Key result
Obesity in resistant hypertension is linked to a stronger urinary sodium-aldosterone correlation versus normal weight.
Why the study?
Having previously found that aldosterone increases with BMI, this study aimed to determine the extent to which that association is related to dietary high salt intake.
Does high dietary salt intake alter aldosterone regulation in obese patients with resistant hypertension compared to normal weight individuals?
Cross-Sectional (n=1,572)
Does high dietary salt intake alter aldosterone regulation in obese patients with resistant hypertension compared to normal weight individuals?
Obese patients with resistant hypertension exhibit a paradoxical increase in aldosterone levels in response to high dietary salt intake, suggesting altered aldosterone regulation.
Obesity may modify aldosterone-salt dynamics in resistant hypertension; leaves open whether this alters management strategies.
BACKGROUND: Having previously reported that aldosterone levels increase progressively with body mass index (BMI), the current analysis was done to determine to what extent this association is related to dietary high salt intake. We anticipated that aldosterone levels would decrease with higher sodium status consistent with classical suppression of aldosterone release secondary to progressive fluid retention induced by high dietary sodium intake. METHODS: Cross-sectional analysis of a large diverse cohort of 2,705 patients with resistant hypertension (HTN) seen in a referral HTN Clinic. Dietary sodium intake was indexed by 24-hour (h) urinary sodium (UNa), aldosterone status was determined by plasma aldosterone concentration, plasma renin activity, and 24 h urinary aldosterone (UAldo). Patients with normal weight served as control. RESULTS: In this study, 1,572 individuals with complete 24 h urine collections were analyzed. Mean BMI was 32.5 ± 7.1 kg/m2 and ranged from 24.6 ± 2.4 kg/m2 (first quartile) to 41.0 ± 4.2 kg/m2 (fourth quartile). BMI was positively associated with 24 h UNa and UAldo levels (P < 0.0001), 24 h UNa and UAldo. There was a positively stronger correlation in obese (r = 0.273, P < 0.0001) compared with normal weight individuals (r = 0.108, P = 0.0342) independent of number and classes of antihypertensive medications. CONCLUSIONS: Our analysis shows that there is an altered regulation of aldosterone in obese patients in the setting of high dietary salt intake.
No takes yet. Share an insight, caveat, or question.
David A. Calhoun (2020) conducted a cross-sectional in Resistant hypertension (n=1,572). Obesity vs. Normal weight was evaluated on Correlation between 24-hour urinary sodium and 24-hour urinary aldosterone (r = 0.273, p=<0.0001). Obesity in patients with resistant hypertension was associated with a stronger positive correlation between 24-hour urinary sodium and aldosterone levels (r=0.273, P<0.0001) than normal weight.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: