Methods for the selection of platelet products for alloimmune-refractory patients.

The ability to efficiently and accurately diagnose the cause(s) of platelet (PLT) refractoriness is paramount in providing effective PLT products for transfusion. Recent advances in methods for detecting and identifying alloantibodies against human leukocyte antigens (HLAs) and human PLT antigens, combined with accurate molecular techniques for HLA typing, have provided a framework for the development of clinical algorithms to support such patients. Alloantibodies may be detected and/or identified by several methods, including complement-dependent cytotoxicity, enzyme-linked immunosorbent assays (ELISA), and microbead-based assays using Luminex or flow cytometry. The primary difference in these assays is the sensitivity of detection and the range of antibody specificities that may be reliably identified. Direct PLT cross-matching to identify compatible PLTs can be accomplished by several methods, including solid-phase red cell adherence, modified antigen capture ELISA, and flow cytometry. A survey of blood centers and laboratories providing transfusion support has identified the heterogeneity of testing options available, areas of concern and need for improvement, and common obstacles in providing appropriate and timely support to immune-refractory PLT patients. Depending on the testing methods and the pool of HLA-typed PLT donors available, there are numerous options for developing suitable algorithms to provide effective support to immune-refractory PLT patients.

Donor-specific antibodies by flow single antigen beads in pediatric living donor kidney transplants: single center experience.

Flow PRA and SAB are now routinely performed to identify HLA antibodies in the recipient sera. The presence of DSA is considered a risk factor for graft failure. However, this risk is not clearly defined. We reviewed all the pediatric recipients of living donor kidney transplants since Flow PRA and Flow SAB became routinely done at our institution. All children had negative CDC and Flow XMs. Comparison of clinical outcome was done between those with and without pretransplant DSA. Six children had positive DSA by Flow SAB. They received thymoglobulin, steroids, tacrolimus, and MMF. Five had anti-HLA class I antibodies and one anti-HLA class II. Only one child had an AR. Graft survival: 100% at last visit with GFR >70 mL/min/1.73 m(2). A control group without DSA was used for comparison (n = 44). They received our standard protocol: basiliximab, tacrolimus, MMF, and steroids. AR rate was 9%. Both groups had similar follow-up time, and patient and graft survival rates. In our small series, we saw excellent outcome despite the presence of DSA pretransplant. No unequivocal ideal to establish the ideal immunosuppressive regimen for this cohort of patients has been established and the long-term outcome of these recipients has not been delineated.