(P-QU-8) Evaluation of Serologic Weak D Testing and RHD Genotyping Strategies to Identify RhD Alloimmunization At-Risk Patient Populations at a Large, Tertiary Pediatric Hospital

Background/Case Studies: The RHD gene is a source of much genetic variation and can lead to variant antigen expression on the surface of RBCs. Variants can result in RhD alloimmunization if the patient is exposed to wild-type antigens that exhibit epitopes their red cells lack. Alloimmunization to RhD is clinically significant, both in the context of pregnancy and transfusion, therefore it is imperative to proactively monitor for at risk patients so appropriate management can be implemented. Serologic testing for the RhD antigen is routinely performed, however methodologies with variable sensitivity limit serologic evaluation of RHD variants. Incorporating RHD genotyping for certain patient populations, such as pregnant women, has been recommended by professional societies, but operationalizing this has proven challenging. In this process improvement activity, we aimed to evaluate RhD serologic testing and RHD genotyping strategies in our pediatric patient population, including prenatal patients, for potential policy revision.

Study

Design/Methods: Hospital transfusion service records were examined for RhD testing results from January 2021 to August 2024. Current process is to perform a serologic weak D test on all Rh negative prenatal patients and potential directed or stem cell donors typing as Rh negative. Additionally, reactions to anti-D reagent of 2+ or less in immediate spin tests undergo discrepancy evaluation per standard operating procedure. RHD molecular typing is determined on a case-by-case basis at the discretion of the transfusion medicine physician. Furthermore, patient samples tested for serologic weak D from 2012 to December 2020 were reviewed.

Results/Findings: There were a total of 39,780 samples processed during the review time period. Of those, 36 samples typed serologically as 2+ or less for the RhD antigen (using automated gel instrument). Of those, 23 had prior transfusions so weak D testing was not performed. For the other 13 samples there was no history of transfusion. Nine had serologic weak D testing performed and was positive (1-3+), 3 had no serologic weak D testing performed and 1 had RHD molecular testing performed. Retrospective review of the samples that had weak D testing performed from 2012 to 2021 showed zero positive weak D results.

Conclusions: Past approaches to sporadically evaluating for RHD variants in our population is not in alignment with current practice recommendations. The pediatric hospital’s increasing adolescent prenatal care, fetal medicine program, and transplant programs increase the probability of identifying a patient with risk of anti-D alloimmunization. The data reviewed provides justification for a defined and organized approach to identifying at risk patients in this pediatric care setting. The data was used to develop a protocol to identify at risk patients and remove practices that have not been beneficial in identifying a variant to date.