Introduction to a structural basis for renal and vascular complications in diabetes and hypertension.

Abstract

An understanding of the structural basis for cardiovascular and renal complications in diabetes and hypertension is critical to design-focused intervention strategies. The processes leading to vascular damage in the kidney and in the arteries in diabetes and hypertension appear to be characterized by hypertrophic/hyperplastic changes in a number of cell types (such as smooth muscle cells, fibroblasts, mesangial cells) and by excessive deposition of extracellular matrix material. Markers of cell growth/proliferation, such as Na(+)-H+ exchange, show increased activity in diabetic patients with renal disease and in patients with essential hypertension. Insulin resistance is a feature of arterial hypertension and diabetes and may contribute to renal and cardiovascular damage in these patients. A number of risk factors for cardiovascular disease cluster in the subset of diabetic patients prone to renal disease. These include dyslipidaemia, left ventricular hypertrophy and hypertension. It is postulated that a familial predisposition to renal and cardiovascular disease is the underlying reason for the susceptibility to the diabetic cardiorenal syndrome. In the management of diabetes and hypertension, it may prove possible to instigate preventive strategies by using therapeutic agents such as angiotensin converting enzyme inhibitors, which have the potential to interfere with the haemodynamic, growth and insulin sensitivity processes that contribute to vascular damage.