Heparin-induced thrombocytopenia/thrombosis (HITP) is thought to be mediated by immunoglobulins that activate platelets in the presence of pharmacologic concentrations of heparin, but the molecular basis for this relatively common and often serious complication of heparin therapy has not been established. We found that plasma from each of 12 patients with HITP contained high titer (. 1:200) Invest. 1994. 93:81-88.)

Highly sensitised patients are at increased risk for antibody mediated rejection (AMR) and reduced graft survival. Highly sensitive assays for detecting recipient preformed anti-HLA antibodies have been developed and identify high immunological risk donors. A 62yo male with end stage renal failure secondary to glomerulonephritis received a T-cell crossmatch negative, deceased donor, renal transplant mismatched at 3 of 6 HLA loci. A donor specific antibody (DSAb) to DR17 (MFI 2073) was present. Given his advancing age, multiple medical comorbidities and broad HLA sensitisation the transplant was accepted, however, shortly before transplantation two atypical results were made available. Firstly a B-cell crossmatch was performed and found to be negative in current serum but strongly positive in peak serum, secondly a further potential DSAb was predicted based on linkage disequilibrium with known donor HLA typing. The donor HLA typing would not be clarified until after the transplant. Despite the increased risk of AMR the transplant proceeded with pre-emptive plasma exchange. The patient developed severe AMR requiring extensive therapy. Incomplete prospective donor HLA typing can generate uncertainty in the interpretation of the virtual crossmatch performed for deceased donor transplants. This may result in clinically relevant sequelae. Advances in antibody detection techniques need to be matched by timely donor HLA typing for its full benefit to be realised.