High Salt Intake Is Independently Associated With Hypertensive Target Organ Damage

The authors tested the hypothesis that high salt intake is associated with hypertensive target organ damage (TOD) independent of blood pressure (BP), and oxidative stress is a modifying factor of this association. A total of 369 community‐dwelling Japanese adults (mean age, 67.5 years; 56.6% women)...

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Bibliographic Details
Published in:The journal of clinical hypertension (Greenwich, Conn.) Conn.), 2016-04, Vol.18 (4), p.315-321
Main Authors: Imaizumi, Yuki, Eguchi, Kazuo, Murakami, Takeshi, Arakawa, Kimika, Tsuchihashi, Takuya, Kario, Kazuomi
Format: Article
Language:English
Subjects:
Aged
Biomarkers - urine
Blood Pressure - drug effects
Blood Pressure Determination
Cross-Sectional Studies
Female
Follow-Up Studies
Humans
Hypertension - epidemiology
Hypertension - physiopathology
Hypertension - urine
Japan - epidemiology
Male
Morbidity - trends
Original Paper
Original Papers
Prognosis
Retrospective Studies
Risk Factors
Sodium Chloride - urine
Sodium Chloride, Dietary - adverse effects
Sodium Chloride, Dietary - pharmacokinetics
Survival Rate - trends
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Summary:The authors tested the hypothesis that high salt intake is associated with hypertensive target organ damage (TOD) independent of blood pressure (BP), and oxidative stress is a modifying factor of this association. A total of 369 community‐dwelling Japanese adults (mean age, 67.5 years; 56.6% women) were examined in this observational study. At the patients' annual health check‐ups, urinary salt excretion (U‐SALT), 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG), and albumin‐creatinine ratio (UACR) were measured from first morning urine. U‐SALT (β=0.14, P=.016) and 8‐OHdG (β=0.13, P=.018) were both independently associated with logUACR. U‐SALT was associated with TOD independent of BP level, and oxidative stress may be a modifying factor in the association between high salt intake and TOD. The elevation of 8‐OHdG may be involved in the pathophysiology of TOD induced by salt intake.
ISSN:1524-6175
1751-7176
1751-7176
DOI:10.1111/jch.12668