Association between Sodium Intake and Change in Uric Acid, Urine Albumin Excretion, and the Risk of Developing Hypertension
Background—In non-hypertensive individuals, a high sodium diet has little acute effect on blood pressure but, for unclear reasons, is associated with hypertension if consumed chronically. We hypothesized that a chronically high sodium intake would be associated with increases in biomarkers of endothelial dysfunction, specifically serum uric acid (SUA) and urine albumin excretion (UAE), and that high sodium intake would be associated with incident hypertension among those with higher SUA and UAE.
Methods and Results—We prospectively analyzed the associations between sodium intake and the change in SUA (N=4062) and UAE (N=4146) among participants of the PREVEND study who were not taking antihypertensive medications. We also examined the association of sodium intake with the incidence of hypertension (N=5556) among non-hypertensive participants. After adjusting for confounders, each 1 gram higher sodium intake was associated with a 1.2μmol/L increase in SUA ( p=0.01) and a 4.6mg/d increase in UAE (p<0.001). The relation between sodium intake and incident hypertension varied according to SUA and UAE. For each 1 gram higher sodium intake, the adjusted hazard ratio for developing hypertension was 0.98 (0.89-1.08) among those in the lowest tertile of SUA, and 1.09 (1.02-1.16) among those in the highest. Corresponding hazard ratios were 0.99 (0.93-1.06) among participants whose UAE was <10mg/d, and 1.18 (1.07-1.29) among those whose UAE was >15mg/d.
Conclusions—Over time, higher sodium intake is associated with increases in SUA and UAE. Among individuals with higher SUA and urine UAE, a higher sodium intake is an independent risk factor for developing hypertension.
- Received January 26, 2012.
- Accepted April 30, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited