Activation of Tissue Factor–Induced Coagulation and Endothelial Cell Dysfunction in Non–Insulin-Dependent Diabetic Patients With Microalbuminuria

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Abstract
Abstract We studied the relationships between albuminuria, tissue factor–induced coagulation, and endothelial cell dysfunction in 67 patients with non–insulin-dependent diabetes mellitus (NIDDM) who were divided into three groups on the basis of their urinary albumin excretion rate (AER). To assess the early phase of tissue factor–induced coagulation, activated factor VII (FVIIa) levels in plasma were measured by a direct fluorogenic assay. As markers of endothelial cell dysfunction, levels of von Willebrand factor (vWF), tissue-type plasminogen activator–plasminogen activator inhibitor–1 (TPA–PAI-1) complex, PAI-1, and tissue factor pathway inhibitor (TFPI) were measured. FVIIa levels were increased in normoalbuminuric NIDDM patients (AER 200 μg/min). In all 67 diabetic patients, AER showed a strong positive correlation with FVIIa ( r =.574, P <.0001) and a weakly but still significant correlation with FVIIa-FVII:Ag ( r =.365, P =.01), vWF ( r =.315, P <.01), and TAT ( r =.323, P <.01). FVIIa showed a weaker correlation with vWF ( r =.244, P <.05). FVIIa generation concomitant with an increase in AER is probably due to endothelial cell damage. Increased plasma FVIIa levels would produce hypercoagulability in NIDDM patients with microalbuminuria and thus may be a risk for cardiovascular disease.