Left ventricular hypertrophy in hypertensive patients with autosomal dominant polycystic kidney disease: influence of blood pressure and humoral and neurohormonal factors.

Left ventricular hypertrophy (LVH) is a common finding in hypertensive autosomal dominant polycystic kidney disease (ADPKD) patients. There are few studies on the influence of blood pressure (BP) and nonhemodynamic factors on LVH in these patients. The aim of this study was to evaluate the relationship between BP, humoral and neurohormonal factors and left ventricular mass (LVM) in hypertensive ADPKD patients. In 20 hypertensive ADPKD patients, ambulatory BP was monitored for 24 h, left ventricular dimensions were estimated by echocardiography, and plasma renin activity (PRA), plasma noradrenaline (NA), angiotensin II (Ang II), aldosterone, atrial natriuretic peptide (ANP) and insulin-like growth factor I (IGF-I) were also determined. Twenty age- and sex-matched essential hypertensive subjects served as controls. Ambulatory BP and LVM index were similar in the two groups, although male ADPKD patients had higher LVM indices than their matched controls. Eight ADPKD patients (40%) and 6 essential hypertensives (30%) showed LVH. PRA, Ang II, aldosterone, ANP and IGF-I levels were similar in the two groups, but plasma NA levels were higher in ADPKD patients than in controls (281 +/- 158 vs. 160 +/- 62 pg/ml, p = 0.004). ADPKD patients with LVH did not differ from those without LVH with regard to humoral and neurohormonal parameters, but had higher ambulatory BP levels. In ADPKD patients, correlation analysis revealed a significant association between LVM index and 24-hour systolic and diastolic BP, but not with any of the hormonal factors evaluated. On multiple regression analysis, 24-hour diastolic BP was the only independent variable linked to LVM index. In conclusion, ambulatory BP is one of the most important determinants of LVM in hypertensive ADPKD patients. Further studies are warranted to elucidate the role of nonhemodynamic factors in the pathogenesis of LVH in this population. Copyright 2000 S. Karger AG, Basel