OBJECTIVE: An increase in urinary albumin excretion (UAE) in type 1 diabetic 
patients might reflect changes in vascular permeability and/or local 
haemodynamic factors. Indeed, transcapillary escape of albumin (TERalb), a 
measure of systemic capillary efflux, is increased in diabetic patients, even in 
those with a modest increase of albuminuria. In normo-albuminuric type 1 
diabetic patients, systemic capillary and glomerular flow is increased. We 
hypothesized that these haemodynamic changes contribute to an elevated TERalb, 
even in the phase preceding micro-albuminuria.
METHODS: We measured TERalb in 39 normo-albuminuric type 1 diabetic patients and 
46 healthy controls. TERalb was calculated from the disappearance curve of 
125I-albumin. Renal and systemic haemodynamics were measured by standard 
techniques. Forearm blood flow (FBF) was measured by plethysmography. 
Endothelial function was assessed by intra-arterial infusion of acetylcholine. 
The structural integrity of the vessel wall was determined by the post-occlusive 
reactive hyperaemia test.
RESULTS: TERalb was increased in diabetic patients (5.53+/-0.40 versus 
4.39+/-0.21 %/h, P = 0.01). Patients were divided into tertiles with respect to 
their TERalb. There were no differences in UAE, blood pressure, metabolic 
parameters, endothelial function or maximal vasodilatation after occlusion 
between the groups. However, filtration fraction and FBF were significantly 
increased in the group of diabetic patients with the highest levels of TERalb. 
Overall, in diabetic patients, FBF was significantly correlated with TERalb.
CONCLUSIONS: TERalb is increased in normo-albuminuric type 1 diabetic patients. 
In these patients with an increased capillary permeability, there is no evidence 
of endothelial dysfunction or vessel wall damage. However, both FBF and 
filtration fraction are increased. Therefore, the increased vascular 
permeability in the early phase of type 1 diabetes is associated with general 
haemodynamic alterations. Notably, such an increase in vascular permeability is 
not necessarily reflected by abnormal UAE. This could be due to either a lack of 
change in glomerular permeability or due to the fact that the threshold for 
tubular reabsorption of albumin has not been exceeded.