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BiBliography
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Bhatt DL, Kandzari DE, O’Neill WW, et al. A controlled trial of renal denervation for resistant hypertension. N Engl J Med.
2014;370(15):1393–1401.
Bisognano JD, Bakris G, Nadim MK, et al. Baroreflex activation therapy lowers blood pressure in patients with resistant hypertension:
results from the double-blind, randomized, placebo-controlled Rheos pivotal trial. J Am Coll Cardiol. 2011;58(7):765–773.
Calhoun DA, Jones D, Textor S, et al. Resistant hypertension: diagnosis, evaluation, and treatment a scientific statement from the
American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Hypertension.
2008;51(6):1403–1419.
Krieger EM, Drager LF, Giorgi DMA, et al. Spironolactone versus clonidine as a fourth-drug therapy for resistant hypertension: the ReHOT
randomized study (Resistant Hypertension Optimal Treatment). Hypertension. 2018;71(4):681–690.
Nerenberg KA, Zarnke KB, Leung AA, et al. Hypertension Canada’s 2018 guidelines for diagnosis, risk assessment, prevention, and
treatment of hypertension in adults and children. Can J Cardiol. 2018;34(5):506–525.
Noubiap JJ, Nansseu JR, Nyaga UF, Sime PS, Francis I, Bigna JJ. Global prevalence of resistant hypertension: a meta-analysis of data
from 3.2 million patients. Heart. 2019;105:98–105.
Pappaccogli M, Covella M, Berra E, et al. Effective of renal denervation in resistant hypertension: A meta-analysis of 11 controlled
studies. High Blood Press Cardiovasc Prev. 2018;25(2):167–176.
Sinnott SJ, Tomlinson LA, Root AA, et al. Comparative effectiveness of fourth-line anti-hypertensive agents in resistant hypertension: A
systematic review and meta-analysis. Eur J Prev Cardiol. 2017;24(3):228–238.
Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention,
detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American
Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2018;138(17):e484–e594.
Williams B, MacDonald TM, Morant SV, et al. Endocrine and haemodynamic changes in resistant hypertension and blood pressure
responses to spironolactone or amiloride: the PATHWAY-2 mechanisms substudies. Lancet Diabetes Endocrinol. 2018;6(6):464–475.
Williams B, MacDonald TM, Webb DJ, et al. Spironolactone versus placebo, bisoprolol, and doxazosin to determine the optimal treatment
for drug-resistant hypertension (PATHWAY-2): a randomised, double-blind, crossover trial. Lancet. 2015;386(10008):2059–2068.
Williams B, Mancia G, Spiering W, et al. 2018 ESC/ESH guidelines for the management of arterial hypertension: the task force for the
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J Hypertens. 2018;36(10):1953–2041.
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Ryan P. Flood, DO, and John R. Montford, MD
QUESTIONS
1. Why is hyperkalemia important to understand in the management of individuals with
hypertension?
Hyperkalemia is one of the most common electrolyte disorders encountered and affects a disproportionate
number of individuals with chronic hypertension. The incidence of hyperkalemia ranges from 1.9% to 38% among
participants of prospectively conducted trials examining the effects of renin-angiotensin-aldosterone system
(RAAS) inhibitors on blood pressure reduction.1 In many studies, higher rates of hyperkalemia accompany patients
with lower estimated glomerular filtration rate (eGFR), older age, and presence of comorbid diabetes mellitus and
cardiovascular disease (CVD). Rates of hyperkalemia are particularly high among participants of trials combining angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEis/ARBs) with mineralocorticoid
receptor antagonists (MRAs) for the treatment of heart failure.
The development of hyperkalemia is associated with higher rates of hospitalization and mortality in virtually
every patient population studied. Hyperkalemia is known to confer direct cardiotoxicity (see following sections),
as well as being a major cause of RAAS inhibitor de-escalation; which, in turn, is linked to increased rates of
health care utilization, poor control of blood pressure, and worse survival. In general, most professional societies
recommend heightened awareness when plasma potassium levels exceed 5.0 mEq/L and de-escalation or discontinuation of RAAS inhibitors with levels greater than 5.5 mEq/L. Practitioners should be aware that underlying
patient characteristics such as the presence of heart failure, acute kidney injury (AKI), critical illness, and rapid
hyperkalemia development appear to be at least as important as the degree of hyperkalemia at conferring poor
patient outcomes.
2. How does the body normally manage potassium?
Potassium is the predominant intracellular cation with only a small percentage (1%–2%) remaining in the extracellular space. The Na+K+-ATPase pump, which is located in the plasma membrane of most nucleated cells in the
body, is responsible for maintaining the high intracellular/low extracellular potassium concentration. The Na+K+ATPase exchanges intracellular sodium for extracellular potassium and is under the influence of many physiological stimuli that serve in a coordinated fashion to buffer acute potassium loads:
• Thepancreasreleasesinsulininresponsetonutritionalglucoseintake,whichsignalsforcellularglucose
uptake. This upregulates the Na+K+-ATPase in glucose responsive tissues like skeletal muscle.
• Catecholaminereleaseandβ2-adrenergic receptor activation increases the activity of the Na+K+-ATPase.
• Elevatedplasmapotassiumconcentrationsdirectlystimulatealdosteronereleasefromthezonaglomerulosaof
the adrenal gland, which activates mineralocorticoid receptors to upregulate Na+K+-ATPase activity.
While the Na+K+-ATPase limits a rapid rise in extracellular potassium concentration after loading, the kidney
maintains long-term balance by accomplishing net potassium excretion with only a small contribution occurring
via gastrointestinal (GI) excretion (∼5%–10% of daily intake). The primary site of potassium handling in the kidney
occurs in the principal cells of the collecting duct of the distal nephron. Potassium excretion by this nephron segment requires adequate distal nephron sodium delivery, a high tubular flow rate, and the presence (and signaling
activity) of aldosterone. A feedback loop also exists between these principal cells and the distal convoluted tubule,
whereby elevated plasma potassium concentrations directly inhibit the thiazide-sensitive sodium chloride cotransporter (NCC), thus augmenting distal sodium delivery and facilitating Na+-K+ exchange in the more distal nephron.
Consequently, any dysregulation in one or more of these processes can contribute significantly to the development
of hyperkalemia.
3
2
CHAPTER 28
3. Define the electrocardiographic changes associated with hyperkalemia.
A wealth of animal studies and extreme human presentations have demonstrated a “typical” progression of myocardial toxicity with acute hyperkalemia occurring in a graded fashion past plasma potassium levels of 5.0 mEq/L.
One of the earliest changes to occur is hyperexcitability, manifesting as “tented” T-waves most prominent in the
precordial electrocardiogram (ECG) leads (Fig. 28.1). As hyperkalemia progresses, elongation of the PR interval
and diminution of the P-wave amplitude occur. An increased QRS complex width is an ominous finding and can
precede a classically described “sine-wave” pattern. Thus hyperkalemia predisposes to both cardiac hyperexcitability (ventricular tachycardia and ventricular fibrillation) and depression (bradycardia, atrioventricular block,
interventricular conduction delay, and asystole), both of which can be fatal.
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Fig. 28.1 “Typical” electrocardiogram (ECG) changes with hyperkalemia. Progression of hyperkalemia begins with hyperpolarization of T-wave amplitude, causing a “tenting” phenomenon, followed by diminution of P-wave amplitude, prolonging of the PR interval,
and widening of the QRS, ultimately progressing to a sine-wave pattern.
However, most human cases of hyperkalemia are of unknown duration and occur among individuals with
different cardiometabolic risk factors, limiting the interpretability of ECG as both a diagnostic and prognostic tool.
The ECG lacks sensitivity and specificity at predicting the degree of hyperkalemia, and there are a host of conditions that can mimic the ECG changes seen with hyperkalemia including sepsis, myocardial infarction, acidosis,
left ventricular hypertrophy, and bundle branch blocks.3 There are even cases of fatal or near-fatal hyperkalemia
occurring in patients with normal ECGs. Ultimately, the ECG alone should not be relied upon to correctly identify
which patients require immediate attention.
4. How should one approach the hypertensive patient with hyperkalemia?
The first step in approaching a hypertensive patient with hyperkalemia is to determine if the finding is artefactual.
Poor phlebotomy technique and certain hematological conditions causing extreme leukocytosis and thrombocytosis should alert the clinician to the possibility of a hemolyzed specimen or pseudohyperkalemia, respectively.
Although excess potassium intake is often implicated, it is usually insufficient to cause hyperkalemia unless
advanced chronic kidney disease (CKD) is present (eGFR <30 mL/min) or acute loading is performed by intravenous potassium administration. Exceptions can occur in patients with distal tubular injury or dysfunction, such as
occurs with urinary obstruction, connective tissue diseases, and distal (type 4) renal tubular acidosis, which can
predispose to hyperkalemia despite a normal or near-normal eGFR. Disruption of the RAAS axis is the most common cause of hyperkalemia in patients with hypertension. There is often a temporal link to incipient hyperkalemia
and initiation or up-titration of ACEis, ARBs, and MRAs. RAAS inhibitors cause hyperkalemia by disrupting aldosterone signaling in the distal nephron, and, in some cases, by lowering of GFR due to angiotensin-2 blockade and
lower glomerular hydrostatic pressure from their antihypertensive effects. However, one must also not overlook
important contributors to hyperkalemia development among hypertensive patients. For example, significant hyperkalemia resulting from a trimethoprim prescription for a soft tissue infection in a hypertensive patient with CKD on
RAAS inhibition can result in dangerous synergy to engender severe hyperkalemia. Table 28.1 highlights many of
the common clinical conditions and medications predisposing individuals to hyperkalemia.
5. What is the role of dietary modification in the prevention of hyperkalemia?
Despite widespread application, advising dietary potassium reduction in individuals prone to hyperkalemia,
particularly those with hypertension, is not supported by evidence, and might even be harmful. Dietary sources
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Table 28.1 Common Conditions Leading to Hyperkalemia
CONDITION ETIOLOGY MECHANISM OF ACTION
Increased intake Intravenous K
+
Exogenous K+ loading
Intravenous K+-containing antimicrobials
Massive blood product transfusion
Impaired redistribution Rhabdomyolysis
Endogenous K+ turnover
Hemolysis
Tumor lysis syndrome
Malignant hyperthermia
Cardiac glycoside toxicity
Impaired Na+K+-ATPase activity
Uremia
Metabolic acidosis
Hypertonicity (hyperglycemia, mannitol)
Altered Na+/K+ extracellular/ intracel-
lular gradient
β2-Adrenergic blockers β2-Adrenergic blockade
Reduced elimination AKI, CKD Low GFR
Urinary obstruction
Distal nephron injury
Sickle cell crisis
Volume depletion
Poor distal Na+ delivery
Heart failure
Amiloride
ENaC blockade
Triamterene
Trimethoprim
CNIs
Pentamidine
Distal (type 4) RTA
Adrenal insufficiency
Impaired aldosterone synthesis,
activity, or MR blockade
a
Diabetes mellitus
Heparin
RAAS inhibitors
MR antagonists
Constipation, bowel obstruction Reduced K+ elimination from GI tract
a
Also can alter K+ redistribution outside the kidney.
b
Only in advanced CKD (GI elimination of K+ upregulated with lower GFR.)
AKI, Acute kidney injury; CKD, chronic kidney disease; CNIs, calcineurin inhibitors; ENaC, epithelial sodium channel; GFR, glomerular
filtration rate; GI, gastrointestinal; MR, mineralocorticoid receptor; RAAS, renin-angiotensin-aldosterone system; RTA, renal tubular
acidosis.
b
of potassium, including meats, fruits, and legumes, are incorporated into many popular diets (such as the Dietary
Approaches to Stop Hypertension [DASH] diet, Mediterranean diet, and plant-based diets) that have an evidence
base supporting general health benefits. Furthermore, adequate dietary potassium intake is linked with lower
blood pressure and associated with lower CVD and overall mortality in a variety of patient populations including
those with hypertension heart failure, and CKD.4 There is also a lack of published data that supports dietary potassium restriction is a particularly efficacious strategy to treat hyperkalemia. It may be reasonable to screen for, and
curtail, excessive sources of dietary potassium intake in patients with hyperkalemia, but practitioners should also
prioritize other aspects of cardiovascular health to tailor an individualized approach. Registered dieticians are an
excellent resource; and visits are often covered by a patient’s insurance. The National Kidney Foundation, Centers
for Disease Control and Prevention, and American Association of Kidney Patients also have excellent online dietary
resources for patients and providers relating to hyperkalemia.
6. Define the role of proper diuretic use in mitigation of hyperkalemia.
Diuretics remain a front-line treatment for hypertension, yet despite the overwhelming evidence of their
therapeutic efficacy, they remain under-prescribed due to concerns of electrolyte imbalances, azotemia, and
other metabolic side effects. Both loop and thiazide/thiazide-like diuretics increase urinary potassium secretion
largely by augmenting urinary flow and sodium delivery to the distal nephron (see Chapters 34 and 35). Often
the prescription of potent K-wasting diuretic is all that is needed to counterbalance the hyperkalemic effects of
RAAS inhibition. Poor compliance with a diuretic prescription, or prescription of shorter acting loop (furosemide,
bumetanide) and thiazide (hydrochlorothiazide) diuretics are potential clues that inadequate distal sodium
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delivery may be contributing to the perpetuation of hyperkalemia. Changing such patients to a longer acting loop
(torsemide) or thiazide-like (indapamide, chlorthalidone) diuretic regimens may prove efficacious at mitigating
both hyperkalemia and untreated hypertension. Often, both diuretics and RAAS inhibitors are de-prescribed due
to concerns of worsening azotemia. Yet data from the Systolic Blood Pressure Intervention Trial (SPRINT) suggest
that, despite an initial larger drop in eGFR with aggressive blood pressure control, participants randomized to a
more aggressive antihypertensive regimen (consisting of high usage of diuretics and RAAS inhibitors) had less
major cardiovascular events and all-cause mortality.5 Furthermore, the acute reduction in GFR with aggressive
blood pressure control in this trial appears to lack many features shared with other causes of AKI, such as markers of tubular damage,6 suggesting this phenomenon results from lower intraglomerular pressure and may not be
deleterious for longer term renal outcomes. The lack of hypertensive individuals with advanced CKD and diabetes
might limit generalizability to this particular cohort of patients. Nevertheless, both SPRINT and other studies
suggest that mild to moderate azotemia occurring after antihypertensive prescription might be tolerable in order
to reduce CVD progression, which has major implications for managing hypertensive patients with higher serum
potassium levels.
7. How can newer potassium-exchange resins be used in hypertensive individuals with
hyperkalemia on RAAS inhibitors?
Patiromer is a nonabsorbable cation exchange polymer that binds free potassium in the GI tract, primarily in the
distal colon, in exchange for calcium and thus enhances potassium losses in the stool. Daily use of oral Patiromer
allows for successful mitigation of chronic hyperkalemia in hypertensive patients with advanced CKD and heart
failure while receiving RAAS blockade.
trolled trial of prophylactic Patiromer administration among individuals with resistant hypertension demonstrated
significantly enhanced compliance with newly prescribed spironolactone versus placebo.9 Patiromer is administered as a dry powder and may be mixed with food or liquids. Starting doses begin at 8.4 g daily up to 12.6 g
twice-daily (BID), demonstrating efficacy in major clinical trials. Patiromer has a tolerable adverse effect profile
consisting of nausea, diarrhea, constipation, abdominal discomfort, and rare hypomagnesemia. It is important to
note that most of the studies performed using Patiromer demonstrate efficacy over a period of weeks to months,
and its use as a short-term agent in the treatment of more urgent hyperkalemia has not been fully examined.
Sodium Zirconium Cyclosilicate (SZC) is a nonabsorbed silicate that captures free potassium in exchange for
hydrogen and sodium along the GI tract. The molecular structure of SZC includes micropores with small diameters
favorably trapping potassium, rather than larger divalent cations like magnesium and calcium and thus limiting
the potential for development of hypocalcemia and hypomagnesemia. Like Patiromer, SZC has shown long-term
efficacy at reducing serum potassium among individuals with hypertension and high RAAS inhibitor usage.
has even shown efficacy at reducing predialysis serum potassium among patients with end-stage renal disease,12
a population with often difficult-to-control hypertension. Furthermore, these studies have demonstrated SZC
works within hours to rapidly lower serum potassium in a dose-dependent fashion. Typical doses of SZC are 5 g
and 10 g BID. SZC appears to also be safe and have a tolerable safety profile similar to Patiromer. It is important to
note the sodium content of one 5-g dose of SZC is 400 mg, and there have been reported instances of edema and
hypertension among patients treated with higher daily doses (>15 g daily) for longer durations.
Overall, Patiromer and SZC appear to be effective therapies for the treatment of individuals with hypertension, diabetes mellitus, CKD, and CVD with hyperkalemia and those at risk of developing hyperkalemia. These
newer exchange resins are rapidly replacing the role of sodium polystyrene sulfate in treating hyperkalemia due to
their studied efficacy and favorable side effect profile.
7,8
Additionally, a recently published prospective, randomized, placebo-con-
10,11
SZC
KEY POINTS
1. Hyperkalemia is a common electrolyte disorder in patients with hypertension and is linked with poor outcomes
including RAAS inhibitor de-escalation, hospitalization, and higher mortality.
2. Hyperkalemia results from a failure of homeostatic mechanisms that redistribute acute potassium loads in the
intracellular space while simultaneously augmenting urinary excretion.
3. Acute and chronic kidney diseases, diabetes mellitus, and commonly prescribed medications can have
synergistic effects to initiate and maintain hyperkalemia.
4. Knowledge of proper diuretic pharmacology serves as the cornerstone to managing and preventing hyperkalemia
in hypertensive individuals.
5. Novel potassium exchange resins such as Patiromer and SZC show great promise in both the acute and
chronic treatment of hyperkalemia, and might allow for better RAAS inhibitor adherence among individuals with
hypertension.
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REFERENCES
1. Kovesdy CP. Management of hyperkalemia in chronic kidney disease. Nat Rev Nephrol. 2014;10(11):653–662.
2. Tromp J, van der Meer P. Hyperkalemia: aetiology, epidemiology, and clinical significance. Eur Heart J Supp. 2019;21(Suppl
A):A6–A11.
3. Montford JR, Linas S. How dangerous is hyperkalemia?. J Am Soc Nephrol. 2017;28(11):3155–3165.
4. Clase CM, Carrero JJ, Ellison DH, et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions
from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2020;97(1):42–61.
5. Wright Jr JT, Williamson JD, Whelton PK, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med.
2015;373(22): 2103–2116.
6. Malhotra R, Craven T, Ambrosius WT, et al. Effects of intensive blood pressure lowering on kidney tubule injury in CKD: a longitudinal
subgroup analysis in SPRINT. Am J Kidney Dis. 2019;73(1):21–30.
7. Pitt B, Anker SD, Bushinsky DA, et al. Evaluation of the efficacy and safety of RLY5016, a polymeric potassium binder, in a doubleblind, placebo-controlled study in patients with chronic heart failure (the PEARL-HF) trial. Eur Heart J. 2011;32(7):820–828.
8. Weir MR, Bakris GL, Bushinsky DA, et al. Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors.
N Engl J Med. 2015;372(3):211–221.
9. Agarwal R, Rossignol P, Romero A, et al. Patiromer versus placebo to enable spironolactone use in patients with resistant
hypertension and chronic kidney disease (AMBER); a phase 2, randomized, double-blind, placebo-controlled trial. Lancet.
2019;394(10208):1540–1550.
10. Kosiborod M, Rasmussen HS, Lavin P, et al. Effect of sodium zirconium cyclosilicate on potassium lowering for 28 days among
outpatients with hyperkalemia. JAMA. 2014;312(21):2223–2233.
11. Spinowitz BS, Fishbane S, Pergola PE, et al. Sodium zirconium cyclosilicate among individuals with hyperkalemia: a 12-month phase
3 study. Clin J Am Soc Nephrol. 2019;14(6):798–809.
12. Fishbane S, Ford M, Fukagawa M, et al. A phase 3b, randomized, double-blind, placebo-controlled study of sodium zirconium
cyclosilicate for reducing the incidence of predialysis hyperkalemia. J Am Soc Nephrol. 2019;30(9):1723–1733.
5 TherapeuTic principles
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LIFESTYLE MODIFICATIONS FOR
HYPERTENSION MANAGEMENT
CHAPTER 29
Hina N. Mehta, MD, and Matthew A. Sparks, MD
QUESTIONS
1. What is the role of lifestyle modifications in the treatment of hypertension?
The 2017 American College of Cardiology/American Heart Association (ACC/AHA) Guideline for the Prevention,
Detection, Evaluation, and Management of High Blood Pressure in Adults recommends lifestyle changes that
can reduce systolic blood pressure (SBP) by approximately 4 to 11 mm Hg in patients with hypertension. These
guidelines stress the importance of maintaining a healthy diet with limited sodium intake, routine exercise,
weight management, tobacco cessation, and decreased alcohol consumption (Tables 29.1 and 29.2). One of the
original trials (published in 2002) that evaluated the efficacy of implementing all of these recommendations was
the diet, exercise, and weight loss intervention trial (DEW-IT), which enrolled 44 adults who were overweight and
had hypertension who were treated with a single blood pressure (BP) medication. DEW-IT consisted of a control
group (no intervention) and a comprehensive intensive lifestyle program (Dietary Approaches to Stop Hypertension
[DASH] diet and an exercise regimen that included 30 to 45 minutes of supervised moderate-intensity aerobic
exercise 3 d/wk, and alcohol restriction). Five energy levels (1350, 1600, 2100, 2600, 3100 kcal/d) of the DASH
Table 29.1 Lifestyle Nonpharmacologic Interventions for Prevention and Treatment of
Hypertension
Adapted from Whelton PK, Carey RM, Aronow WS, et al. ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the
prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/
American Heart Association task force on clinical practice guidelines. J Am Coll Cardiol. 2018;71:e127–248.
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Table 29.2 Dietary Nonpharmacologic Interventions for Prevention and Treatment of
Hypertension
DASH, Dietary Approaches to Stop Hypertension.
Adapted from Whelton PK, Carey RM, Aronow WS, et al. ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the
prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/
American Heart Association task force on clinical practice guidelines. J Am Coll Cardiol. 2018;71:e127–248.
diet were used, depending on the energy requirements of each participant. The DASH diet provided 18% kcal from
protein, 55% kcal from carbohydrate, and 27% kcal from fat. After 9 weeks of intervention, the lifestyle group lost
an average of 5.5 kg, whereas the control group had a mean weight loss of 0.6 kg. The mean change in 24-hour
SBP and diastolic blood pressure (DBP) was −10.5/−5.9 mm Hg in the lifestyle group and −1.1/−0.6 mm Hg in
the control group. BP reductions of this degree are similar to those accomplished with pharmacotherapy.
2. How do you follow a low-sodium diet?
The United States Department of Agriculture (USDA) 2015–2020 Dietary Guidelines for Americans describe how
Americans eat more sodium than recommended—an average of more than 3400 mg or 100 mEq of sodium daily!
The USDA guidelines recommend limiting sodium intake to less than 2300 mg/d (roughly 1 teaspoon of salt) and
patients with prehypertension or hypertension to reduce their sodium intake to 1500 mg/d. Reducing sodium
intake can decrease BP by approximately 5/3 mm Hg (see Table 29.2). About 75% of dietary sodium comes from
eating packaged and restaurant foods, whereas only a small portion (11%) comes from directly adding salt to
food when cooking or eating. Foods such as bread, stock (broth) cubes, and breakfast cereals are often high in
salt, which is often overlooked. Of note, current guidelines differ in the recommended amount of sodium intake for
patients with heart failure. Observational studies uphold that sodium restriction improves heart failure outcomes,
whereas other randomized controlled trials infer that dietary sodium restriction can cause hypovolemia and increased neurohormonal activation. Thus there remains controversy surrounding restricting dietary sodium content
especially in regards to heart failure.
3. How do you calculate how much sodium is in foods or beverages?
There is a misconception that “salt” and “sodium” are synonymous terms. In reality, sodium (Na) is a mineral
and a chemical element with the atomic number 11. Sodium also is a chemical element (other than chloride
[Cl]) found in salt (sodium chloride [NaCl]). Foods and beverages may contain no salt (NaCl), but they still may be
high in sodium because of the presence of naturally occurring sodium. Salt (NaCl) contains a 1:1 ratio of Na and
Cl ions. The molar mass of Na is 22.99 g/mol and of Cl is 35.45 g/mol. One mole of NaCl equals 58.44 g NaCl.
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Therefore 100 g of NaCl contains 39.34 g Na and 60.66 g Cl, thus sodium (Na) is roughly 40% of the weight of
salt, and chloride is the remaining 60%. Nutritionists often suggest diminishing salt intake, but it is sodium you
will see listed on food labels (Fig. 29.1). If you are cooking and want to figure out how much sodium you are adding, convert grams of salt to milligrams of sodium, then divide the amount of salt in grams by 2.5, and then finally
multiply by 1000 to get milligrams. The amount of sodium in a serving of food is listed in milligrams (mg) and as a
percent of the daily value on the nutrition label. The percent daily value (% daily value) for sodium gives a general
idea of how much sodium a serving adds to your total daily diet. The percent daily value for sodium on the nutrition label shown here is baseline on a daily maximum value of 2300 mg.
4. How effective is the DASH diet?
The DASH diet is a widely used dietary intervention for hypertension. The DASH diet emphasizes fruits, vegetables,
and low-fat dairy products with reduced intake in saturated fat and cholesterol. In terms of macronutrient
Fig. 29.1 Typical food label.
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Table 29.3 Effect of DASH Diet and Sodium Reduction on Blood Pressure
DIET
Control diet
Control diet
SODIUM LEVELS
RESTRICTION CHANGES
b
b
High to intermediate −2 mm Hg ∼133–131 mm Hg
Intermediate to low −5 mm Hg ∼131–126 mm Hg
SBP CHANGE
A
(mm Hg)
SBP ABSOLUTE
CHANGE (mm Hg)
DASH diet High to intermediate −1 mm Hg ∼126–125 mm Hg
DASH diet Intermediate to low −2 mm Hg ∼125–123 mm Hg
a
High sodium level = 3500 mg; intermediate sodium level = 2400 mg; low sodium level = 1500 mg.
b
Control diet: typical of what many people in the United States eat.
DASH, Dietary Approaches to Stop Hypertension; SBP, systolic blood pressure.
Adapted from Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the dietary approaches
to stop hypertension diet. N Engl J Med. 2001;344(1):3–10.
Table 29.4 Comparison of Control Diet against DASH Diet with Varying Sodium Levels
SODIUM LEVELS
A
DIET CHANGES
B
SBP CHANGE
(mm Hg)
SBP ABSOLUTE
CHANGE (mm Hg)
High Control to DASH diet −6 mm Hg ∼133–126 mm Hg
Intermediate Control to DASH diet −5 mm Hg ∼131–125 mm Hg
Low Control to DASH diet −2 mm Hg ∼126–123 mm Hg
a
High sodium level = 3500 mg; intermediate sodium level = 2400 mg; low sodium level = 1500 mg.
b
Control diet: typical of what many people in the United States eat.
DASH, Dietary Approaches to Stop Hypertension; SBP, systolic blood pressure.
Adapted from Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the dietary approaches
to stop hypertension diet. N Engl J Med. 2001;344(1):3–10.
composition, the nutrient goals of the DASH diet are as follows: total fat (27% of calories), saturated fat (6% of
calories), protein (18% of calories), and carbohydrates (55% of calories). It includes a sodium goal of 2300 mg and
potassium goal of 4700 mg. The original trial (Appel et al., NEJM, 1997) demonstrated the DASH diet reducing BP
(reduced SBP by 11.4 mm Hg and DBP by 5.5 mm Hg) in subjects with known hypertension, but it also showed
reductions in BP in subjects without hypertension (reduced SBP by 3.5 mm Hg and DBP by 2.1 mm Hg) compared
to the control diet.
5. Is the DASH diet more effective with the addition of sodium restriction?
Because the DASH trial was conducted independent of testing the effect of sodium restriction, a subsequent
multicenter, randomized trial was conducted to examine the combined effect of the DASH diet with sodium restriction on BP. The DASH diet showed to lower BP at high (3500 mg/d; typical of current US sodium consumption),
intermediate (2400 mg/d; reflecting the upper limit of current US recommendations), and lower levels (1500 mg/d;
reflecting potentially optimal sodium levels) of sodium intake, but the lowest SBP and DBP were seen in patients
who were on the DASH diet with the lowest amount of sodium intake (Tables 29.3 and 29.4). Thus the combined
effects of low sodium intake (1500 mg/d) and DASH diet were greater than the effects of either intervention alone
and they were substantial. In addition, in participants with hypertension, the effects were equal to or greater than
those of single drug therapy. Although the DASH diet has been endorsed by the Joint National Committee, the
American Diabetic Association, and the National Heart, Lung and Blood Institute Lifestyle Guidelines, the adherence to the DASH diet remains suboptimal across all races/ethnicities, education levels, and income levels across
the United States.
6. Can the DASH diet be used in patients with diminished kidney function to lower BP?
More than two thirds of US adults with chronic kidney disease (CKD) have uncontrolled hypertension. Lowering BP
to recommended treatment targets slows down the progression of CKD, and the DASH diet may have an important
role in BP control. In a pilot study, 11 participants with moderate CKD (epidermal growth factor receptor between
30 and 59 mL/min/1.73 m2) were monitored after completing 1 week of reduced-sodium, run-in diet followed by a
reduced-sodium DASH diet. The pilot date showed minimal acute metabolic abnormalities in adults with moderate
CKD and a possible improvement in nocturnal BP. Overall, mean serum potassium was significantly higher after
DASH diet week 1, but it was not significantly different from baseline after DASH diet week 2.
7. Does the Mediterranean diet result in BP effects?
There have been considerable efforts to test how adoption of a Mediterranean diet impacts cardiovascular health.
The Mediterranean diet consists of a diet heavy in fish, monounsaturated fats from olive oil, fruits, vegetables,
whole grains, legumes, nuts, and moderate alcohol consumption. The diet can graphically be represented in
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