Journal Article

Reversal of left ventricular hypertrophy with angiotensin converting enzyme inhibition in hypertensive patients with autosomal dominant polycystic kidney disease.

T Ecder, C L Edelstein, A B Chapman, A M Johnson, L Tison, E A Gill, G M Brosnahan and R W Schrier

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 14, issue 5, pages 1113-1116
Published in print May 1999 | ISSN: 0931-0509
Published online May 1999 | e-ISSN: 1460-2385 | DOI: http://dx.doi.org/10.1093/ndt/14.5.1113
Reversal of left ventricular hypertrophy with angiotensin converting enzyme inhibition in hypertensive patients with autosomal dominant polycystic kidney disease.

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BACKGROUND: Hypertension occurs commonly and early in the natural history of autosomal dominant polycystic kidney disease (ADPKD), affecting both renal and patient outcome. Activation of the renin angiotensin aldosterone system due to cyst expansion and local renal ischaemia plays an important role in the development of ADPKD related hypertension and left ventricular hypertrophy (LVH), a known important risk factor for cardiovascular morbidity and mortality. The aim of this study was to investigate the effects of an angiotensin converting enzyme (ACE) inhibitor, enalapril, on renal function, blood pressure and LVH in hypertensive ADPKD patients. METHODS: Fourteen hypertensive ADPKD patients (11 men, 3 women; mean age: 40 years) were included in the study. All patients had LVH and creatinine clearance (Cer) greater than 50 ml/min/1.73 m2. The patients were followed for 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 left ventricular mass index (LVMI) were 110 +/- 2 mmHg, 84 +/- 6 ml/min/1.73 m2 and 146 +/- 4 g/m2, 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 baseline). There was also a significant decrease in LVMI (131 +/- 6 g/m2, P < 0.05) after year 1 which continued to decrease until the end of the study reaching 98 +/- 6 g/m2 (P < 0.01 vs year 1 and baseline). Although Ccr remained stable after year 1, a significant decrease was observed after 7 years of follow-up (59 +/- 6 ml/min, P < 0.001 vs year 1 and baseline). CONCLUSIONS: ACE inhibition in hypertensive ADPKD patients provided long-term reversal of LVH in association with a mean 3.6 ml/min/year decline of Ccr. These preliminary results have potential important implications for cardiovascular and renal protection in ADPKD.

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Subjects: Nephrology

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