Forty-six transplant patients had lower platelet serotonin and higher plasma beta-thromboglobulin (beta-TG) than normal controls. These abnormalities were more pronounced in acute rejection (AR) than in chronic rejection (CR), but were also present in normally functioning transplants (FT). Patients also showed lower serum levels of thromboxane B2 (TxB2) than controls. Plasma fibrinopeptide A (FPA) was higher in AR, but not in CR and in FT, than in controls. Therefore, in renal transplant recipients, platelets continue to circulate after in vivo activation, the abnormalities being roughly proportional to the extent of graft injury. Granule-bound substances secreted into the circulation might produce ischaemia and platelet aggregates, damaging the graft and aggravating the rejection lesions.
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