Zout en hoge bloeddruk*
Uit een Nederlands-Amerikaanse studie blijkt dat hoge (keuken)zout inname leidt tot beschadigingen van de bloedvaten waardoor de kans op
hoge bloeddruk toeneemt. In de studie werd gekeken naar de zoutinname van ruim vijfduizend Nederlanders. Hoge zoutinname resulteerde in hoge urinewaarden urinezuur en albumine. Beide zijn markers voor schade aan de bloedvaten. Verder bleek dat meer schade ook betekende meer kans op hoge bloeddruk.
Asociation Between Sodium Intake and Change in Uric Acid, Urine Albumin Excretion, and the Risk of Developing Hypertension
1. John P. Forman, MD, MSc; 2. Lieneke Scheven, MD; 3. Paul E. de Jong, MD, PhD;
4. Stephan J.L. Bakker, MD, PhD; 5. Gary C. Curhan, MD, ScD*; 6. Ron T. Gansevoort, MD, PhD*
+ Author Affiliations
1. From the Renal Division and Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (J.P.F., G.C.C.), and Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands (L.S., P.E.d.J., S.J.L.B., R.T.G.).
1. Correspondence to John P. Forman, MD, Msc, Kidney Clinical Research Institute, 41 Ave Louis Pasteur, Boston, MA 02115. E-mail jforman@partners.org
1. ↵* Drs Curhan and Gansevoort contributed equally to this article.
Abstract
Background—A high-sodium diet has little short-term effect on blood pressure in nonhypertensive individuals but, for unclear reasons, is associated with hypertension if consumed long term. 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 Prevention of Renal and Vascular End Stage Disease (PREVEND) study who were not taking antihypertensive medications. We also examined the association of sodium intake with the incidence of hypertension (n=5556) among nonhypertensive participants. After adjustment for confounders, each 1-g-higher sodium intake was associated with a 1.2-μmol/L increase in SUA (P=0.01) and a 4.6-mg/d increase in UAE (P<0.001). The relation between sodium intake and incident hypertension varied according to SUA and UAE. For each 1-g-higher sodium intake, the adjusted hazard ratio for developing hypertension was 0.98 (95% confidence interval, 0.89–1.08) among those in the lowest tertile of SUA and 1.09 (1.02–1.16) among those in the highest tertile. Corresponding hazard ratios were 0.99 (confidence interval, 0.93–1.06) among participants whose UAE was <10 mg/d and 1.18 (confidence interval, 1.07–1.29) among those whose UAE was >15 mg/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.
De volledige studie.
(Juli 2012)
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