Abstract
Several are the recent experimental data regarding the pathogenesis of diabetic microangiopathy, even if the comprehensive picture of this condition is still rather incomplete. The functional and structural alterations of several organs involved (first of all kidney and retina) are especially dependent on the activation of the polyol pathway and on the increase of the nonenzymatic glycosylation. An important determinant of diabetic microangiopathy is the increase of permeability, at first charged especially to the haemodynamic alterations and partly reversible, and later supported by irreversible variations of the cellular and extracellular components of the vascular wall. Genetic factors certainly contribute to the explanation of the diverse gravity of microvascular damage in diabetic patients, even if the mechanisms by which they interfere are only partly known. Furthermore, the links between arterial hypertension and diabetic nephropathy, and also the reduction in glycosaminoglycans in the basal membranes are perhaps genetically originated.
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