Microalbuminuria is closely related to impaired arterial elasticity in untreated patients with essential hypertension

Abstract

Background/aim: Although an increase in urinary albumin excretion (UAE) and impaired arterial mechanics have both been identified as predictors of cardiovascular events in hypertensive subjects, the interaction between arterial pressure wave contour and microalbuminuria (MA) has not been well defined.

Methods: MA was determined from three nonconsecutive 24-hour urine samples in a group of 130 untreated hypertensive subjects. The arterial pressure waveform was recorded by carotid artery applanation tonometry and expressed as the augmentation index (AIx), the ratio of the augmented pressure (the difference between the early and late systolic shoulder) to pulse pressure. The subjects were classified according to their arterial pressure waveform into type A (Aix >0.12), type B (0 < Aix <or= 0.12), and type C (Aix <or= 0).

Results: Patients with MA (n = 48) were matched for demographics with those without MA (n = 82). Subjects with MA had significantly increased left ventricular mass index (101 vs. 85 g/m(2), p < 0.0001), blood pressure (164/100 vs. 146/94 mm Hg, p < 0.005), and AIx (0.16 vs. 0.04, p < 0.03). Hypertensive patients with type A arterial pressure waveform had significantly increased values of the log 24-hour UAE as compared with those with type B and C pressure waveforms. The proportion of patients with type A waveform was significantly higher in microalbuminuric patients as compared with normoalbuminuric patients (67 vs. 33%, p < 0.005); in contrast, the proportion of patients with type B or C waveform was significantly higher in normoalbuminuric patients as compared with microalbuminuric patients (68 vs. 36%, p < 0.005). By multiple regression analysis and analysis of variance, it was revealed that an increased AIx was significantly and independently associated with increased values of UAE (p < 0.05).

Conclusions: Hypertensive patients with MA exhibited an earlier systolic augmentation of the arterial pressure, reflecting a more impaired arterial elasticity as compared with hypertensive subjects without MA. These findings suggest that worse cardiovascular outcomes may be associated with the presence of an increased UAE in hypertensive subjects.