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 andexperimental 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 organdamage. Little is known about the relationships between aldosteronaemia and left ventricularmass 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) ALDplasma levels, both by radioimmunological assay. Moreover, we also performed 24-hour ambulatoryblood pressure monitoring (ABPM) and echocardiogram. Left ventricular mass (LVM),calculated according to the formula of the American Society of Echocardiography, was indexedfor height2.7 (LVMH2.7). Glomerular filtration rate (eGFR) was estimated by the 4-variablesequation of the MDRD study.Results: The patients with CKD and LV hypertrophy (LVH), [LVMH2.7 >51 g/m2.7) showedhigher levels of ALD (p = 0.001), when compared to those without LVH; this difference held evenafter 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 confoundingfactors, such as age, gender, 24-hour SBP, BMI, albuminuria, PRA and eGFR in multiple regressionanalysis (beta = 0.22; p = 0.001).Conclusions: Our results seem to suggest that the increase of LVM, previously documented inpatients with renal dysfunction, even of mild-to-moderate degree, may be mediated, at least inpart, by increased levels of aldosterone.
|Number of pages||1|
|Publication status||Published - 2011|