Background/Case Studies: Background/Case Studies: A 4-year-old male presented with pneumonia with empyema, thrombotic microangiopathy (hemoglobin 5.8/g/dL, platelets (PLT) 78x10^9/L) and acute kidney injury. Streptococcus pneumoniae associated atypical hemolytic uremic syndrome (aHUS) was suspected on the basis of a positive urinary antigen immunochromatographic membrane assay and pleural fluid analysis showing many leukocytes and gram-positive cocci in pairs.
Study
Design/Methods: Study Design/ Methods: ABORh forward and reverse grouping was performed using monoclonal anti-A, -B, -D, Rh control, A1 and B cells at immediate spin (IS). Direct antiglobulin tests (DAT) were performed using polyspecific antihuman globulin (PS), monospecific anti-IgG (IgG), monospecific anti-C3b,d (C3) and saline control (S) at IS and room temperature incubation (RT). Testing of patient red blood cells (RBC) against donor plasma and lectins (Arachis hypogaea, Dolichos biflorus, Salvia sclarea, Salvia horminum and Glycine soja) was evaluated at IS using group O and A1 reagent cells as negative controls.
Results/Findings: Results/Findings: Initial ABORh results were invalid; Anti-A(4+), -B(1+), -D(4+), Rh control(1+), A1 cells(0) and B cells(4+). The DAT was also invalid; S(1+). Repeat testing with warm washed patient RBC showed group A positive and a positive DAT with C3. Warm washed patient RBC were also tested against ABO-compatible donor plasma (A and AB), group A cord-sera and an autocontrol. All ABO-compatible plasma tested were positive, whereas the autocontrol and cord sera were negative. An abbreviated lectin panel was performed using the patient’s warm washed RBC. Positive reactions were observed with A. hypogea, D. biflorus and G. soja; negative reactions were observed with both Salvia lectins (Table 1). Conclusions:
Conclusion: The reactivity suggests polyagglutination due to exposure of the Thomsen-Friedenreich (T) crypt antigen (T activated). Most normal human sera has naturally occurring IgM anti-T. Exposure of the T antigen can occur with S. pneumoniae infection through the desialyation of RBC, PLT and glomerular epithelial cells which results in agglutination of patient RBC when tested against human sera. Since the widespread use of murine and monoclonal reagents, polyagglutination is not often detected, but may be evaluated with lectins to resolve ABORh grouping discrepancies or for clinical correlation to strengthen the diagnosis of aHUS. Avoidance of plasma transfusion and washing of RBCs and PLTs was initially implemented out of an abundance of caution, but was discontinued to support the patient on extracorporeal membrane oxygenation.
Importance of research: Lectin testing is not routinely performed or widely available in most hospital transfusion services. This case highlights the utility of lectin testing to the blood bank, the clinical team, and the transfusion management of the patient. Identification of T antigen activation helped resolve the patient’s ABO discrepancy, strengthened the diagnosis, and guided transfusion recommendations.
