Reversal of left ventricular hypertrophy with angiotensin converting enzyme inhibition in hypertensive patients with autosomal dominant polycystic kidney disease
T. Ecder et al., Reversal of left ventricular hypertrophy with angiotensin converting enzyme inhibition in hypertensive patients with autosomal dominant polycystic kidney disease, NEPH DIAL T, 14(5), 1999, pp. 1113-1116
Background. Hypertension occurs commonly and early in the natural history o
f autosomal dominant polycystic kidney disease (ADPKD), affecting both rena
l and patient outcome. Activation of the renin-angiotensin-aldosterone syst
em due to cyst expansion and local renal ischaemia plays an important role
in the development of ADPKD related hypertension and left ventricular hyper
trophy (LVH), a known important risk factor for cardiovascular morbidity an
d mortality. The aim of this study was to investigate the effects of an ang
iotensin converting enzyme (ACE) inhibitor, enalapril, on renal function, b
lood pressure and LVH in hypertensive ADPKD patients.
Methods. Fourteen hypertensive ADPKD patients (II men, 3 women; mean age: 4
0 years) were included in the study. All patients had LVH and creatinine cl
earance (Cer) greater than 50ml/min/1.73m(2). The patients were followed fo
r 7 years on enalapril therapy. The effects of enalapril on renal function,
blood pressure and LVH were investigated.
Results. Baseline measurements of mean arterial pressure (MAP), Ccr and lef
t ventricular mass index (LVMI) were 110+/-2mmHg, 84+/-6ml/min/1.73m(2) and
146 +/- 4 g/m(2), respectively. After one year of enalapril therapy there
was a significant decrease in MAP (94 +/- 3 mmHg, P< 0.005) which remained
stable until the end of the study at 7 years (94 +/- 1 mmHg, P < 0.005 vs b
aseline). There was also a significant decrease in LVMI (131+/-6 g/m(2), P<
0.05) after year I which continued to decrease until the end of the study
reaching 98 +/- 6 g/m(2) (P < 0.01 vs year 1 and baseline). Although Ccr re
mained stable after year I, a significant decrease was observed after 7 yea
rs of follow-up (59 +/- 6 ml/min, P<0.001 vs year 1 and baseline).
Conclusions. ACE inhibition in hypertensive ADPKD patients provided long-te
rm reversal of LVH in association with a mean 3.6 ml/min/year decline of Cc
r. These preliminary results have potential important implications for card
iovascular and renal protection in ADPKD.