The uraemic state is commonly complicated by a haemorrhagic tendency due to an abnormality of the primary haemostatic response. Whilst renal anaemia contributes to the defect, platelet dysfunction has also been implicated. Tests of coagulation and platelet reactivity performed ex vivo on anticoagulated blood samples have not provided an adequate explanation for the haemostatic defect. We have therefore studied events at the site of tissue injury by serial assays of beta-thromboglobulin (BTG), thromboxane B2(TxB2) and fibrinopeptide A (FPA) in blood samples issuing from a standardised skin bleeding time incision in 7 uraemic subjects and matched healthy controls. Generation of TxB2and FPA were normal, but the concentration of BTG in bleeding time blood was markedly reduced throughout the first 5 min in the uraemic subjects. We conclude that a defect of platelet release occurring at the site of tissue injury may contribute to the haemostatic abnormality in uraemia and this finding could be relevant to the therapeutic strategy adopted in the management of bleeding episodes.