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November 24, 1997

Salt: A Perpetrator of Hypertensive Target Organ Disease?

Author Affiliations

From the Department of Internal Medicine, Section on Hypertensive Diseases, Ochsner Clinic and Alton Ochsner Medical Foundation, New Orleans, La (Dr Messerli), the Department of Medicine, University of Erlangen-Nuremberg, Nuremberg, Germany (Dr Schmieder), and the Division of Nephrology, Department of Medicine, University of Maryland, Baltimore (Dr Weir).

Arch Intern Med. 1997;157(21):2449-2452. doi:10.1001/archinte.1997.00440420077006

Experimental and clinical data suggest salt intake to be an important factor in the pathogenesis of essential hypertension. However, the relationship between dietary sodium and blood pressure has been found to be relatively weak, perhaps because casual blood pressure levels fluctuate considerably. We hypothesized that a closer correlation could be expected between salt intake and the degree of hypertensive target organ disease. We reviewed the literature for studies dealing with 24-hour urinary sodium excretion (as a measure of salt intake) and hypertensive target organ disease as assessed by left ventricular structure and function, microproteinuria, cerebrovascular disease, and arterial compliance. Salt intake as assessed by 24-hour urinary sodium excretion was found to be a close independent determinant of left ventricular mass in 9 different studies worldwide. A reduction in dietary sodium has been shown to reduce left ventricular hypertrophy. There is clinical and experimental evidence, particularly in salt-sensitive patients, that salt intake directly affects hypertensive renal disease, cerebrovascular disease, and compliance of the large arteries. The close and partially independent correlation between salt intake and hypertensive target organ disease suggests dietary sodium to be a direct perpetrator of cardiovascular disease.

Arch Intern Med. 1997;157:2449-2452