Jk. Rockstroh et al., BLOOD-PRESSURE INDEPENDENT EFFECTS OF NITRENDIPINE ON CARDIAC STRUCTURE IN PATIENTS AFTER RENAL-TRANSPLANTATION, Nephrology, dialysis, transplantation, 12(7), 1997, pp. 1441-1447
Left ventricular hypertrophy is well established as a blood pressure i
ndependent cardiovascular risk factor in patients on renal replacement
therapy. The effects of antihypertensive treatment on myocardial stru
cture and function in renal transplant recipients have been so far onl
y rarely investigated. In a double-blind, placebo-controlled study pat
ients were randomized to the calcium channel blocker nitrendipine or p
lacebo if the transplanted kidney had developed a stable phase. Normot
ensive patients received nitrendipine 2 x 5 mg daily or placebo, hyper
tensive patients received 2 x 10 mg up to 2 x 20 mg nitrendipine daily
or placebo. To achieve adequate blood pressure control, all patients
with still elevated blood pressure on study medication received antihy
pertensive drugs other than calcium channels blockers. Ambulatory bloo
d pressure recording and 2D-guided M-mode echocardiography were perfor
med at baseline and upon completion of the study. In addition, laborat
ory workup (including serum creatinine and lipids) was done, and serum
aldosterone, plasma renin activity, plasma angiotensin II and blood g
lucose levels were measured in all patients at baseline and after at l
east 12 months of therapy. Ambulatory blood pressure was almost identi
cal between both groups at study baseline and follow-up. In renal tran
splant patients on nitrendipine, posterior wall thickness (-0.10 +/- 1
.77 mm) and septal wall thickness (-0.83 +/- 2.23 mm) did not change s
ignificantly from baseline. In contrast, posterior wall thickness (0.7
1 +/- 0.92 mm, P < 0.01) and septal wall thickness (0.97 +/- 2.20 mm,
P < 0.05) increased in patients on placebo, which differed from the ob
served changes on nitrendipine (ANOVA: P = 0.093 and P = 0.048, respec
tively). Relative wall thickness, a parameter for concentric left vent
ricular hypertrophy, became numerically smaller on nitrendipine therap
y from 0.46 +/- 0.07 to 0.44 +/- 0.09 (-0.02 +/- 0.09, NS) but increas
ed from 0.42 +/- 0.08 to 0.48 +/- 0.08 in the placebo arm (+0.04 +/- 0
.08, P < 0.02), which was also significant between the two groups (ANO
VA: P = 0.036). Endocrine parameters, lipids and blood glucose were no
t different between the two groups. We conclude from these data that t
he calcium channel blocker nitrendipine exerted beneficial effects on
cardiac structure in patients after renal transplantation independent
of blood pressure.