Arterial stiffness: an independent determinant of adaptive glomerular hyperfiltration after kidney donation

After kidney donation, the remaining kidney tends to hyperfiltrate, thus limiting the initial loss of renal function. The potential determinants of this adaptive glomerular hyperfiltration (GHF) and specifically the influence of arterial function are poorly known. In 45 normotensive healthy kidney donors [51 ± 10 yr (mean ± SD), 39 females], glomerular filtration rate (GFR) was measured as the clearance of continuously infused 99mTc-DTPA and timed urine collections at baseline, i.e., before donation, and 1 yr after donation. GHF was computed as postdonation GFR minus half of baseline GFR. Arterial function was assessed as baseline carotid-femoral pulse wave velocity (PWV) and carotid augmentation index (AIx). After kidney donation, no significant change in blood pressure (BP) was observed, but two subjects developed hypertension. GFR decreased from 107 ± 19 to 73 ± 15 ml·min−1·1.73 m−2, and mean GHF was 20 ± 10 ml·min−1·1.73 m−2. In univariate analysis, GHF was inversely correlated to age ( r2 = 0.24, P = 0.01), baseline PWV ( r2 = 0.23, P = 0.001), and Aix ( r2 = 0.11, P = 0.031). Nevertheless, GHF was not correlated to baseline peripheral or central BP. In multivariate analysis, baseline PWV, but not AIx, remained inversely correlated to GHF, independently of age, baseline mean BP, and GFR (model r2 = 0.34, P < 0.001). In healthy subjects selected for renal donation, increased arterial stiffness is associated with decreased postdonation compensatory hyperfiltration.

Geometry is a major determinant of flow reversal in proximal aorta

The aim of this study is to quantify aortic backward flow (BF) using phase-contrast cardiovascular magnetic resonance (PC-CMR) and to study its associations with age, indexes of arterial stiffness, and geometry. Although PC-CMR blood flow studies showed a simultaneous presence of BF and forward flow (FF) in the ascending aorta (AA), the relationship between aortic flows and aging as well as arterial stiffness and geometry in healthy volunteers has never been reported. We studied 96 healthy subjects [47 women, 39 ± 15 yr old (19–79 yr)]. Aortic stiffness [arch pulse wave velocity (PWVAO), AA distensibility], geometry (AA diameter and arch length), and parameters related to AA BF and FF (volumes, peaks, and onset times) were estimated from CMR. Applanation tonometry carotid-femoral pulse-wave velocity (PWVCF), carotid augmentation index, and time to return of the reflected pressure wave were assessed. Whereas FF parameters remained unchanged, BF onset time shortened significantly ( R2 = 0.18, P < 0.0001) and BF volume and BF-to-FF peaks ratio increased significantly ( R2 = 0.38 and R2 = 0.44, respectively, P < 0.0001) with aging. These two latter BF indexes were also related to stiffness indexes (PWVCF, R2 > 0.30; PWVAO, R2 > 0.24; and distensibility, R2 > 0.20, P < 0.001), augmentation index ( R2 > 0.20, P < 0.001), and aortic geometry (AA diameter, R2 > 0.58; and arch length, R2 > 0.31, P < 0.001). In multivariate analysis, aortic diameter was the strongest independent correlate of BF beyond age effect. In conclusion, AA BF estimated using PC-CMR increased significantly in terms of magnitude and volume and appeared earlier with aging and was mostly determined by aortic geometry. Thus BF indexes could be relevant markers of subclinical arterial wall alterations.

Lack of age-associated elevations in 24-h systolic and pulse pressures in women who exercise regularly

We tested the hypothesis that the elevations in 24-h arterial systolic (SBP) and pulse (PP) pressures with age in sedentary adult females are absent or smaller in women who exercise regularly. Four groups of healthy normotensive women were studied: premenopausal ( n = 12; 29 ± 1 yr, mean ± SE) and postmenopausal ( n = 20; 62 ± 1) sedentary, and premenopausal ( n = 14; 30 ± 1) and postmenopausal ( n= 12; 58 ± 1) endurance-exercise trained (distance runners). In the sedentary group, 24-h SBP and PP (Spacelabs ambulatory monitor 90207) were ∼10 mmHg higher ( P < 0.05) in the postmenopausal women than in the premenopausal controls; this was because of higher daytime and nighttime SBP and PP levels in the postmenopausal women. In contrast, 24-h, daytime and nighttime SBP and PP were not different with age in the endurance-trained women. SBP variability and SBP load (% of all recordings > 140 mmHg) generally were greater with age in the sedentary women (e.g., SBP load = 14 ± 4 vs. 3 ± 1%, P < 0.05) but not in the endurance-trained women. In the pooled population, 24-h SBP and PP were related to waist-to-hip ratio (measure of abdominal adiposity) ( r = 0.48 and 0.49, respectively, P < 0.001) and carotid augmentation index (measure of arterial stiffness) ( r = 0.43 and 0.53, P < 0.005). In the sedentary women, accounting for the influence of either of these factors eliminated the significant age-associated differences in 24-h SBP and PP ( P > 0.3). Our results suggest that the elevations in 24-h SBP and PP with age in sedentary adult females may not occur in women who regularly perform endurance exercise. This appears to be related to the absence of age-associated increases in abdominal adiposity and arterial stiffness in the exercising women.