Microalbuminuria is associated with an increased risk of cardiovascula
r disease (CVD) in insulin-dependent diabetes mellitus (DDM) patients,
but the pathophysiological basis of this association is not clear. To
see whether or not hemostatic dysfunctions might contribute to explai
n this association, we measured tissue plasminogen activator (t-PA), p
lasminogen activator inhibitor-1 (PAI-1), factor VII activity, plasma
fibrinogen, and plasma endothelin-1 (ET-1) in 13 microalbuminuric (alb
umin excretion rate [AER], 20-200 mug/min) and in 13 comparable normoa
lbuminuric (<20 mug/min) IDDM patients. t-PA and ET-1 were similar in
the two groups, whereas PAI-1 activity (5.65 +/- 1.92 vs. 0.85 +/- 0.5
8 IU/ml, P < 0.05), factor VII (87.85 +/- 4.94 vs. 76.54 +/- 2.31%, P
< 0.05), and plasma fibrinogen (3.38 +/- 0.21 vs. 2.65 +/- 0.13 g/l, P
< 0.05) were significantly higher in microalbuminuric than in normoal
buminuric patients. Plasma fibrinogen was related to AER (i2 = 0.23, P
< 0.05), whereas triglycerides and factor VII were related to PAI-1 (
i2 = 0.39, P < 0.001 and i2 = 0.10, P < 0.05). These results suggest t
hat microalbuminuria iss associated with a hypercoagulative and hypofi
brinolytic state. Hemostatic dysfunctions might be a pathogenetic link
between microalbuminuria and CVD.