[The feasibility and current limits in the prevention of diabetic nephropathy]

Diabetic nephropathy is the leading cause of uremia in Italy and other industrialized countries: once diabetic nephropathy commences, it advances slowly but inexorably to uremia. Prevention begins with strict control of blood sugar to inhibit or normalize glomerular hyperfiltration, and control of blood pressure to prevent glomerular hypertension and decrease microalbuminuria. Pharmacological measures include ACE-inhibitors and calcium channel blockers, alone or in combination, to reduce proteinuria and preserve renal function. It is believed that some classes of anti-hypertensive drugs have a direct pharmacological depressive effect on cell growth factors that lead to mesangial sclerosis: ACE-inhibitors would thus depress angiotensin II, and the calcium channel blockers would inhibit the increase in intracellular calcium of the mesangial cells which increases gene expression of early growth. Dietary sodium restriction seems to correct the expansion of the sodium pool and related volemic expansion hypertension. A protein-poor diet limits the precapillary glomerular vasodilatation resulting from protein-induced hyperaminoacidemia. The earlier dietetic and pharmacological measures are taken, the more effective they become: while they cannot arrest diabetic nephropathy once it has commenced, they are able to delay evolution of the disease to uremia.