RESUMO
Reduction of bloodpressure has been known, from the work of Parving et al (1987), to reduce the rate of decline of renal function in the nephropathy associated with Type-1 diabetes mellitus (IDDM), using conventional anti-hypertensive agents. More recently, interest in angiotensin-converting enzyme inhibitors (ACE-Is), and calcium channel blockers (CCBs) in the treatment of diabetic nephropathy, has been forthcoming. In diabetic nephropathy, induced in rats by streptozotocin, ACE-Is clearly alter renal haemodynamics and reduce proteinuria. Reduction of proteinuria is also seen in humans with diabetic nephropathy, and there is a suggestion of preservation of renal function, although no long-term studies have been published. Two studies are underway in non-hypertensive microalbuminuric subjects, but these have also not been published. The group of ACE-Is appears to have similar action in reducing proteinuria in diabetic nephropathy, but the same cannot be said for the CCBs. They differ in their action in reducing proteinuria, and dilitiazem may stand alone in reducing proteinuria in human diabetic nephropathy. Debate continues on the mechanism for reduction in proteinuria. Amelioration in systemic hypertension plays a role for all classes of antihypertensive drugs used, but the ACE-Is may alter glomerular permselectivity and thereby bring about reduction in proteinuria. Dietary reduction or protein intake may also play a protein preserving renal function as may reduction of lipids (AU)
