Due to its hemodynamic, metabolic and growth promoting effects, angiotensin
II (AII) may play an important role in the pathogenesis of diabetic kidney
disease. Consequently, decreasing the production or cellular action of AII
is a rational target for therapeutic attempts aimed at slowing the progres
sion of diabetic nephropathy. Based on their superior renoprotective perfor
mance in recent landmark studies, currently ACE inhibitors are the drugs of
choice in diabetic patients with microalbuminuria or overt proteinuria. A
new class of antihypertensive medications, the AT1 receptor antagonists may
represent an alternative to ACE inhibitors in the treatment of diabetic ne
phropathy. They provide a more complete blockade of the renal renin-angiote
nsin system and are generally better tolerated than ACE inhibitors. On the
other hand, AT1 receptor antagonists do not increase bradykinin levels, an
effect that may contribute to the high level of renoprotection achieved by
ACE inhibitors. Although human data are not available at: this point, ACE i
nhibitors and AT1 receptor antagonists have similar beneficial effects on p
roteinuria, renal hypertrophy and glomerulo-sclerosis in animal models of d
iabetic kidney disease. Currently several prospective studies are being con
ducted to compare the efficacy of ACE inhibitors and AT1 receptor antagonis
ts in the treatment of human diabetic nephropathy. Copyright (C) 1999 John
Wiley & Sons, Ltd.