There is a clear relationship between hypertension and the microvascul
ar complications of diabetes. Genetic predisposition to hypertension h
as been correlated to the risk of diabetic nephropathy in type I diabe
tes, and hypertension is a well known risk factor for developing nephr
opathy in patients with type II diabetes. Multiple studies have emphas
ized the importance of hypertension on renal disease progression, and
blood pressure control with conventional antihypertensive drugs slows
the rate of renal function loss in diabetic nephropathy. Furthermore,
evidence of the role of renin-angiotensin system (RAS) on progression
of renal damage has focused much interest on the therapeutic action of
the RAS blockade. In patients with type I diabetes, blocking the RAS
with angiotensin converting enzyme (ACE) inhibitors prevents progressi
on from microalbuminuria to overt nephropathy, and in overt nephropath
y decreases the gradual loss of renal function beyond its blood pressu
re lowering effect. Less clinical information is available in type II
diabetic nephropathy, but our experience and some recent studies sugge
st that ACE inhibitors also have a renoprotective action in type II di
abetes. The role of calcium channel blockers in diabetic nephropathy i
s not clear. Several short-term studies with the first generation dihy
dropyridine calcium antagonists showed a lower effect on urinary album
in excretion and a more rapid progression to renal failure than with A
CE inhibitors. However, other calcium channel blockers, particularly o
f the non-dihydropyridine type, have been shown to have a beneficial e
ffect on diabetic nephropathy, decreasing proteinuria and slowing prog
ression.