1. What nonpharmacologic strategies can be used to treat hypertension?

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).

2. How effective is salt restriction?

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.

3. How effective is the dash diet?

Americans, besides consuming excess salt, eat foods high in saturated fats and low in fiber and potassium. Low dietary potassium predisposes to sodium retention, volume expansion, and hypertension. Potassium supplementation can decrease blood pressure in hypertensive patients. The mechanism by which fiber may prevent hypertension is not well delineated, although a meta-analysis showed that diets supplemented by fiber lower blood pressure (–1.13/–1.26 mm Hg). The DASH diet emphasizes fruits and vegetables and low-fat foods. During an 8-week trial, the DASH diet, in patients with and without hypertension, lowered blood pressures by −5.5/–3 mm Hg. If the DASH diet is coupled with low sodium intake (1.5 g daily), blood pressures will decrease by –8.9/–4.5 mm Hg compared to an average American diet. Unfortunately, the National Health and Nutrition Examination Survey (NHANES) data reveal that nearly 91% of Americans consume more than 2300 mg of sodium daily. Only 1.2% patients who would benefit from reducing dietary sodium to ≤1.5 g (i.e., African Americans, patients ≥51 years, or patients with diabetes mellitus, hypertension, or chronic kidney disease) actually restrict dietary sodium appropriately. Over 60% of these patients consume more than 3 g of sodium daily. DASH dietary instructions have been published for easy reference.

While the appropriateness of the DASH diet for chronic kidney disease patients has not been studied extensively, a small pilot study of 11 patients recently showed that the DASH diet is safe for patients with moderate kidney disease (i.e., an estimated glomerular filtration rate of 30 to 59 mL/min per 1.73 m ² ). No significant hyperkalemia occurred during the 2-week study, and nighttime systolic blood pressure decreased by 5.3 mm Hg.

4. How effective is the treatment of OSA?

Patients with OSA experience oxygen desaturation and sympathetic activation. Persistent, untreated OSA leads to hypertension. In the Wisconsin Sleep Cohort Study, 709 patients were followed for 4 years, and those patients with an apnea-hypopnea index of ≥5 had a more than twofold higher risk for hypertension, compared to patients with no apnea-hypopnea events. A meta-analysis of five randomized, controlled trials revealed that continuous positive airway pressure (CPAP) therapy improved the blood pressure control of OSA patients: 24-hour systolic and diastolic ambulatory blood pressures decreased 4.78 and 2.95 mm Hg, respectively, compared to no treatment. While nocturnal ambulatory systolic blood pressure did not change significantly with CPAP, nocturnal ambulatory diastolic blood pressure fell 1.53 mm Hg.

OSA is common in chronic kidney disease—up to 60% of these patients may have OSA—and chronic kidney disease may increase sleep apnea severity. Severe OSA (apnea-hypopnea index ≥ 30), in conjunction with resistant hypertension, increases the odds of chronic kidney disease by more than 13-fold. It is possible that treatment of OSA in chronic kidney disease patients may improve blood pressure control and kidney outcomes.