The pathogenesis of the diabetic glomerular lesion is unknown. However, cumulative indirect evidence favors hemodynamic factors associated with the abnormal endocrine environment as the cause of
diabetic angiopathy. Experimental evidence suggests that the increased hydrostatic pressures in capillary beds, a hallmark of the early stages of
insulin-dependent diabetes, are associated with macromolecular leakage leading to the typical thickening of glomerular capillary basement membrane and increased glomerular mesangial matrix even prior to the occurrence of systemic
hypertension. Patients with renal or
carotid artery stenosis seem to be protected against
diabetic nephropathy and retinopathy on the stenosed side. The first signal of
diabetic nephropathy even before deterioration of the renal function is microalbuminuria detected by sensitive methods such as radioimmunoassay. Not only in hypertensive, but even in normotensive diabetic patients with microalbuminuria
antihypertensive therapy has been shown to reduce
albumin excretion rate and to slow the progression of
diabetic nephropathy. Once overt
diabetic nephropathy has been established,
hypertension is a constant accompaniment of the disease. Thus,
hypertension may be a cause as well as a result of
diabetic nephropathy. Tight control of
blood sugar in close association with
antihypertensive treatment reducing blood pressure to a lower normal limit, possibly with agents that specifically decrease glomerular capillary hydraulic pressure are the corner stone in protection against progression of the
diabetic angiopathy.