The present study confirms the high prevalence of LVH in patients with mild or moderate renal dysfunction. In the patients studied (all with a GFR of 30 mL/min per 1.73 m(2)), the association between LVM and GFR was independent of potential confounders, including 24 h blood pressure load. Taking into account the negative prognostic impact of LVH, further studies focusing on a deeper comprehension of the mechanisms underlying the development of LVH in chronic kidney disease patients are needed.

Our results seem to corroborate the concept that the RI may be considered as a marker of systemic vascular changes and therefore a predictor of cardiovascular risk.

Our results suggest that in patients with essential hypertension, MAU and CRP are independently associated with an increased aortic stiffness.

The authors aimed to analyze the relationship between subclinical renal damage, defined as the presence of microalbuminuria or an estimated glomerular filtration rate (eGFR) between 30 mL/min/1.73 m 2 and 60 mL/min/ 1.73 m 2 and short-term blood pressure (BP) variability, assessed as average real variability (ARV), weighted standard deviation (SD) of 24-hour BP, and SD of daytime and nighttime BP. A total of 328 hypertensive patients underwent 24-hour ambulatory BP monitoring, 24-hour albumin excretion rate determination, and eGFR calculation using the Chronic Kidney Disease Epidemiology Collaboration equation. ARV of 24-hour systolic BP (SBP) was significantly higher in patients with subclinical renal damage (P=.001). This association held (P=.04) after adjustment for potential confounders. In patients with microalbuminuria, ARV of 24-hour SBP, weighted SD of 24-hour SBP, and SD of daytime SBP were also independently and inversely related to eGFR. These results seem to suggest that in essential hypertension, short-term BP variability is independently associated with early renal abnormalities. J Clin Hypertens (Greenwich). 2015;17:473-480. ª 2015 Wiley Periodicals, Inc.Since the pioneering observations of Stephen Hales during the 18th century it has been recognized that blood pressure (BP) is not a constant parameter; rather, it shows marked spontaneous oscillations over shortterm (minutes to hours) and long-term (days to months) periods. Far from being a "background noise" that hindered assessment of "true BP," short-term BP variability (BPV) seems to be relevant to the pathophysiology of target organ damage and to the incidence of clinical events, as suggested by studies performed in humans by invasive continuous 24-hour BP measurements 1,2 and as clearly shown by investigations conducted in sinoaortic-denervated rats.3-6 Although the precise quantification of short-term BPV requires beatto-beat BP recording, 7 its assessment is also possible, even if less accurately, through the use of intermittent noninvasive 24-hour ambulatory BP monitoring (ABPM). However, studies in which short-term BPV was estimated by ABPM yielded conflicting results. 8-32Short-term BP variability has been usually estimated by 24-hour, daytime, or nighttime standard deviation (SD) of average BP. However, the limitations of the SD as a measure of short-term BPV have stimulated the search of more refined BPV estimates. 6,7,10,13,20,21 One of these is the average real variability (ARV) of 24-hour BP, ie, the average of the absolute differences of consecutive measurements. 20 This statistical parameter is sensitive to the individual BP measurement order and less sensitive to low sampling frequency of ABPM. 21Some studies suggest that ARV better predicts cardiovascular (CV) risk in comparison to the traditional SD. 20,22,23 Another new index of short-term BPV is the "weighted" SD of the 24-hour mean value, ie, the average SD of daytime and nighttime BP, each weighted for the duration of the day and night periods, respectively. This in order ...

Several studies documented an association between metabolic syndrome (MetS) and left ventricular (LV) hypertrophy. However, only in a few of these studies the impact of MetS on left ventricular mass (LVM) was separately analysed by gender, with conflicting results. The aim of our study was to verify, in a wide sample of essential hypertensive patients, the influence of gender, if any, on the relationship between MetS and LVM. We enrolled 475 non-diabetic subjects (mean age: 46 ± 11 years), with mild-to-moderate essential hypertension, of whom 40% had MetS, defined on the basis of Adult Treatment Panel III (ATPIII) criteria. All the patients underwent a 24-h ambulatory blood pressure monitoring and an echocardiogram. LVM indexed for height 2.7 (LVMH 2.7 ) was significantly (Po0.001) higher in women with MetS (n ¼ 83) than in those without it (n ¼ 97; 54 ± 17 vs 42±11 g m À2.7). An equally significant difference in LVMH 2.7 was documented also in male gender between the two groups with (n ¼ 105) and without MetS (n ¼ 190; 51 ± 14 vs 43±11 g m À2.7 ; Po0.001). The relationship between MetS and LVMH 2.7 remained statistically significant (Po0.001) in both sexes, in multiple regression analyses, even after adjustment for potential confounding factors. Our results seem to suggest that the relationship between MetS and LVM is not significantly affected by gender, being LVM increased in both hypertensive women and men with MetS.