Relationship Between Short-Term Blood Pressure Variability and Subclinical Renal Damage in Essential Hypertensive Patients.

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.

Unfavourable interaction of microalbuminuria and mildly reduced creatinine clearance on aortic stiffness in essential hypertension.

The aim of our study was to assess the independent relationships of urinary albumin excretion rate (AER), of creatinine clearance (CrCl) and of their interaction with aortic stiffness in hypertensive patients without overt renal insufficiency. We studied 222 untreated nondiabetic essential hypertensives. In patients with reliable 24-h urine collections, AER and CrCl were determined. Microalbuminuria (MAU) was defined as an AER of 20 to 200 µg/min. Aortic stiffness was assessed by measurement of carotid-femoral pulse wave velocity (c-f PWV). C-f PWV was higher in subjects with MAU than in those without it (p<0.001, even after adjustment for age, sex and mean arterial pressure) and in subjects with CrCl below 90 ml/min/1.73 m(2) when compared to those with greater values of CrCl (p=0.04 after correction for age, sex and mean arterial pressure). There was a significant interaction of MAU and reduced CrCl regarding c-f PWV (p=0.04). In multiple regression analysis, AER and CrCl remained independently associated with aortic stiffness (ß=0.22; p<0.001 and ß=-0.13; p=0.02, respectively). In essential hypertensive patients microalbuminuria and mildly reduced CrCl are related independently of each other with increased c-f PWV and exert a synergistic unfavourable effect on aortic stiffness.

Inverse relationship between ambulatory arterial stiffness index and glomerular filtration rate in arterial hypertension.

BACKGROUND: Arterial stiffness and mild-to-moderate renal dysfunction are predictors of cardiovascular (CV) morbidity and mortality. Recently, the ambulatory arterial stiffness index (AASI) has been proposed as a surrogate index of arterial stiffness. It has been associated with an enhanced risk of stroke. The aim of our study was to assess the relationship between AASI and glomerular filtration rate (GFR) in a group of hypertensive patients with no CV complications. METHODS: A total of 143 untreated hypertensive subjects (mean age: 44 +/- 12 years; men 57%), with serum creatinine <1.5 mg/dl, were enrolled. AASI was calculated as one minus the regression slope of diastolic on systolic blood pressure (BP) obtained by individual 24-h BP recordings. GFR was computed from the scintigraphic determination of the technetium-99m diethylenetriaminepentaacetic acid uptake within the kidneys, by the Gates' method. RESULTS: Hypertensive patients with AASI above the median value (n = 71) had lower GFR than those with AASI below the median (n = 72) (98.3 +/- 31 vs. 122.4 +/- 32 ml/min/1.73 m(2); P < 0.001). This difference held even after adjustment for age and gender. The linear regression analysis disclosed a significant inverse correlation between GFR and AASI (r = -0.30; P < 0.001), that was replicated (beta = -0.19; P = 0.02) in a multiple regression model including, as independent variables (besides AASI), age, gender, high-density lipoprotein cholesterol, body mass index, 24-h pulse pressure (PP) and nocturnal reduction in BP. CONCLUSIONS: AASI is inversely related to GFR in arterial hypertension. This may help to explain the increased CV risk associated with mild-to-moderate renal dysfunction.