Abstract P383: High Sodium Intake is Independently Associated with Subclinical Hypercortisolism in Hypertensive Patients
2018; Lippincott Williams & Wilkins; Volume: 72; Issue: Suppl_1 Linguagem: Inglês
10.1161/hyp.72.suppl_1.p383
ISSN1524-4563
AutoresGiacomo Rossitto, Giuseppe Maiolino, Silvia Lerco, Valeria Bisogni, Maurizio Cesari, Giulio Ceolotto, Rhian M. Touyz, Alessio Pinato, Mario Plebani, Gian Paolo Rossi, Christian Delles,
Tópico(s)Hormonal Regulation and Hypertension
ResumoThe widely accepted notion of an increase in water intake to compensate for a similar increase in salt consumption has recently been challenged by evidence of long-term renal and metabolic mechanisms favouring endogenous water accrual and body fluid preservation. A glucocorticoid-driven catabolic state is instrumental to this aim and is prevented by increased food intake in rodents. Demonstration of these mechanisms in large human populations is lacking and their relevance for cardiovascular disease is therefore unknown. We explored the association between sodium intake (estimated by 24h urine sodium excretion; USE) and 24h urinary free cortisol (UFC) in 145 patients screened for secondary causes of hypertension in a tertiary referral centre, after washout from drugs affecting the renin-angiotensin-aldosterone system (63 males, 43.3%; age, 48 [38-56] years; BMI, 27.1 [24.3-31.0] kg/m 2 ). USE was directly associated with UFC (Spearman’s rho=0.407, p<0.001), as well as male gender (r=0.381, p<0.001), BMI (r=0.243, p=0.006), creatinine clearance (r=0.637, p<0.001) and, borderline, to plasma glucose (r=0.268, p=0.065). Importantly, UFC increased across classes of sodium intake (Low < 2.3g/d, Medium 2.3-5g/d and High > 5g/d) in lean and overweight groups (n=41, ANOVA p = 0.005 and n= 49, ANOVA p < 0.001, respectively), but not in obese subjects (n=35; p = 0.083). Linear regression analysis showed that (square root-transformed) USE was the strongest explanatory variable for UFC after correction for age, gender, BMI, eGFR and aldosterone:renin ratio (β = 0.04, p < 0.0005). A regression model that also included (Log-transformed) BMI as a surrogate of excess food intake (β = -0.51, p = 0.042), explained 23% of UFC variability in the cohort. We conclude that sodium intake, as estimated by USE, is an independent predictor of subclinical hypercortisolism in lean and overweight but possibly not in obese subjects. These data, in a population at increased cardiovascular risk, suggest a link between sodium intake and subclinical metabolic derangement, which could further add to the overall risk profile.
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