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Hypertension. 1995;25:1339-1344

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(Hypertension. 1995;25:1339-1344.)
© 1995 American Heart Association, Inc.


Articles

Salt-Induced Increases in Systolic Blood Pressure Affect Renal Hemodynamics and Proteinuria

Matthew R. Weir; Donald R. Dengel; M. Theresa Behrens; Andrew P. Goldberg

From the Division of Nephrology and Clinical Research Unit, Division of Gerontology, Geriatrics Service and Geriatric Research, Education and Clinical Center, Department of Medicine, University of Maryland School of Medicine and Baltimore VA Medical Center, Baltimore, Md.

Abstract Nine white and 13 black hypertensive patients with normal serum creatinine were randomized to receive either 2 weeks of a low-salt (40 mEq Na+/d) or high-salt (200 mEq Na+/d) diet followed by 2 weeks of the other diet separated by a 1-week washout on their regular diet. The entire study was conducted in an outpatient setting with intensive dietary instruction and monitoring of blood pressure and 24-hour collections of urine for analysis. Urine electrolyte measurement showed that the patients were able to achieve only a modestly reduced (100±14 mEq Na+/24 h [mean±SEM]) low-salt diet as outpatients, while the higher-salt diet (236±22 mEq Na+/24 h) was more easily achieved. Eleven patients (8 black, 3 white) were classified as modestly salt sensitive on the basis of an increase or decrease in mean arterial pressure of >=3 mm Hg going from lower- to high- or high- to lower-salt diets, respectively. In the salt-sensitive patients, the increase in dietary salt intake increased glomerular filtration rate by 29% (71.2±6.6 to 85.8±7.3 mL · min-1 · 1.73 m2, P=.05), with no significant change in renal plasma flow (412.7±36.4 to 399.6±27.8 mL · min-1 · 1.73 m2). There were no changes in these parameters in the salt-resistant patients. Increased dietary salt intake in the salt-sensitive patients was associated with a 15% increase in glomerular filtration fraction (0.18±0.02 to 0.22±0.01, P=.09), whereas in the salt-resistant group, glomerular filtration fraction did not change (0.16±0.01 to 0.17±0.02, P=.47). Greater dietary salt intake also resulted in an increase in 24-hour urine protein excretion in the salt-sensitive population (74.0±8.3 to 139.0±31.3 mg/24 h), while there was no significant change in the salt-resistant population (115.5±16.6 to 86.4±14.3 mg/24 h, P=.03 versus salt sensitive). The salt-induced increase in proteinuria was related to the increase in systolic blood pressure on the high-salt diet (r=.54, P=.04). These studies demonstrate that in the presence of modest salt sensitivity (mean arterial pressure increase >=3 mm Hg), an increase in systolic blood pressure is predictive of potentially adverse renal hemodynamic responses to higher dietary salt in essential hypertensive patients. Consequently, modest salt restriction may reduce the risk for acute changes in renal hemodynamics in salt-sensitive patients, which may be important for long-term protection and prevention of deterioration of renal function.


Key Words: blood pressure • hypertension, salt-dependent • salt • kidney • proteinuria




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