Relationship between Plasma Aldosterone and Left Ventricular Mass in Hypertensive Subjects with Mild-to-Moderate Chronic Kidney Disease

Abstract

Introduction: Plasma aldosterone (ALD) levels are generally increased in subjects with chronic kidney disease (CKD), especially in those with end-stage renal disease. Convincing clinical and experimental data indicate that aldosterone plays a fundamental role in determining functional and structural changes of the heart. On the other hand, it is known that hypertensive patients with renal dysfunction, also of mild degree, show an increased prevalence of cardiovascular organ damage. Little is known about the relationships between aldosteronaemia and left ventricular mass in subjects with mild-to-moderate CKD. Aim: To analyse the relationships between ALD and left ventricular mass (LVM), in a group of hypertensive patients with stages I-III CKD. Methods: We enrolled 194 hypertensive patients with stages I-III CKD (mean age 46 –12 years,males 70%). All the subjects performed 24-hour urine collection to assay albuminuria, and electrolytes,and underwent, where necessary after a wash-out pharmacological period of 2 weeks, blood collection to assay biochemical routine parameters, plasma renin-activity (PRA) ALD plasma levels, both by radioimmunological assay. Moreover, we also performed 24-hour ambulatory blood pressure monitoring (ABPM) and echocardiogram. Left ventricular mass (LVM), calculated according to the formula of the American Society of Echocardiography, was indexed for height2.7 (LVMH2.7). Glomerular filtration rate (eGFR) was estimated by the 4-variables equation of the MDRD study. Results: The patients with CKD and LV hypertrophy (LVH), [LVMH2.7 >51 g/m2.7) showed higher levels of ALD (p = 0.001), when compared to those without LVH; this difference held even after adjustment (p < 0.01) for age, gender, 24-hour systolic blood pressure (SBP), BMI and PRA. A statistically significant correlation was observed between ALD and LVMH2.7 (r = 0.26; p < 0.001). This association remained significant even taking into account various confounding factors, such as age, gender, 24-hour SBP, BMI, albuminuria, PRA and eGFR in multiple regression analysis (beta = 0.22; p = 0.001). Conclusions: Our results seem to suggest that the increase of LVM, previously documented in patients with renal dysfunction, even of mild-to-moderate degree, may be mediated, at least in part, by increased levels of aldosterone.