A study of the coagulolytic balance as well as platelet aggregation was carried out in 64 nephrotic patients. The data were correlated, in a prospective attempt, with the clinical demonstration of thrombo-embolic events. Activating factors (factors I, VIIIc, VIIIr:Ag) were increased as well as certain clotting inhibitors, alpha-1-antitrypsin and alpha-2-macroglobulin. There was a platelet hyperaggregability in 31.5% of our patients. Thrombo-embolic complications occurred in six subjects (9%). The data of these six patients were compared with that of the other patients; no significant correlation were found between clotting abnormalities and thrombosis. Low level of ATm (less than 0.8 U.Fr) and severe hypoalbuminemia (less than 20 g/liter) were of no predictive value for the occurrence of thrombo-embolic events.

LM. Genetic risk factors in acute coronary disease. Haemostasis 1999 (in press). 2. Brattstrom L, Wilcken DE, Ohrvik J, Brudin L. Common methylenetetrahydrofolate reductase gene mutation leads to hyperhomocysteinemia but not to vascular disease: the result of a meta-analysis.

SummaryAdhesion of platelets to endothelium has been shown to induce important changes in endothelial properties. In this study, we examined the effect of platelet-endothelial cell interactions on the expression of urokinase-type plasminogen activator (u-PA) by human microvascular endothelial cells. After incubation of endothelial cells with platelets, a dose-dependent increase in the expression of u-PA Ag was observed and reached a plateau for a ratio of 300 platelets per endothelial cells. The u-PA Ag upregulation resulted from an increase in u-PA mRNA that originated from a synthesis by endothelial cells since no u-PA mRNA was detected in platelets. The platelet-induced u-PA synthesis was inhibited when the endothelial cells were pre-treated with phospholipase C to remove the u-PA receptor, or when the platelets were incubated with an antibody that blocks the binding of u-PA to u-PAR. Taken together, these data indicate that u-PA present on the platelet surface interacts with u-PAR on the endothelial cells and induces the u-PA synthesis. This mechanism may represent a physiological control of platelet-mediated intravascular fibrin deposition.

We applied the standard treatment with streptokinase to 52 cases of deep venous thrombosis and 35 cases pulmonary embolism. Angiography demonstrated total lysis of the clot 22 times, partial lysis 42 times, and no lysis 23 times. The absence of lysis was more frequent in venous clots than in pulmonary clots. Early treatment was more effective, achieving complete lysis in 21 of 22 cases. Nevertheless, in deep venous thrombosis, late treatment can result in partial lysis and set an important venous junction free. With the standard treatment, the biologic controls showed good lysis in 75% of the cases, insufficient lysis in 15%, and no lysis in 10%. The extent of the thrombosis is an important point. The clot was totally lysed in 9 of 10 cases of localized deep venous thrombosis. In patients with pulmonary embolism, about 30% of the obstructed surface is cleared. Nevertheless, in such cases we must take into consideration not only the nonperfused pulmonary area, but also the venous starting point of the clot.

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