Obesity in young hypertensive patients was associated with a lower renin-aldosterone ratio compared to non-obese patients (19 vs 27), with no difference in 24-hour urinary sodium excretion.
Observational (n=49)
No
Do demographic, clinical, and biochemical factors differ between obese and non-obese young hypertensive patients?
In young hypertensive patients, obesity is associated with a lower renin-aldosterone ratio but does not appear to correlate with increased sympathetic nervous system activation markers like heart rate or pulse pressure.
Absolute Event Rate: 19% vs 27%
Objective: Obesity is a well-known risk factor for hypertension; however, the underlying pathological mechanisms are complex. Sympathetic nervous stimulation and activation of renin angiotensin aldosterone syndrome are some of the mechanisms implicated in development of hypertension in obese individuals. In this report, we compare demographic, clinical and biochemistry findings in obese (body mass index (BMI)> 30 kg/m2) and non-obese individuals in a cohort of patients with young onset hypertension (< 40 years of age). Design and method: We conducted analysis of 49 patients referred to a specialist hypertension clinic as part of prospective service evaluation collecting data on all young hypertensives referred to our tertiary centre between 2023-2025. The mean age of onset of hypertension was 29 years (range 10 to 40 years). Twenty-four subjects were non-obese (BMI <30) and twenty five were obese (BMI equal to and over 30). Age, BP, HR, creatinine and electrolytes, 24-hour urine electrolytes, renin and aldosterone was compared in the two cohorts. Results: There was no difference between the average BP between the two groups at the point of their referral to our service: 147/96 mmHg vs 146/94mmHg, however, 64% (n=16) of referred patients with BMI equal to or over 30, was already on antihypertensive treatment, compared to 41% patients in a none-obese group (n=10). Obese patients were found to have lower renin-aldosterone ratio (RAA) than non-obese: 19 vs 27, respectively, but equal 24-hr urinary sodium excretion, pulse pressure, HR and creatinine. Conclusions: The effect of obesity on the RAA system varies and is likely not generalizable. We found that lower RAA values in obese population did not correlate with increased 24-hr urinary sodium excretion, which could be used as an indirect indicator of daily salt consumption. Obesity is also postulated to activate SNS but we found no difference in HR and pulse pressure in these two groups. More patients will be included in our analysis as we experience increasing referral rate for young-onset hypertensives.
Gray et al. (Fri,) conducted a observational in young onset hypertension (n=49). Obesity (BMI ≥ 30 kg/m2) vs. Non-obese (BMI < 30 kg/m2) was evaluated on renin-aldosterone ratio (RAA). Obesity in young hypertensive patients was associated with a lower renin-aldosterone ratio compared to non-obese patients (19 vs 27), with no difference in 24-hour urinary sodium excretion.