264 The complement-dependent antibody lymphocytotoxicity (cross match) assay has been used to detect the presence of recipient antibodies directed against donor lymphocyte antigens. However, detection of antibodies by the standard NIH crossmatch (NIH-XM) technique may be too insensitive to detect low level of antibodies. A modified lymphocytotoxicity technique using antihuman globulin (AHG-XM) has been employed to increase the cross-match sensitivity. The clinical relevance of the additional reactivity detected by this technique is still a matter of debate. In the present study we analysed the impact of positive historical AHG-XM on kidney graft survival in 87 presensitized patients, consecutively transplanted in a single center between 1985 and 1991. All the patients had a negative NIH-XM on historical and current sera and the AHG-XM on current serum was also negative. Seventee three patients had a negative historical AHG-XM (group A) and 14 had a positive historical AHG-XM(group B) Actuarial patient survival in groups A and B was 96% and 100% at 1 year, and 88% and 100% at 8 years, respectively. Actuarial graft survival in group A and B was not significantly different at 1 year (92% vs 100%) and at 8 years (62% vs 77% p>0.05). Mean serum creatinine values were not significantly different at 1 year (160μmol/l) and at 8 years (156 μmol/l vs 149 μmol/l). Patients with a positive historical AHG-XM did not experience a significantly greater number of acute rejection episodes than the recipients with a negative historical AHG-XM (1.5 vs 1.29 p >0.05) Censoring death with a functioning allograft did not modify the results. CONCLUSION: an historical positive antihuman glubulin cross match does not impede long-term allograft survival, and the use of this technique could generate undue prolonged waiting time for renal transplantation canditates.

Fifty polytransfused patients were prospectively studied to determine the frequency of post-transfusion alloimmunization and its influence on the response to platelet transfusion. Platelet- and HLA-specific antibodies were detected by means of the standard and antiglobulin-augmented lymphocytotoxicity techniques (LCT), the platelet suspension indirect immunofluorescence test (PSIIFT), and monoclonal antibody immobilization of platelet antigens (MAIPA). HLA antibodies were detected in 13 patients (26%) (IgM = 6; IgG = 6; IgM + IgG = 1). The standard LCT was positive in 12 of these 13 patients. Complement-independent HLA antibodies, only detectable in the PSIIFT and the antiglobulin-augmented LCT, were documented in two patients and were associated with poor post-transfusion platelet recovery in the patient who could be evaluated. All the HLA antibodies were detected in the PSIIFT, while only four were detected in the MAIPA. Platelet-specific alloantibodies were found in two patients by means of PSIIFT or MAIPA and may have led to poor post-transfusion platelet recovery in one patient. Platelet autoantibodies were detected in two patients but were not associated with platelet refractoriness. Paraformaldehyde-dependent platelet antibodies were detected in 11 patients but were not associated with platelet refractoriness.

Immune and nonimmune causes of platelet refractoriness were evaluated in a group of 50 patients with multiple perfusions in a prospective study. Our results suggest that these two factors are equally important and HLA alloimmunization is the major immune obstacle to successful platelet transfusion.