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Abstract Thrombomodulin (TM) IS a surface glycoprotein which neutralizes thrombin clotting and platelet aggregatory activity and acts as a cofactor for thrombin catalyzed activation of anticoagulant protein c. Circulating thrombomodulin is not constantly secreted by endothelial cells but results from cellular damage. Unlike von Willebrand factor and tissue plasminogen activator, circulating TM is not a maker of endothelial cell stimulation, and the endothelial membrane TM is hardly leaked in absence of endothelial inJurY The liver is considered the major site of clearance of circulating TM, and patients with liver disease especially fulminant hepatitis were reported to have elevated plasma TM levels (Takahashi et al., 1992) In addition the change in urinary excretion of TM may modifi,· its plasma (Ishii and Majerus, 1985). Plasma TM has been frequently reported to be elevated in a variety of diseases including DIC, pulmonary thromboembolism, acute respiratory distress. chronic renal failure. collagen diseases, hematological malitmancies as well as in thrombotic diseases These findings suggest that the endothelial damage may occur more frequently than hitherto supposed (Ta Kahashi et a!., 1992 ). Subclinical elevation of urinarY albumin, microalbwninurea. is well described as being a predictor for cardiovascular disease in both diabetic and nondiabetic subjects It reflects the presence of generalized vascular damage and represents a crucial event in the natural histories of diabetes melhtus and essential hypertension (Yudkin et al., 1988). An increased risk of cardiovascular mortalitv in both insuhn - dependent ODD) and noninsulin-dependent (NIDD 1 diabetics has been recorded in association with microalbwninurea and the risk becomes 10 - to 40 fold higher with development of clinical proteinuria, macroalbuminurea in IDD (Borch et a!., 1985). |