The relation between urinary albumin excretion rate (UAE), transcapillary escape 
rate of albumin (TERalb), haemostatic factors, ambulatory blood pressure, and 
metabolic variables was investigated in 45 Type II (non-insulin-dependent) 
diabetic patients without overt nephropathy or uncontrolled blood pressure. We 
enrolled 44 patients in a placebo controlled study to test the effects of 3 week 
long treatment with low-molecular weight heparin (tinzaparin) on the same 
variables. BMI, 24 h systolic and diastolic blood pressure, plasma 
concentrations of triglycerides, fasting glucose, factor VIII, von Willebrand 
factor (vWf), fibrinogen, alpha-2 macroglobulin, and fibronectin were notably 
higher in patients with increased albuminuria compared with normoalbuminuric 
patients, whereas the TERalb was similar in the two groups. TERalb correlated 
with fasting plasma glucose. UAE correlated more closely than TERalb with 24 h 
ambulatory blood pressure, vWf, and factor VIII. Urinary albumin excretion rate 
was unchanged during tinzaparin [28.9+/-5.6 vs 28.1+/-6.0 microg/min (geometric 
mean (antilog SD)] vs placebo (18.0+/-5.4 vs 17.6+/-5.3 microg/min), and no 
change was found in TERalb [6.3+/-1.6 vs 6.0+/-1.5%/h (means +/- SD), and 
6.3+/-1.5 vs 5.6+/-1.8%/h; tinzaparin versus placebo, respectively]. Only minor 
changes were observed in blood pressure, lipids, glycaemic control and 
haemostatic factors. This study shows no correlation between albuminuria and 
transcapillary escape rate in Type II diabetic patients without overt 
nephropathy or uncontrolled-blood pressure. UAE is related to markers of 
atherosclerosis, endothelial injury and dysfunction, and haemostatic factors. 
Moreover, UAE correlates much more than TERalb with 24 h ambulatory blood 
pressure, von Willebrand factor, and factor VIII. Finally, short-term treatment 
with tinzaparin does not change the transvascular or glomerular leakage of 
albumin. These results indicate that TERalb is not a sensitive marker of 
microvascular dysfunction in such patients and that factors other than abnormal 
glycosaminoglycan metabolism may contribute to the vascular damage of these 
patients.