Gl. Bakris et al., CALCIUM-CHANNEL BLOCKERS VERSUS OTHER ANTIHYPERTENSIVE THERAPIES ON PROGRESSION OF NIDDM ASSOCIATED NEPHROPATHY, Kidney international, 50(5), 1996, pp. 1641-1650
Treatment of hypertension with ACE inhibitors in diabetic patients red
uces proteinuria and slows progression of nephropathy compared with ag
ents that do not maintain declines in proteinuria. Calcium channel blo
ckers (CCBs) have variable effects on proteinuria; their long-term eff
ects on progression of diabetic nephropathy are not known. The current
study examines the hypothesis that CCBs that maintain reductions in p
roteinuria slow progression of nephropathy associated with non-insulin
dependent diabetes mellitus (NIDDM) by a degree comparable to ACE inh
ibitors, given similar levels of blood pressure control. To test this
hypothesis we randomized 52 patients with NIDDM associated nephropathy
and hypertension, mean age of 63 +/- 8 years, to either the ACE inhib
itor, lisinopril (N = 18), nondihydropyridine CCBs (NDCCBs), verapamil
SR (N = 8) or diltiazem SR (N = 10), or the beta blocker, atenolol (N
= 16). Goal blood pressure was less than or equal to 140/90 mm Hg. Pa
tients were followed for a mean period of 63 +/- 7 months. The primary
end point was change in creatinine clearance (C-Cr) slope in each gro
up. There was no significant difference in mean arterial pressure redu
ction among the groups over the study period (P = 0.14). The mean rate
of decline in C-Cr was greatest in the atenolol group (-3.48 ml/min/y
ear/1.73 m(2); P < 0.0001). There was no difference in the C-Cr slopes
between lisinopril and NDCCBs groups (P = 0.36). Proteinuria was redu
ced to a similar extent in the lisinopril and NDCCBs groups (P > 0.99)
. Therefore, in persons with renal insufficiency secondary to NIDDM, s
imilar levels of blood pressure control with either lisinopril or NDCC
Bs slowed progression of renal disease to a greater extent than atenol
ol. Moreover, this enhanced slowing of renal disease progression corre
lated with sustained and significant reductions in proteinuria, findin
gs not observed in the atenolol group.