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