dithiothreitol, which denatures Kell antigens and other disulfide-dependent systems. In addition, there was no reactivity against three untreated k-negative red cells, which, together with the K+k- phenotype, defined anti-k (titer 2, score 16). In March 2026, nivolumab was started; the following month, positive autocontrol and eluate reactive with the entire panel appeared, findings of limited interpretation due to transfusion in the interval and absence of testing against k-negative red cells. Indirect bilirubin remained normal, with no other markers of hemolysis. After ruling out autologous donation due to severe anemia and erythropoietin refractoriness, the National Rare Blood Registry was activated, obtaining k-negative units from the state inventory and, by air transport, from a blood center in another federal unit, which were transfused without adverse reactions. However, the patient died due to progression of the neoplasm. Discussion: The concentration of dithiothreitol determined the course of the investigation: 0.01 M in serum inactivates IgM, whereas abolishing Kell antigens requires 0.2 M in test red cells. Another important issue is the habit of attributing any panagglutinating reactivity to an autoantibody, which, in the context of a k-negative phenotype, may be entirely due to the alloantibody. Without testing the eluate against k-negative red cells, one cannot assert overlapping autoimmunity, and the association with immunotherapy remains a hypothesis. Conclusion: In the presence of generalized agglutination in a patient with a rare phenotype, extended phenotyping combined with a panel treated with 0.2 M dithiothreitol and k-negative red cells resolves specificity without the need for adsorption. This case also reinforces the role of the National Rare Blood Registry in supporting patients alloimmunized against high-frequency antigens.
SN - 2531-1379
SN - 2531-1387
ER -