The Impact of Blood Pressure and Visceral Adiposity on the Association of Serum Uric Acid With Albuminuria in Adults Without Full Metabolic Syndrome
Open Access
- 26 August 2016
- journal article
- research article
- Published by Oxford University Press (OUP) in American Journal of Hypertension
- Vol. 29 (12), 1335-1342
- https://doi.org/10.1093/ajh/hpw098
Abstract
The impact of metabolic phenotypes on the association of uricemia with urinary albumin/creatinine ratio (uACR) remains unresolved. We evaluated the association between serum uric acid and uACR in persons with 0, and 1–2 metabolic syndrome (MetS) components and determined the modification effects of visceral adiposity index (VAI), mean arterial pressure (MAP), and fasting glucose on this association. Using data from a cross-sectional survey of a representative Czech population aged 25–64 years (n = 3612), we analyzed 1,832 persons without decreased glomerular filtration rate 2, diabetes, and MetS. MetS components were defined using the joint statement of the leading societies. Of the 1,832 selected participants, 64.1% (n = 1174) presented with 1–2 MetS components (age 46.3±11.2; men 51.7%), whereas 35.9% (n = 658) were free of any component (age 39.4±10.0; men 34.2 %). In fully adjusted multiple linear regression models for uricemia, uACR was an independent factor for increase in uric acid levels only in persons with 1–2 MetS components (standardized beta (Sβ) 0.048; P = 0.024); however, not in those without any component (Sβ 0.030; P = 0.264). Uric acid levels increased by the interaction of uACR with VAI (Sβ 0.06; P = 0.012), and of uACR with MAP (Sβ 0.05; P = 0.009). Finally, the association of uACR with uricemia was confined to persons whose VAI together with MAP were ≥the median of 1.35 and 98mm Hg, respectively (Sβ 0.190; P < 0.001). We demonstrated a strong modification effect of VAI and MAP on the association between uACR and uricemia, which suggests obesity-related hypertension as the underlying mechanism.Keywords
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