The relation between urinary albumin excretion rate (UAE), transcapillary escape rate of albumin (TER_alb), 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, α-2 macroglobulin, and fibronectin were notably higher in patients with increased albuminuria compared with normoalbuminuric patients, whereas the TER_alb was similar in the two groups. TER_alb correlated with fasting plasma glucose. UAE correlated more closely than TER_alb 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 μg/min (geometric mean (antilog SD)] vs placebo (18.0 ± 5.4 vs 17.6 ± 5.3 μg/min), and no change was found in TER_alb [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 TER_alb 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 TER_alb 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. [Diabetalogia (1999) 42: 60–67]