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Several nonpharmacologic strategies are available to improve blood pressure control among essential hypertensive patients. By extension, similar strategies may be effective among patients with chronic kidney disease. These strategies include salt restriction, weight loss, exercise, moderation of alcohol intake, and treatment of obstructive sleep apnea (OSA).
Although some experts recommend caution in advocating for dietary sodium restriction, as some studies show an inverse relation between dietary sodium and mortality, we feel that it is an effective modality for hypertension management. Sodium restriction has been shown to reduce blood pressure, both in randomized trials and in meta-analyses. The Dietary Approaches to Stop Hypertension (DASH) trial revealed a –6.7/–3.5 mm Hg blood pressure reduction when dietary sodium was reduced from 3 to 1.5 g. A large meta-analysis found that a reduction of approximately 2.3 g in dietary sodium reduced systolic blood pressure by 3.7 mm Hg among hypertensive patients, an effect that was more pronounced among older patients. Sodium sensitive hypertensive patients who restrict dietary sodium convert from nondipping to dipping status (dipping refers to ≥10% decrease in blood pressure while asleep; nondipping, hypertensive patients are at increased cardiovascular risk compared to dipping patients). Dietary sodium restriction reduces left ventricular hypertrophy, improves the anti-proteinuric effects of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers for both diabetic and nondiabetic chronic kidney disease patients, and may reduce kidney disease progression. Long-term follow-up of patients enrolled in the Trials of Hypertension Prevention revealed that a reduction of dietary sodium of approximately 750 to 1000 mg daily reduced cardiovascular events (myocardial infarction, coronary bypass surgery, coronary angioplasty, stroke, or cardiovascular death) by 25%.
A 24-hour urine collection that quantifies sodium excretion provides a reasonable estimate of dietary sodium intake, and a recently published analysis of patients enrolled in the Chronic Renal Insufficiency Cohort (CRIC) study revealed interesting results regarding dietary sodium intake and cardiovascular events. The CRIC study is a prospective cohort study of chronic kidney disease patients that evaluates the risk factors for kidney disease progression and cardiovascular disease. Among a group of nearly 3800 racially diverse patients, those patients whose dietary sodium (estimated from a mean of three 24-hour urine collections over the first 2 years of the study) resided in the highest quartile (≥4548 mg) experienced a 36% relative risk increase in nonfatal cardiovascular events (a composite of stroke, myocardial infarction, or congestive heart failure), a 34% relative risk increase in congestive heart failure, and an 81% relative risk increase for nonfatal stroke, compared to those patients whose dietary sodium was in the lowest quartile (<2894 mg). Every 1000 mg increase in daily dietary sodium increased the risk for the composite end-point 10%, the risk for congestive heart failure 9%, and the risk for nonfatal stroke 16%.
The National Academy of Sciences and the American Heart Association recommend that dietary sodium be limited to 1.5 g daily—a goal that would need both government and industry cooperation. The U.S. Department of Health and Human Services also recommends dietary sodium restriction: no more than 1.5 g daily for adult African Americans, patients ≥51 years, or patients with diabetes mellitus, hypertension, or chronic kidney disease. The Kidney Disease Improving Global Outcomes guidelines also recommend low dietary sodium for chronic kidney disease patients, though only to a level of <2 g. While sodium restriction may initially be difficult, patients become acclimated to the diet over several weeks. A population-wide reduction of dietary sodium to 1200 mg may save approximately $10 billion to $24 billion annually in health care costs.
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