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Potassium

Nutrient Name: Potassium.
Synonym: Kali.
Elemental Symbol: K.
Forms: Potassium aspartate, potassium bicarbonate, potassium chloride, potassium citrate, potassium gluconate, potassium iodide, potassium-R-lipoate, potassium oratate, potassium para-aminobenzoate.

Summary Table
nutrient description

Chemistry and Forms

Potassium aspartate, potassium bicarbonate, potassium chloride, potassium citrate, potassium gluconate, potassium orotate, potassium tartrate.

Physiology and Function

Cell membrane excitability, ion transport, and energy production are central functions of potassium in human physiology. Potassium, sodium, and chloride are the essential dietary minerals that serve as the major electrolytes in the human body within a triangular equilibrium. Directly and through these relationships, potassium participates in the regulation of water balance, osmotic equilibrium, acid-base balance, and blood pressure, and it plays a critical role in the contractility of smooth, cardiac, and skeletal (striated) muscle, particularly through its contribution to nerve function and carbohydrate and protein metabolism. It participates in glucose metabolism through its involvement with insulin in the movement of blood glucose into cells and conversion of blood glucose into glycogen for storage in the muscles and liver. Potassium (K+) is the principal cation in intracellular fluid, whereas sodium (Na+) is the principal extracellular cation. Potassium concentrations are tightly regulated both inside and outside of cells, with a differential of 30 times, and this sodium-potassium concentration gradient creates the membrane potential on which all contractility and nerve function depend.

Water balance is maintained by using ion pumps in the cell membrane, especially the sodium-potassium-adenosinetriphosphatase (Na+, K+-ATPase) pumps, to move potassium into cells in exchange for sodium being pumped out of cells. The proper functioning of nerve impulse transmission, muscle contraction, and cardiac function all require tight control of cell membrane potential. The critical function of these ion pumps is demonstrated in their exchange activities, accounting for 20% to 40% of the resting energy expenditure (of ATP) in a typical adult. The activity of the adenosine triphosphate (ATP)–sensitive K+channel plays an important role in mitochondrial cell-signaling pathways for ischemic protection and gene transcription, “roles that appear to depend on the ability of mitochondrial K(ATP) opening to trigger increased mitochondrial production of reactive oxygen species.” 1 Beyond Na+, K+-ATPase, potassium is required as a cofactor in the activity of only a few other enzyme systems, such as pyruvate kinase, central to carbohydrate metabolism. Potassium is also essential for proper kidney and adrenal function.

Potassium salts are inherently highly soluble, and dietary potassium intake is readily absorbed, 85% to 98%, principally in the small intestine. Average body content of potassium is 180 grams, and the intracellular fluid holds approximately 98% of the total body potassium. Dietary potassium is primarily excreted in the urine (∼ 77%-90%), with minimal renal capacity for conservation and minimal elimination of unabsorbed and intestinally secreted potassium eliminated via feces. The correlation between dietary potassium intake and urinary potassium content is high ( r = 0.82). Small amounts of potassium are excreted, along with other electrolytes, through perspiration and saliva.

nutrient in clinical practice

Known or Potential Therapeutic Uses

Potassium is among the nutrients more frequently prescribed in conventional medical practice, particularly in the context of hypertension and drug-induced depletion, as well as diarrhea and other causes of acute electrolyte depletion or disequilibrium. Although the legal limitation of potassium in over-the-counter (OTC) preparations to 99 mg in the United States is unique, much higher dosage levels are often prescribed in conjunction with potassium-wasting diuretics, or simply are attainable through consumption of a few pieces of fruit daily (or many electrolyte-rich “sports” drinks). Professional supervision and regular monitoring of serum potassium concentrations are appropriate whenever potassium is coadministered with conventional medications. Notably, perioperative outcomes are better in cardiac surgery patients with adequate potassium levels than those in patients with low preoperative serum potassium levels, who are at increased risk of developing arrhythmias and more likely to require cardiopulmonary resuscitation. 2 Conversely, hyperkalemia can occur when excess potassium accumulates because of decreased urinary potassium excretion as a result of diminished renal elimination, or more rarely, acute excessive intake. Apart from unintended effects of potassium-sparing diuretics, acute or chronic renal failure and hypoaldosteronism constitute the most common causes of hyperkalemia. Hemolysis, traumatic tissue damage, severe burns, and tumor lysis syndrome may also produce hyperkalemia as a result of a rapid shift of intracellular potassium into general circulation.

Historical/Ethnomedicine Precedent

The simple admonition to eat plenty of fruits and vegetables, especially those grown in soil rich with minerals, represents a time-honored recommendation that would encompass a healthful dietary potassium intake.

Possible Uses

Allergies, asthma, atherosclerosis, cancer, cardiac arrhythmia, congestive heart failure, Crohn's disease, diabetes mellitus (mild), diarrhea (especially in infants), electrolyte depletion, glaucoma, hypertension, hypokalemia, inflammatory bowel disease, muscle cramping and spasms, muscle fatigue and weakness, nephrolithiasis, osteoporosis, premenstrual syndrome, stroke, ulcerative colitis.

Deficiency Symptoms

Potassium deficiency can lead to a broad range of adverse effects across multiple body systems. These effects primarily derive from alterations in membrane potential and cellular metabolism and include muscle weakness, fatigue, listlessness, irritability, apprehension, mental confusion, drowsiness, nerve conduction irregularities, respiratory failure, reduced or absent reflexes, paralysis, cardiac disturbances (particularly arrhythmia), hypotension, muscle cramping and spasms, anorexia, nausea, abdominal bloating, delayed gastric emptying, constipation, paralytic ileus, polydypsia, and polyuria. Severe hypokalemia can be fatal as a result of cardiac arrhythmias and muscular paralysis. Electrocardiographic (ECG) changes accompanying hypokalemia are ST depression, flat T waves, U waves, and dysrhythmias. The pulse will alternate between fast and slow. It is necessary to monitor for digitalis toxicity in digitalized patients.

Most incidents of hypokalemia (i.e., abnormally low plasma potassium concentration) result from excessive loss of potassium, but inadequate or unbalanced intake can make a significant contribution. Thus, gross deficiencies of potassium are most often associated with use of potassium-depleting diuretics or glucocorticoids but can also result from severe or prolonged vomiting, diarrhea or perspiration, gastrointestinal (GI) disturbances caused by parasites, ostomy, laxative abuse or food reactions, some forms of renal disease, or other metabolic disturbances (e.g., acidosis) associated with alcoholism, anorexia nervosa, bulimia, rapid weight loss, congestive heart failure, chronic obstructive pulmonary disease, diabetes mellitus, or magnesium depletion. To a lesser degree, because potassium losses increase with perspiration, exercise and heat exposure, particularly hot humid climate, can adversely affect potassium status. In another clinical scenario, fluid shifting from the extracellular to the intracellular fluid compartment as a result of elevated insulin levels in the treatment of diabetic ketoacidosis is the most common cause of a drop in serum potassium levels. Subsequently, potassium is pulled from the intracellular space to the serum and then excreted through the kidneys in the hyperglycemic phase. At that point, serum potassium levels appear elevated, even though the stores are being lost with polyuria. Consequently, in the absence of replacement, serum potassium can drop to dangerously low levels if insulin is administered to reduce the hyperglycemia and potassium returns to the intracellular space. In a less dramatic process, potassium can become depleted during periods of stress as the adrenal glands secrete increased levels of adrenaline, which pulls potassium from the cells to be lost by the kidneys’ excretion. Similarly, overproduction of corticosteroids resulting from Cushing's syndrome, hyperaldosteronism, or other endocrine disorders (or exogenous administration) can provoke sodium retention and increase potassium excretion.

Absolute potassium deficiency is relatively rare, but relative potassium deficiency (i.e., in relation to sodium excess) is common, even in those with apparently healthy diets. In 2001 the Third National Health and Nutrition Examination Survey (NHANES-III) found that the modern American diet, especially when dominated by salt and processed foods, contains an average of 2300 mg of potassium daily for adult females and 3100 mg daily for adult males; slightly more than minimum daily requirements but approximately one-quarter to one-third the estimated daily potassium intake of hunter-gatherers or other “primitive” diets. Moreover, with daily potassium intake in modern diets being half as much as the typical daily sodium intake, most experts recommend significantly higher levels of dietary potassium, for example, a ratio of at least 5:1 or optimally 10:1 potassium/sodium intake or more, especially in the form of fresh fruits and vegetables. Dietary intake for reducing risk of hypertension, heart disease, and stroke is at least in the range of 4 to 5 g daily. Thus, even though low dietary intakes of potassium will generally not produce hypokalemia, insufficient dietary potassium probably increases significantly the risk of a wide range of chronic diseases, especially in the context of an imbalanced or poor-quality diet.

Several commonly consumed substances may induce lowered potassium levels. Caffeine and tobacco can reduce potassium absorption. Apart from the major adverse impact on potassium status associated with sodium intake, magnesium can also cause increased excretion of potassium in the stool with excess intake. Rare case reports describe hypokalemia subsequent to continued intake of large doses of licorice; the herb (but usually not the candy) contains glycyrrhizic acid, which can increase urinary excretion of potassium in a manner similar to aldosterone.

Dietary Sources

Fruits and vegetables are generally the richest dietary sources of potassium, and an individual who eats a diet high in these can have a high potassium intake (8-11 g/day). Notably, however, U.S. Department of Agriculture (USDA) data (2004) documented changes in food composition for 43 garden crops indicating that the nutrient content of many vegetables and fruits declined significantly from 1950 to 1999. 3

Bananas, orange juice, prunes and prune juice, raisins, avocados, cantaloupes, peaches, tomato juice, potatoes (baked with skin), soy flour, white beans, lima beans (cooked), lentils (cooked), acorn squash (cooked), parsnips (cooked), turnips (cooked), artichokes (cooked), and spinach (cooked) contain more than 300 mg of potassium per serving. Other foods providing moderate amounts of potassium include oranges, tomatoes, other fruits and vegetables, mint leaves, molasses, whole grains, sunflower seeds, almonds, flounder, salmon, cod, milk, chicken, and red meat.

Common herbs also considered sources of potassium include red clover, sage, catnip, hops, horsetail, nettle, plantain, and skullcap.

The potassium/sodium ratio in foods varies considerably and is more influential than the potassium content per se. Beans, peas, potatoes, grains, nuts, and fruits are among the foods with the highest potassium/sodium ratio. Thus, bananas or navy beans contain more than 1000 times more potassium than sodium, and Brazil nuts or corn contain more than 700 times more potassium than sodium. In comparison, eggs, beef, and fish contain 6 to 10 times more potassium than sodium, and spinach, celery, and beets contain only about 2.5 to 4 times more potassium than sodium, as do whole milk, chicken, and lamb. Many health care professionals advise using potassium chloride, rather than sodium chloride, as a seasoning to shift the potassium/sodium balance.

Nutrient Preparations Available

Potassium preparations can be potassium salts (chloride and bicarbonate), potassium bound to various mineral chelates (e.g., aspartate, citrate), or food-based potassium sources. Forms of potassium used as supplemental nutrients or as pharmaceutical agents include potassium aspartate, potassium bicarbonate, potassium chloride (oral, effervescent, or injection), potassium citrate, potassium gluconate, potassium iodide (oral solution or syrup), potassium-R-lipoate, potassium orotate, and potassium para-aminobenzoate. Potassium gluconate and potassium citrate are the most common supplemental forms. Potassium is administered parenterally when oral replacement is not possible or if hypokalemia is life threatening. Intravenous (IV) administration without cardiac monitoring should not exceed 10 mEq/hr.

Available forms are composed of potassium bound to other nonmetallic substances that render it chemically stable. Pure potassium is never available as a supplement or prescription item because it is a highly reactive metal that spontaneously ignites when exposed to water. Potassium bicarbonate or citrate is the form most conducive to a reduced risk of kidney stones. 4,5Among the chelated forms used orally, potassium citrate is generally better tolerated (and possibly more efficacious), whereas potassium chloride is less well tolerated, although it is used as a substitute for table salt and, in solution, for IV administration. A large amount given rapidly after sedation and neuromuscular paralysis is used as part of execution by lethal injection because it stops cardiac electrical activity and thus cardiac function.

Prescription preparations of potassium usually contain an inorganic form of potassium, usually potassium chloride, along with nonnutritive additives, and are dispensed as timed-release tablets, liquids, powders, and effervescent tablets, typically in the dosage range of 1.5 to 3 g (20-40 mEq) daily. Potassium iodide is also the preferred agent recommended by some governmental bodies as a protective measure against iodine-131 radiation-induced thyroid cancer in cases of nuclear radiation contamination.

Potassium is available generically from numerous manufacturers as an over-the-counter (OTC) product, but it is limited to 99 mg per serving as a nutritional supplement, which is small compared with the U.S. Institute of Medicine's recommendation for a dietary intake of 4700 mg daily. More significant quantities of supplemental potassium require a physician's prescription. Notably, so-called salt substitutes, such as Morton Salt Substitute, Lite Salt, No Salt, and Nu-Salt, are basically potassium chloride at the dosage level of 530 mg of potassium per ⅙ teaspoon.

Dosage Forms Available

Divided doses, taken with or near food, throughout the day are generally best for availability and tolerance.

Over-the-counter potassium supplements, singly or within multivitamin/mineral formulations, typically contain 99 mg of potassium per recommended daily dose, the legal nonprescription limit in the United States, as established by the Food and Drug Administration (FDA), for non-food-based forms. Notably, so-called salt substitutes, such as Morton Salt Substitute, Lite Salt, No Salt, and Nu-Salt, are basically potassium chloride at the dosage level of 530 mg potassium per ⅙ tsp.

Dosage Range

Adult

Dietary: A daily intake of 2000 mg (51 mEq) is generally considered an adequate (i.e., minimum) requirement of potassium for adult men and women, including for pregnant and nursing women. The need to ensure a (minimal) daily potassium intake of 2.5 to 3.5 g, a supply from fruits and vegetables (chiefly as citrate or malate, through daily intake of 0.6-0.8 mg/kg) represents the underlying rationale for the often-repeated “5 to 10 servings per day” recommendations from official bodies. Many practitioners experienced in nutritional medicine recommend 6 to 9 g from food sources as an optimal daily intake.

In 2004 the Food and Nutrition Board (FNB) of the U.S. Institute of Medicine established, for the first time, a recommended adequate intake (AI) level of 4700 mg (120 mEq) per day of potassium for adult, based on intake levels that have been found to lower blood pressure, reduce salt sensitivity (particularly in African-American men), and minimize the risk of kidney stones. However, the AI for potassium during lactation is set at 5100 mg (130 mEq)/day (4700 + 400 mg). 6 In the United Kingdom the average adult daily diet provides 2562 mg for women and 3279 mg for men.

Supplemental/Maintenance: No dosage level has been officially established for use as a dietary supplement. Potassium supplementation is not normally necessary in the presence of a balanced diet.

Pharmacological/Therapeutic: An oral dose of 1500 to 4000 mg daily, with plenty of fluid, is usually indicated in correction of mild deficiency or to lower blood pressure. More broadly, therapeutic doses can range from 100 to 6000 mg per day.

As a prescription medication, potassium is usually measured according to milliequivalents (mEq) or millimoles (mmol) rather than as milligrams (mg). To convert mg of elemental potassium to mEq, take mg and divide it by 39.0983 (atomic weight of potassium). For example, 90 mg is equivalent to 2.30 mEq, and 99 mg is equivalent to 2.53 mEq. Conversely, if you know the mEq, multiply by 39.0983 to find the elemental potassium weight in mg. For example, 2 mEq is equal to 78.0 mg. A typical therapeutic dosage of potassium is between 10 and 20 mEq, three to four times daily; professional supervision is recommended.

Toxic: Daily intakes exceeding 17 g, difficult to obtain from oral supplements, would be required to produce potassium toxicity. Hyperkalemia from oral administration is virtually unknown in individuals with normal renal function. Thus, the U.S. FNB noted that in “otherwise healthy individuals (i.e., individuals without impaired urinary potassium excretion from a medical condition or drug therapy), there is no evidence that a high level of potassium from foods has adverse effects,” and concluded that “a Tolerable Upper Intake Level (UL) for potassium from foods is not set for healthy adults.” 6

Pediatric (<18 Years)

Dietary: As of 2004, official U.S. recommendations for AI were established for the first time 6 :

  • Children, 1 to 3 years: 3000 mg (77 mEq)/day
  • Children, 4 to 8 years: 3800 mg (97 mEq)/day
  • Children, 9 to 13 years: 4500 mg (115 mEq)/day
  • Children, 14 to 18 years: 4700 mg (120 mEq)/day

Supplemental/Maintenance: Usually not recommended for children under 12 years of age with healthy, balanced diet.

Pharmacological/Therapeutic: Not established.

Toxic: Not established.

Laboratory Values

The accuracy of laboratory assessment of potassium status is severely limited because most potassium in the human body is within cells. Consequently, measuring levels of free potassium in the serum will only detect deficiency in extreme depletion states. Measurement of potassium levels in red blood cells (RBCs), white blood cells (WBCs), or other intracellular tissues can provide a more accurate index of tissue potassium stores and thus reveal potassium insufficiency more readily.

Serum Potassium (K+)

Normal levels are 3.5 to 5.0 mmol/L. (To convert mg of elemental potassium to mEq, take mg and divide it by 39.0983 [atomic weight of potassium].) Low serum potassium levels may reflect a shift to intracellular space or to depletion from the total body stores. Hyperkalemia is indicated by an increase in the serum potassium concentration above 5.5 mEq/L (plasma potassium >5.0).

Urinary Potassium (24 Hour)

Normal levels are 26 to 123 mmol/day.

Ranges depend on dietary intake. Because potassium excretion in the urine varies with intake and concentrations are affected by fluid intake, 24-hour measurement of urinary potassium provides a more consistent value.

Erythrocyte Potassium

Normal levels are approximately 100 mmol/L RBCs. This test most accurately reflects tissue stores.

  • Note:   Pseudohyperkalemia is defined as a difference between serum and plasma potassium greater than 0.4 mmol/L. Cases have been reported in which potassium is released from platelets, WBCs, or RBCs into the serum as blood clots, giving a falsely high value. This has occurred in polycythemia rubra vera, other myeloproliferative disorders with a high hematocrit or high platelet count, release of potassium from platelets during coagulation, RBC hemolysis during or after collection, and a protracted interval between blood sampling and separation of serum. Such misleading findings can be avoided, and a more accurate estimation obtained, by use of plasma instead of serum. 7

safety profile

Overview

At moderate or high dosage levels, potassium salts taken orally can cause symptoms of nausea, vomiting, abdominal discomfort, diarrhea, and ulcers. A single dose of several hundred milligrams in tablet form can produce gastric irritation, especially when ingested on an empty stomach, with potassium chloride particularly well known for adverse effects, even in liquid forms. Microencapsulated forms are generally better tolerated. In contrast, modified-release preparations (e.g., potassium chloride with enteric coating) have been associated with GI ulceration. Adverse effects can usually be prevented or reduced by taking potassium with meals. Potassium in dietary forms, at any intake level, is generally not associated with adverse effects, except that occasionally, ingestion of potassium-rich fruit has been reported to produce hyperkalemia in the context of potassium-sparing diuretics and ACE inhibitor medications. Most adverse effects associated with potassium result from depletion and deficiency. Chronic renal insufficiency requires dietary restriction of potassium (and magnesium) with careful monitoring of blood levels.

Nutrient Adverse Effects

Gastrointestinal (GI) symptoms constitute the most common adverse effects associated with nondietary potassium intake, with nausea, vomiting, abdominal discomfort, and diarrhea quite common and ulceration less frequent. When indicated, high-potency potassium chloride tablets should only be administered in a slow-release form (e.g., Slow K), to minimize the risk of GI distress or bleeding ulcers often attributable to the high amounts of chloride in the tablets.

The most serious adverse reaction to potassium is hyperkalemia. Abnormally elevated serum potassium concentrations [K+] occur when potassium intake exceeds the capacity of renal elimination. The accumulation of excess potassium can occur with decreased urinary potassium excretion due to acute or chronic renal failure, hypoaldosteronism, or the use of potassium-sparing diuretics, ACE inhibitors, or other drugs. More acutely, a shift of intracellular potassium into the circulation, most often resulting from hemolysis or sudden tissue damage, can also cause hyperkalemia. Thus, hyperkalemia is almost always caused by metabolic derangement due to pathophysiology (especially compromised kidney function) or medications that interfere with metabolic feedback systems; close monitoring is always appropriate when treating such patients.

A toxic reaction with severe hyperkalemia could potentially result from rapid ingestion of oral doses greater than 17 g (434 mEq) by individuals not acclimated to high intake, even with normal renal function. 6 Ingestion of a dose this size would be difficult and unlikely to occur unintentionally.

Potassium is generally considered to be neither a mutagen nor a carcinogen in standard forms at typical doses.

Adverse Effects Among Specific Populations

Individuals with compromised renal function, especially chronic renal failure, are at greatest risk for complications.

Pregnancy and Nursing

Specific data on potassium administration or supplementation in pregnancy and nursing are lacking. However, typical supplemental dosage levels are at or below recommended dietary intake levels or doses from typical intake of many common (and healthful) foods.

Infants and Children

Specific data on potassium administration or supplementation in infants and children are lacking. However, typical supplemental dosage levels would be at or below recommended dietary intake levels or doses from typical intake of many common (and healthful) foods.

Contraindications

Limited risk with food-level doses, but excessive doses should be avoided outside professional supervision and close monitoring: Addison's disease; compromised renal function, especially chronic renal failure; heart block; peptic ulcer; GI ulceration or obstruction; acute dehydration; severe burns.

Precautions and Warnings

Concurrent medications that alter potassium metabolism or interfere with potassium regulation, except with supervision and monitoring, including amiloride, spironolactone, triamterene, or other potassium-sparing diuretics, and ACE inhibitors such as captopril, enalapril, or lisinopril. Note that in such cases, consumption of foods providing potassium at recommended level (4.5-4.7 g/day) may develop excessive potassium levels. Caution also warranted in individuals undergoing trimethoprim-sulfamethoxazole therapy.

The 2004 recommendations from the U.S. FNB state: “Overall, because of the concern for hyperkalemia and resultant arrhythmias that might be life-threatening, the proposed AI [Adequate Intake: 4700 mg per day for adults] should not be applied to individuals with chronic kidney disease, heart failure, or type 1 diabetes, especially those who concomitantly use ACE inhibitor therapy. Among otherwise healthy individuals with hypertension on ACE inhibitor therapy, the AI should apply as long as renal function is unimpaired.” 6

interactions review

Strategic Considerations

A cursory review of standard information on the therapeutic applications, effects and risks, interactions, and depletion patterns associated with potassium typically focuses on hypertension, diabetes, and renal disease, or frank hypokalemia/hyperkalemia, often to the exclusion of the diverse effects of numerous medications on the key physiological functions of potassium and its many clinical applications. A deeper and broader review of the scientific literature looking at therapeutic applications beyond mere “supplementation” reveals both subtle and profound, gradual and rapid, obvious and complex effects of potassium insufficiency, deficiency, or excess, even when not necessarily at the threshold of hypokalemia or hyperkalemia. Health care professionals applying the information available through such an integrative analysis can discover many opportunities for enriching their therapeutic repertoire and enhancing clinical outcomes while avoiding or carefully navigating some of the more problematic encounters between potassium and various drugs, particularly in the context of treating patients with chronic disease or metabolic maladaption.

Potassium is one of the primary mineral nutrients, which, along with magnesium, are the most susceptible to drug-induced depletion. Such depletion patterns, particularly in early stages, are typically difficult to detect at the intracellular level, where hypokalemia can be most significant, especially for normal cardiac muscle and electrical activity. Potassium-wasting diuretics, particularly the thiazide and loop diuretics, represent the most widely recognized examples of medications that inherently increase risks of potassium depletion and hypokalemia. However, long-term, repeated, and high-dose use of numerous pharmaceutical agents, such as beta-2-adrenoceptor agonists, colchicine, amphotericin B, and laxatives or stool softeners, can impair potassium absorption, deplete potassium, and interfere with its physiological activity. Hypokalemia resulting from these drugs, particularly in combination with steroids or digoxin, may contribute to edema, acute cardiac rhythm irregularities, aggravation of asthma, or other adverse responses. Compensatory increase in potassium intake can usually, but not always, prevent or correct drug-induced adverse effects, and sometimes the corrective remedy is simply regular intake of several pieces of potassium-rich fruit. However, in situations such as cyclosporine-induced nephrotoxicity and hyperkalemia, adverse effects can be either rapid or gradual in onset, and attempts at mitigating drug toxicity through nutrient support can be of limited effectiveness. Likewise, the risks accompanying diuretic therapy or renal impairment can become unpredictable and complex, especially when interacting with agents such as digoxin, which can intrinsically impair potassium function; digoxin toxicity increases with hypokalemia, and digoxin overdose can cause hyperkalemia. In this case, as in many others, the intimate relationship between potassium and magnesium (as well as other key nutrients) reveals itself in physiology, therapeutics, interactions, and parallel depletion patterns and demonstrates the need for a comprehensive risk assessment and nutrient support strategy. As with many drug-induced depletion patterns, evidence of benefit from nutrient coadministration is often present in clinical practice but lacking in the scientific literature. Close monitoring is imperative in patients with intertwined pathologies, multiple medications, and comorbidities such as renal impairment, cardiac conditions, organ allografts, or other complicating factors.

Serum/plasma concentrations indicate critical deficiency or excess and disequilibrium or dysregulation, but potassium depletion at the intracellular level is difficult to detect with conventional laboratory assessment of blood constituents. Increasing potassium intake with potassium-rich foods, salt substitutes, and supplements is generally indicated and effective, although increased vigilance is necessary in the setting of compromised renal function or other medications altering potassium status.

Mineral wasting caused by renal tubular damage occurs in patients being treated with cisplatin or aminoglycosides, particularly in elderly and compromised populations, and hypokalemia often results. potassium depletion can further potentiate renal insufficiency or failure in such cases. Concurrent potassium therapy may prevent or correct adverse effects with long-term or repeated drug therapy, but evidence is limited. With cisplatin, however, refractory hypokalemia may require concomitant administration of both potassium and magnesium, possibly because of the magnesium dependence of the Na+,K+-ATPase membrane “pump” enzyme. Some agents, such as carbonic anhydrase inhibitors, can decrease renal blood flow and glomerular filtration rate. However, other than furosemide and acetazolamide, these may not adversely impact potassium status in most individuals. Nevertheless, given the potential for significant disequilibrium in carbon dioxide and bicarbonate transport, risks may be significantly elevated in certain individuals.

Hypokalemia, whether from disease, drugs, or physiological degeneration, can increase risks associated with many pharmaceutical agents that require stable levels of potassium and other key nutrients. For example, hypokalemia of various origins can significantly increase risk of acute cardiac rhythm irregularities and adverse reactions to quinidine and other antiarrhythmic drugs, especially when accompanied by hypomagnesemia.

Certain medications lead to increased potassium levels and potential for hyperkalemia, with the attendant risk of severe adverse events, sometimes acute, often chronic. Notably, hyperkalemia was virtually unknown except in renal failure until introduction of several drug classes in recent years. This rapid escalation of occurrence of hyperkalemia represents a major challenge in the chronic care of patients with multiple intertwined and complex patterns of dysfunction and disease, debilitation, and comedication.

In the context of certain medical conditions and comedications, some drugs can create or aggravate a risk of hyperkalemia and the potential for sudden onset of severe symptoms. Amiloride or other potassium-sparing diuretics carry an implicit risk of hyperkalemia when combined with a significant increase in potassium intake, especially with compromised renal function and concomitant ACE inhibitor therapy. Likewise, beta-adrenergic blockers can also elevate potassium levels and cause hyperkalemia through uncertain and often unpredictable mechanisms. Similarly, losartan and other angiotensin II receptor antagonists inherently carry a risk of hyperkalemia.

In these cases, potassium intake needs to be limited and patients educated as to the various sources (and relative dosages) of potassium. Some medications, such as trimethoprim, alone or in combination with sulfamethoxazole, can elevate potassium levels and may occasionally cause hyperkalemia, usually through effects on renal function; although uncommon and often reversible, severe adverse effects can be acute, and renal failure is possible. High-risk patients, such as those with compromised physiological function, with human immunodeficiency virus (HIV) infection, or receiving polypharmacy affecting renal function, should always be monitored closely. Perhaps more importantly than any absolute prohibition, patients need to avoid rapid or significantly increased potassium intake (e.g., new use of salt substitute) outside professional supervision.

As a mineral, potassium has variable risk for pharamacokinetic interference in which binding between the drug and potassium impairs biovailability and decreases therapeutic effect of both agents. Risks of clinically significant adverse effects are generally minimized by separating oral intake by several hours.

In a few cases, administration of potassium is relatively contraindicated in patients with specific pathological conditions or being treated with specific medications. Nevertheless, such contraindication is often cautionary, and coadministration of these agents is safe, or even beneficial in certain patients, but requires regular monitoring and close supervision by health care professionals trained and experienced in the various modalities and their integrative application.

nutrient-drug interactions
Albuterol/Salbutamol, Rimiterol, and Related Beta-2-Adrenoceptor Agonists
Amiloride
Aminoglycoside Antibiotics, Including Gentamicin, Neomycin, and Tobramycin
Amphotericin B (AMB; Fungizone)
Angiotensin-Converting Enzyme (ACE) Inhibitors
Benazepril (Lotensin); combination drug: benazepril and amlodipine (Lotrel); captopril (Capoten); combination drug: captopril and hydrochlorothiazide (Acezide, Capto-Co, Captozide, Co-Zidocapt); cilazapril (Inhibace), enalapril (Vasotec); enalapril combination drugs: enalapril and felodipine (Lexxel); enalapril and hydrochlorothiazide (Vaseretic); fosinopril (Monopril), lisinopril (Prinivil, Zestril); combination drug: lisinopril and hydrochlorothiazide (Prinzide, Zestoretic); moexipril (Univasc), perindopril (Aceon), quinapril (Accupril), ramipril (Altace), trandolapril (Mavik).
Minimal to Mild Adverse Interaction—Vigilance Necessary
Potentially Harmful or Serious Adverse Interaction—Avoid
Drug-Induced Effect on Nutrient Function, Supplementation Contraindicated, Professional Management Appropriate

Probability: 2. Probable
Evidence Base: Consensus

Effect and Mechanism of Action

The ACE inhibitors can increase serum levels of potassium in certain individuals, particularly those with diabetes or compromised renal function. 33-35 The increased levels of intracellular potassium and magnesium associated with ACE inhibitor therapy may be an important mechanism by which ACE inhibitors reduce arrhythmias. 36-38 Some ACE inhibitors, such as enalapril, can significantly inhibit plasma aldosterone concentration and urinary excretion of aldosterone. 39 In general, these effects appear to be similar for long-acting ACE inhibitors such as enalapril and short-acting ACE inhibitors such as captopril.

The concomitant use of potassium with an ACE inhibitor drug increases the risk of hyperkalemia, especially with rapid introduction. 12 Potassium levels may become further elevated with simultaneous use of potassium-sparing diuretics, potassium-based salt substitutes, very-low-calorie diets, and NSAIDs (which reduce renal excretion of ACE inhibitors). 40-42 All these risks are amplified in the context of renal insufficiency.

Research

The concomitant use of ACE inhibitor and potassium-sparing diuretic therapy is a contraindication rather than a potassium interaction; in such cases, both potassium and potassium-sparing medications should be avoided. For example, Burnakis and Mioduch 43 noted the significant risk of hyperkalemia in patients receiving combined therapy with captopril and potassium. Chiu et al. 12 conducted a retrospective chart review of five patients, all with diabetes and older than 50, who were seen for hyperkalemia in emergency care after having amiloride HCl/hydrochlorothiazide added to an ACE inhibitor drug regimen 8 to 18 days before presenting. They stated that these findings “highlight the dangers of a precipitous rise in serum potassium levels in patients at risk for renal insufficiency, already receiving an angiotensin-converting enzyme (ACE) inhibitor, who are given a potassium-sparing diuretic.”

Ohya et al. 39 administered enalapril (5 mg once daily) and captopril (12.5 mg three times daily) to 11 patients with mild essential hypertension and normal renal function for 1 week each in a crossover design, to compare effects of long-acting (enalapril) and short-acting (captopril) ACE inhibitors on serum electrolytes and circadian rhythm of urinary electrolyte excretion in relation to aldosterone status. Both agents “significantly decreased urinary K excretion” while “not significantly alter[ing] serum K level.” Notably, the amplitude of urinary K excretion was decreased by both drugs, although the circadian rhythm (acrophase) was not affected by either drug. Both enalapril and captopril “significantly reduced blood pressure” (to a similar degree) while enalapril, but not captopril, “significantly inhibited plasma aldosterone concentration and urinary aldosterone excretion.” Thus, although the primary finding of this trial was that “enalapril caused more sustained inhibition of aldosterone secretion” than captopril, they also noted that “both drugs showed similar effects on the K homeostasis in patients with mild essential hypertension.” 39

Nevertheless, the effects of ACE inhibitor therapy on potassium and magnesium may play an important role in their therapeutic effect. O’Keeffe et al. 36 investigated the effect of captopril therapy on lymphocyte potassium and magnesium concentrations in patients with congestive heart failure (CHF). They compared lymphocyte potassium and magnesium in 18 patients taking furosemide and potassium for CHF before and 3 months after the introduction of captopril to 32 healthy controls. Nine of the treatment subjects exhibited decreased baseline lymphocyte magnesium and potassium concentrations, despite similar plasma electrolyte levels. Notably, there was a “significant increase in both lymphocyte potassium and magnesium levels” after 3 months’ treatment with captopril and furosemide in these patients. Furthermore, nine patients “who had been taking a potassium-sparing combination diuretic also had an increase in lymphocyte magnesium” after the introduction of captopril. These authors concluded that “increased intracellular potassium and magnesium may be one mechanism whereby [ACE] inhibitors reduced arrhythmias and improve survival” in CHF patients. 36 In contrast, however, some of these same researchers subsequently examined the effect of 6 months’ captopril (or nifedipine) therapy on lymphocyte magnesium and potassium levels in 28 patients treated for hypertension. They observed “no difference in serum or lymphocyte concentrations in the two groups compared to 45 healthy, normotensive controls.” 37

Overall, as summarized by Shionoiri 41 in a review of pharmacokinetic drug interactions involving ACE inhibitors (1993): “When ACE inhibitors are given, hyperkalaemia may occur in patients with renal insufficiency, those taking potassium supplements or potassium-sparing diuretics, and in diabetic patients with mild renal impairment.”

Reports

Numerous case reports have been published describing hyperkalemia in patients undergoing ACE inhibitor therapy. 35,44-46 Stoltz and Andrews 40 described severe hyperkalemia during very-low-calorie diets and ACE inhibitor use. Ray et al. 42 reported two cases of severe hyperkalemia resulting from the concomitant use of salt substitutes (KCl) in hypertensive patients taking ACE inhibitors, in what they warned was “a potentially life threatening interaction.” Serum potassium stabilized in the normal range after cessation of the salt substitute in each case. The authors concluded that “without vigilance the contribution of the salt substitute to hyperkalaemia would have been overlooked and an ACE inhibitor erroneously withdrawn.” 42

Clinical Implications and Adaptations

Health care professionals treating patients taking an ACE inhibitor are strongly encouraged to counsel these individuals to avoid unsupervised increases in potassium intake, in the form of supplements but also as high-potassium foods (e.g., fruit) or salt substitutes, on the basis of the increased risk for problematic reactions. A clinically significant increase in blood potassium levels represents an uncommon yet potentially serious adverse effect associated with ACE inhibitors. The importance of frank inquiry and detailed inventory of concomitant (or even occasional) medications, diet, nutrients and herbs cannot be overemphasized. Close supervision and regular monitoring are essential, particularly in individuals with compromised renal function. The prescription of potassium chloride or potassium-sparing medications is generally contraindicated during ACE inhibitor therapy.

Beta-Adrenoceptor Antagonists (Beta-Adrenergic Blocking Agents)
Carbenoxolone (CBX)
Carbonic Anhydrase Inhibitors, Potassium Depleting
Cisplatin
Colchicine
Corticosteroids, Oral
Cotrimoxazole (Sulfamethoxazole and Trimethoprim)
Cyclosporine
Digoxin and Related Cardiac Glycosides
Diuretics, Potassium Depleting, Including Loop and Thiazide Diuretics
Ipecac
Laxatives and Stool Softeners
Losartan and Related Angiotensin II Receptor Antagonists
Magnesium-Containing Antacids
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Quinidine and Related Antiarrhythmic Drugs
Spironolactone and Triamterene
Trimethoprim-Sulfamethoxazole
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Acetylsalicylic Acid (Aspirin)
Amphetamines and Related Stimulant Medications
Calcium Channel Blockers
Epinephrine and Related Beta-Adrenergic Agonists
Fluoroquinolone (4-Quinolone) Antibiotics
Haloperidol (Haldol)
Heparin
Insulin
Pseudoephedrine, Phenylpropanolamine, and Related Decongestants
Tetracycline Antibiotics
Theophylline/Aminophylline and Related Beta-2 Sympathomimetics (Oral and Inhalant)
Thioridazine
nutrient-nutrient interactions
Magnesium and Magnesium-Containing Antacids
herb-nutrient interactions
Diuretic Herbs
Ipecac
Licorice Root
Senna
Citations and Reference Literature
  • 1.Garlid KD, Paucek P. The mitochondrial potassium cycle. IUBMB Life 2001;52:153-158.View Abstract
  • 2.Wahr JA, Parks R, Boisvert D et al. Preoperative serum potassium levels and perioperative outcomes in cardiac surgery patients. Multicenter Study of Perioperative Ischemia Research Group. JAMA 1999;281:2203-2210.View Abstract
  • 3.Davis DR, Epp MD, Riordan HD. Changes in USDA food composition data for 43 garden crops, 1950 to 1999. J Am Coll Nutr 2004;23:669-682.
  • 4.Lemann J Jr, Pleuss JA, Gray RW, Hoffmann RG. Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected]. Kidney Int 1991;39:973-983.View Abstract
  • 5.Sakhaee K, Alpern R, Jacobson HR, Pak CY. Contrasting effects of various potassium salts on renal citrate excretion. J Clin Endocrinol Metab 1991;72:396-400.
  • 6.Panel on Dietary Reference Intakes for Electrolytes and Water, Food and Nutrition Board, US Institute of Medicine. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: National Academy Press; 2004:173-246.
  • 7.Teh MM, Zaman MJ, Brooks AP, Li Voon Chong JS. When is a high potassium not a high potassium? J R Soc Med 2003;96:354-355.
  • 8.Spector SL. Adverse reactions associated with parenteral beta agonists: serum potassium changes. N Engl Reg Allergy Proc 1987;8:317-321.View Abstract
  • 9.Phillips PJ, Vedig AE, Jones PL et al. Metabolic and cardiovascular side effects of the beta 2-adrenoceptor agonists salbutamol and rimiterol. Br J Clin Pharmacol 1980;9:483-491.View Abstract
  • 10.Edner M, Jogestrand T. Oral salbutamol decreases serum digoxin concentration. Eur J Clin Pharmacol 1990;38:195-197.View Abstract
  • 11.Ramsay LE, Hettiarachchi J, Fraser R, Morton JJ. Amiloride, spironolactone, and potassium chloride in thiazide-treated hypertensive patients. Clin Pharmacol Ther 1980;27:533-543.View Abstract
  • 12.Chiu TF, Bullard MJ, Chen JC et al. Rapid life-threatening hyperkalemia after addition of amiloride HCl/hydrochlorothiazide to angiotensin-converting enzyme inhibitor therapy. Ann Emerg Med 1997;30:612-615.View Abstract
  • 13.Barr GA, Mazze RI, Cousins MJ, Kosek JC. An animal model for combined methoxyflurane and gentamicin nephrotoxicity. Br J Anaesth 1973;45:306-312.View Abstract
  • 14.Mazze RI, Cousins MJ. Combined nephrotoxicity of gentamicin and methoxyflurane anaesthesia in man: a case report. Br J Anaesth 1973;45:394-398.View Abstract
  • 15.Kes P, Reiner Z. Symptomatic hypomagnesemia associated with gentamicin therapy. Magnes Trace Elem 1990;9:54-60.View Abstract
  • 16.Valdivieso A, Mardones JM, Loyola MS, Cubillos AM. [Hypomagnesemia associated with hypokalemia, hyponatremia and metabolic alkalosis: possible complication of gentamicin therapy]. Rev Med Chil 1992;120:914-919.
  • 17.Parsons PP, Garland HO, Harpur ES, Old S. Acute gentamicin-induced hypercalciuria and hypermagnesiuria in the rat: dose-response relationship and role of renal tubular injury. Br J Pharmacol 1997;122:570-576.View Abstract
  • 18.Barton CH, Pahl M, Vaziri ND, Cesario T. Renal magnesium wasting associated with amphotericin B therapy. Am J Med 1984;77:471-474.View Abstract
  • 19.British National Formulary (BNF 52); London: BMJ Publishing Group and RPS Publishing; 2006.
  • 20.Bernardo JF, Murakami S, Branch RA, Sabra R. Potassium depletion potentiates amphotericin-B-induced toxicity to renal tubules. Nephron 1995;70:235-241.View Abstract
  • 21.Utz JP. Amphotericin B toxicity: general side effects. Ann Intern Med 1964;61:340-343.View Abstract
  • 22.Butler WT, Hill GJ 2nd, Szwed CF, Knight V. Amphotericin B renal toxicity in the dog. J Pharmacol Exp Ther 1964;143:47-56.View Abstract
  • 23.Butler WT, Hill GJ 2nd. Intravenous administration of amphotericin B in the dog. J Am Vet Med Assoc 1964;144:399-402.View Abstract
  • 24.Butler WT, Bennett JE, Hill GJ 2nd. Electrocardiographic and electrolyte abnormalities caused by amphotericin B in dog and man. Proc Soc Exp Biol Med 1964;116:857-863.View Abstract
  • 25.Butler WT, Bennett JE, Alling DW et al. Nephrotoxicity of amphotericin B: early and late effects in 81 patients. Ann Intern Med 1964;61:175-187.View Abstract
  • 26.Butler WT. Amphotericin B toxicity: changes in renal function. Ann Intern Med 1964;61:344-349.View Abstract
  • 27.Craven PC, Gremillion DH. Risk factors of ventricular fibrillation during rapid amphotericin B infusion. Antimicrob Agents Chemother 1985;27:868-871.
  • 28.Wazny LD, Brophy DF. Amiloride for the prevention of amphotericin B–induced hypokalemia and hypomagnesemia. Ann Pharmacother 2000;34:94-97.View Abstract
  • 29.Smith SR, Galloway MJ, Reilly JT, Davies JM. Amiloride prevents amphotericin B related hypokalaemia in neutropenic patients. J Clin Pathol 1988;41:494-497.View Abstract
  • 30.Bearden DT, Muncey LA. The effect of amiloride on amphotericin B–induced hypokalaemia. J Antimicrob Chemother 2001;48:109-111.View Abstract
  • 31.Pasic S, Flannagan L, Cant AJ. Liposomal amphotericin (AmBisome) is safe in bone marrow transplantation for primary immunodeficiency. Bone Marrow Transplant 1997;19:1229-1232.View Abstract
  • 32.Da Silva PS, de Oliveira Iglesias SB, Waisberg J. Hypokalemic rhabdomyolysis in a child due to amphotericin B therapy. Eur J Pediatr 2007;166(2):169-171.
  • 33.Rado JP. Prediction of hyperkalemia associated with prolonged treatment with captopril by glucose-induced acute serum potassium changes. Exp Clin Endocrinol 1984;84:143-147.View Abstract
  • 34.Rush JE, Merrill DD. The safety and tolerability of lisinopril in clinical trials. J Cardiovasc Pharmacol 1987;9 Suppl 3:S99-S107.View Abstract
  • 35.Good CB, McDermott L, McCloskey B. Diet and serum potassium in patients on ACE inhibitors. JAMA 1995;274:538.View Abstract
  • 36.O’Keeffe S, Grimes H, Finn J et al. Effect of captopril therapy on lymphocyte potassium and magnesium concentrations in patients with congestive heart failure. Cardiology 1992;80:100-105.
  • 37.Lavin F, O’Keeffe S, Grimes H et al. Effect of prolonged nifedipine or captopril therapy on lymphocyte magnesium and potassium levels in hypertension. Cardiology 1993;82:405-408.
  • 38.Sifton DW et al. Physicians’ Desk Reference. Montvale, NJ: Medical Economics Company; 2000:1965-1968.
  • 39.Ohya Y, Ueno M, Takata Y et al. Crossover comparison of the effects of enalapril and captopril on potassium homeostasis in patients with mild hypertension. Int J Clin Pharmacol Ther 1994;32:655-659.View Abstract
  • 40.Stoltz ML, Andrews CE Jr. Severe hyperkalemia during very-low-calorie diets and angiotensin converting enzyme use. JAMA 1990;264:2737-2738.
  • 41.Shionoiri H. Pharmacokinetic drug interactions with ACE inhibitors. Clin Pharmacokinet 1993;25:20-58.View Abstract
  • 42.Ray K, Dorman S, Watson R. Severe hyperkalaemia due to the concomitant use of salt substitutes and ACE inhibitors in hypertension: a potentially life threatening interaction. J Hum Hypertens 1999;13:717-720.View Abstract
  • 43.Burnakis TG, Mioduch HJ. Combined therapy with captopril and potassium supplementation: a potential for hyperkalemia. Arch Intern Med 1984;144:2371-2372.View Abstract
  • 44.Warren SE, O’Connor DT. Hyperkalemia resulting from captopril administration. JAMA 1980;244:2551-2552.
  • 45.Grossman A, Eckland D, Price P, Edwards CR. Captopril: reversible renal failure with severe hyperkalaemia. Lancet 1980;1:712.View Abstract
  • 46.Burnakis TG. Captopril and increased serum potassium levels. JAMA 1984;252:1682-1683.View Abstract
  • 47.Rosa RM, Silva P, Young JB et al. Adrenergic modulation of extrarenal potassium disposal. N Engl J Med 1980;302:431-434.View Abstract
  • 48.Lundborg P. The effect of adrenergic blockade on potassium concentrations in different conditions. Acta Med Scand Suppl 1983;672:121-126.View Abstract
  • 49.Arthur S, Greenberg A. Hyperkalemia associated with intravenous labetalol therapy for acute hypertension in renal transplant recipients. Clin Nephrol 1990;33:269-271.View Abstract
  • 50.Rodriguez M, Solanki DL, Whang R. Refractory potassium repletion due to cisplatin-induced magnesium depletion. Arch Intern Med 1989;149:2592-2594.View Abstract
  • 51.Whang R, Whang DD, Ryan MP. Refractory potassium repletion: a consequence of magnesium deficiency. Arch Intern Med 1992;152:40-45.View Abstract
  • 52.Buckley JE, Clark VL, Meyer TJ, Pearlman NW. Hypomagnesemia after cisplatin combination chemotherapy. Arch Intern Med 1984;144:2347-2348.View Abstract
  • 53.Bianchetti MG, Kanaka C, Ridolfi-Luthy A et al. Chronic renal magnesium loss, hypocalciuria and mild hypokalaemic metabolic alkalosis after cisplatin. Pediatr Nephrol 1990;4:219-222.View Abstract
  • 54.Roe DA. Drug-Induced Nutritional Deficiencies. 2nd ed. Westport, Conn: Avi Publishing; 1985:159-160.
  • 55.Werbach MR. Foundations of Nutritional Medicine. Tarzana, Calif: Third Line Press; 1997:223-224.
  • 56.Thorn GW. Clinical considerations in the use of corticosteroids. N Engl J Med 1966;274:775-781.View Abstract
  • 57.Hormones, adrenal cortical steroids, glucocorticoids. In: Threlkeld DS, ed. Facts and Comparisons Drug Information. St Louis: Facts and Comparisons; April 1991:128b.
  • 58.Stanbury RM, Graham EM. Systemic corticosteroid therapy—side effects and their management. Br J Ophthalmol 1998;82:704-708.View Abstract
  • 59.Kelly TM, Nelson DH. Sodium excretion and atrial natriuretic peptide levels during mineralocorticoid administration: a mechanism for the escape from hyperaldosteronism. Endocr Res 1987;13:363-383.
  • 60.Krishna GG, Kapoor SC. Potassium depletion exacerbates essential hypertension. Ann Intern Med 1991;115:77-83.View Abstract
  • 61.Krishna GG, Kapoor SC. Potassium supplementation ameliorates mineralocorticoid-induced sodium retention. Kidney Int 1993;43:1097-1103.View Abstract
  • 62.Chacko M, Fordtran JS, Emmett M. Effect of mineralocorticoid activity on transtubular potassium gradient, urinary [K]/[Na] ratio, and fractional excretion of potassium. Am J Kidney Dis 1998;32:47-51.View Abstract
  • 63.Coruzzi P, Gualerzi M, Parati G et al. Potassium supplementation improves the natriuretic response to central volume expansion in primary aldosteronism. Metabolism 2003;52:1597-1600.View Abstract
  • 64.Newnham DM. Asthma medications and their potential adverse effects in the elderly: recommendations for prescribing. Drug Saf 2001;24:1065-1080.View Abstract
  • 65.Wenzl HH, Fine KD, Santa Ana CA et al. Effect of fludrocortisone and spironolactone on sodium and potassium losses in secretory diarrhea. Dig Dis Sci 1997;42:119-128.View Abstract
  • 66.Imbriano LJ, Durham JH, Maesaka JK. Treating interdialytic hyperkalemia with fludrocortisone. Semin Dial 2003;16:5-7.View Abstract
  • 67.Olyaei AJ, de Mattos AM, Bennett WM. Immunosuppressant-induced nephropathy: pathophysiology, incidence and management. Drug Saf 1999;21:471-488.View Abstract
  • 68.You CW, Park YH, Lee ES et al. Effects of thyroxine on hyperkalemia and renal cortical Na+, K+-ATPase activity induced by cyclosporin A. J Korean Med Sci 2002;17:625-632.View Abstract
  • 69.Caliskan Y, Kalayoglu-Besisik S, Sargin D, Ecder T. Cyclosporine-associated hyperkalemia: report of four allogeneic blood stem-cell transplant cases. Transplantation 2003;75:1069-1072.View Abstract
  • 70.Heering PJ, Kurschat C, Vo DT et al. Aldosterone resistance in kidney transplantation is in part induced by a down-regulation of mineralocorticoid receptor expression. Clin Transplant 2004;18:186-192.View Abstract
  • 71.Takami A, Asakura H, Takamatsu H et al. Isolated hyperkalemia associated with cyclosporine administration in allogeneic stem cell transplantation for renal cell carcinoma. Int J Hematol 2005;81:159-161.View Abstract
  • 72.Laine J, Holmberg C. Renal and adrenal mechanisms in cyclosporine-induced hyperkalaemia after renal transplantation. Eur J Clin Invest 1995;25:670-676.View Abstract
  • 73.Qvist E, Laine J, Ronnholm K et al. Graft function 5-7 years after renal transplantation in early childhood. Transplantation 1999;67:1043-1049.View Abstract
  • 74.Higgins R, Ramaiyan K, Dasgupta T et al. Hyponatraemia and hyperkalaemia are more frequent in renal transplant recipients treated with tacrolimus than with cyclosporine: further evidence for differences between cyclosporin and tacrolimus nephrotoxicities. Nephrol Dial Transplant 2004;19:444-450.
  • 75.Stigant CE, Cohen J, Vivera M, Zaltzman JS. ACE inhibitors and angiotensin II antagonists in renal transplantation: an analysis of safety and efficacy. Am J Kidney Dis 2000;35:58-63.View Abstract
  • 76.Schmidt A, Gruber U, Bohmig G et al. The effect of ACE inhibitor and angiotensin II receptor antagonist therapy on serum uric acid levels and potassium homeostasis in hypertensive renal transplant recipients treated with CsA. Nephrol Dial Transplant 2001;16:1034-1037.View Abstract
  • 77.Singer M, Coluzzi F, O’Brien A, Clapp LH. Reversal of life-threatening, drug-related potassium-channel syndrome by glibenclamide. Lancet 2005;365:1873-1875.
  • 78.Lown B, Black H, Moore FD. Digitalis, electrolytes and the surgical patient. Am J Cardiol 1960;6:309-337.View Abstract
  • 79.Smith TW, Willerson JT. Suicidal and accidental digoxin ingestion: report of five cases with serum digoxin level correlations. Circulation 1971;44:29-36.View Abstract
  • 80.Whang R, Oei TO, Watanabe A. Frequency of hypomagnesemia in hospitalized patients receiving digitalis. Arch Intern Med 1985;145:655-656.View Abstract
  • 81.Schmidt TA, Bundgaard H, Olesen HL et al. Digoxin affects potassium homeostasis during exercise in patients with heart failure. Cardiovasc Res 1995;29:506-511.
  • 82.Martin BJ, Milligan K. Diuretic-associated hypomagnesemia in the elderly. Arch Intern Med 1987;147:1768-1771.View Abstract
  • 83.Kroenke K, Wood DR, Hanley JF. The value of serum magnesium determination in hypertensive patients receiving diuretics. Arch Intern Med 1987;147:1553-1556.View Abstract
  • 84.Zuccala G, Pedone C, Cocchi A et al. Older age and in-hospital development of hypokalemia from loop diuretics: results from a multicenter survey. GIFA Investigators, Multicenter Italian Pharmacoepidemiologic Study Group. J Gerontol A Biol Sci Med Sci 2000;55:M232-M238.View Abstract
  • 85.Franse LV, Pahor M, Di Bari M et al. Hypokalemia associated with diuretic use and cardiovascular events in the Systolic Hypertension in the Elderly Program. Hypertension 2000;35:1025-1030.View Abstract
  • 86.Ruml LA, Pak CY. Effect of potassium magnesium citrate on thiazide-induced hypokalemia and magnesium loss. Am J Kidney Dis 1999;34:107-113.View Abstract
  • 87.Ruml LA, Gonzalez G, Taylor R et al. Effect of varying doses of potassium-magnesium citrate on thiazide-induced hypokalemia and magnesium loss. Am J Ther 1999;6:45-50.View Abstract
  • 88.Ritsema GH, Eilers G. Potassium supplements prevent serious hypokalaemia in colon cleansing. Clin Radiol 1994;49:874-876.View Abstract
  • 89.Moriarty KJ, Kelly MJ, Beetham R, Clark ML. Studies on the mechanism of action of dioctyl sodium sulphosuccinate in the human jejunum. Gut 1985;26:1008-1013.View Abstract
  • 90.Ewe K, Holker B. [The effect of a diphenolic laxative (bisacodyl) on water and electrolyte transport in the human colon] (author’s translation). Klin Wochenschr 1974;52:827-833.
  • 91.Farack UM, Gruber E, Loeschke K. The influence of bisacodyl and deacetylbisacodyl on mucus secretion, mucus synthesis and electrolyte movements in the rat colon in vivo. Eur J Pharmacol 1985;117:215-222.View Abstract
  • 92.Fleming BJ, Genuth SM, Gould AB, Kamionkowski MD. Laxative-induced hypokalemia, sodium depletion and hyperreninemia: effects of potassium and sodium replacement on the renin-angiotensin-aldosterone system. Ann Intern Med 1975;83:60-62.View Abstract
  • 93.Gastrointestinal drugs, laxatives. In: Threlkeld DS, ed. Facts and Comparisons Drug Information. St Louis: Facts and Comparisons; May 1991:319a.
  • 94.Perazella MA. Drug-induced hyperkalemia: old culprits and new offenders. Am J Med 2000;109:307-314.View Abstract
  • 95.Sica DA. Antihypertensive therapy and its effects on potassium homeostasis. J Clin Hypertens (Greenwich) 2006;8:67-73.View Abstract
  • 96.Brenner BM, Cooper ME, de Zeeuw D et al. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med 2001;345:861-869.View Abstract
  • 97.Dahlof B, Devereux RB, Kjeldsen SE et al. Cardiovascular morbidity and mortality in the Losartan Intervention for Endpoint Reduction in Hypertension Study (LIFE): a randomised trial against atenolol. Lancet 2002;359:995-1003.View Abstract
  • 98.Toto R, Shultz P, Raij L et al. Efficacy and tolerability of losartan in hypertensive patients with renal impairment. Collaborative Group. Hypertension 1998;31:684-691.View Abstract
  • 99.Shahinfar S, Dickson TZ, Ahmed T et al. Losartan in patients with type 2 diabetes and proteinuria: observations from the RENAAL Study. Kidney Int Suppl 2002:64-67.View Abstract
  • 100.Schepkens H, Vanholder R, Billiouw JM, Lameire N. Life-threatening hyperkalemia during combined therapy with angiotensin-converting enzyme inhibitors and spironolactone: an analysis of 25 cases. Am J Med 2001;110:438-441.
  • 101.Wrenger E, Muller R, Moesenthin M et al. Interaction of spironolactone with ACE inhibitors or angiotensin receptor blockers: analysis of 44 cases. BMJ 2003;327:147-149.View Abstract
  • 102.Angiotensin II receptor antagonists and heart failure: angiotensin-converting-enzyme inhibitors remain the first-line option. Prescrire Int 2005;14:180-186.
  • 103.Kauffmann R, Orozco R, Venegas JC. [Severe hyperkalemia associated to the use of losartan and spironolactone: case report]. Rev Med Chil 2005;133:947-952.View Abstract
  • 104.Saito M, Takada M, Hirooka K et al. Serum concentration of potassium in chronic heart failure patients administered spironolactone plus furosemide and either enalapril maleate, losartan potassium or candesartan cilexetil. J Clin Pharm Ther 2005;30:603-610.
  • 105.Fujii H, Nakahama H, Yoshihara F et al. Life-threatening hyperkalemia during a combined therapy with the angiotensin receptor blocker candesartan and spironolactone. Kobe J Med Sci 2005;51:1-6.
  • 106.Miyahara Y, Miyazaki T, Tanaka Y et al. [A case of intraoperative hyperkalemia induced with administration of an angiotensin II receptor antagonist (AIIA) and intake of dried persimmons]. Masui 2004;53:543-546.View Abstract
  • 107.Bailie GR. Acute renal failure. In: Young LY, Kradjan WA, et al, eds. Applied Therapeutics: the Clinical Use of Drugs. 6th ed. Vancouver, W ash: Applied Therapeutics; 1995:29-33.
  • 108.Poirier TI. Reversible renal failure associated with ibuprofen: case report and review of the literature. Drug Intell Clin Pharm 1984;18:27-32.View Abstract
  • 109.Whelton A, Stout RL, Spilman PS, Klassen DK. Renal effects of ibuprofen, piroxicam, and sulindac in patients with asymptomatic renal failure: a prospective, randomized, crossover comparison. Ann Intern Med 1990;112:568-576.View Abstract
  • 110.Po SS, Wang DW, Yang IC et al. Modulation of HERG potassium channels by extracellular magnesium and quinidine. J Cardiovasc Pharmacol 1999;33:181-185.View Abstract
  • 111.Roden DM, Iansmith DH. Effects of low potassium or magnesium concentrations on isolated cardiac tissue. Am J Med 1987;82:18-23.View Abstract
  • 112.Sadowski DC. Drug interactions with antacids: mechanisms and clinical significance. Drug Saf 1994;11:395-407.View Abstract
  • 113.Teplick JG, Teplick SK, Ominsky SH, Haskin ME. Esophagitis caused by oral medication. Radiology 1980;134:23-25.View Abstract
  • 114.Eng J, Sabanathan S. Drug-induced esophagitis. Am J Gastroenterol 1991;86:1127-1133.View Abstract
  • 115.Jackson PR, Ramsay LE, Wakefield V. Relative potency of spironolactone, triamterene and potassium chloride in thiazide-induced hypokalaemia. Br J Clin Pharmacol 1982;14:257-263.View Abstract
  • 116.Sawyer N, Gabriel R. Progressive hypokalaemia in elderly patients taking three thiazide potassium-sparing diuretic combinations for thirty-six months. Postgrad Med J 1988;64:434-437.View Abstract
  • 117.Schnaper HW, Freis ED, Friedman RG et al. Potassium restoration in hypertensive patients made hypokalemic by hydrochlorothiazide. Arch Intern Med 1989;149:2677-2681.View Abstract
  • 118.Stepan VM, Hammer HF, Krejs GJ. Hyperkalaemia and diarrhoea in a patient with surreptitious ingestion of potassium sparing diuretics. Eur J Gastroenterol Hepatol 1997;9:1001-1004.View Abstract
  • 119.Greenberg S, Reiser IW, Chou SY, Porush JG. Trimethoprim-sulfamethoxazole induces reversible hyperkalemia. Ann Intern Med 1993;119:291-295.View Abstract
  • 120.Velazquez H, Perazella MA, Wright FS, Ellison DH. Renal mechanism of trimethoprim-induced hyperkalemia. Ann Intern Med 1993;119:296-301.View Abstract
  • 121.Perazella MA. Trimethoprim-induced hyperkalaemia: clinical data, mechanism, prevention and management. Drug Saf 2000;22:227-236.View Abstract
  • 122.Alappan R, Perazella MA, Buller GK. Hyperkalemia in hospitalized patients treated with trimethoprim-sulfamethoxazole. Ann Intern Med 1996;124:316-320.View Abstract
  • 123.Alappan R, Buller GK, Perazella MA. Trimethoprim-sulfamethoxazole therapy in outpatients: is hyperkalemia a significant problem? Am J Nephrol 1999;19:389-394.
  • 124.Choi MJ, Fernandez PC, Patnaik A et al. Brief report: trimethoprim-induced hyperkalemia in a patient with AIDS. N Engl J Med 1993;328:703-706.View Abstract
  • 125.Modest GA, Price B, Mascoli N. Hyperkalemia in elderly patients receiving standard doses of trimethoprim-sulfamethoxazole. Ann Intern Med 1994;120:437; author reply 438.View Abstract
  • 126.Pennypacker LC, Mintzer J, Pitner J. Hyperkalemia in elderly patients receiving standard doses of trimethoprim-sulfamethoxazole. Ann Intern Med 1994;120:437; author reply 438.View Abstract
  • 127.Canaday DH, Johnson JR. Hyperkalemia in elderly patients receiving standard doses of trimethoprim-sulfamethoxazole. Ann Intern Med 1994;120:437-438.View Abstract
  • 128.Koc M, Bihorac A, Ozener CI et al. Severe hyperkalemia in two renal transplant recipients treated with standard dose of trimethoprim-sulfamethoxazole. Am J Kidney Dis 2000;36:E18.View Abstract
  • 129.Smith MJH, Smith PK. The Salicylates: a Critical Bibliographic Review. New York: Interscience; 1966.
  • 130.Casis O, Espina L, Gallego M. Effects of amphetamine on calcium and potassium currents in rat heart. J Cardiovasc Pharmacol 2000;36:390-395.View Abstract
  • 131.Bowyer JF, Masserano JM, Weiner N. Inhibitory effects of amphetamine on potassium-stimulated release of [3H]dopamine from striatal slices and synaptosomes. J Pharmacol Exp Ther 1987;240:177-186.View Abstract
  • 132.Freed MI, Rastegar A, Bia MJ. Effects of calcium channel blockers on potassium homeostasis. Yale J Biol Med 1991;64:177-186.View Abstract
  • 133.Raab W. Cardiotoxic effects of emotional, socioeconomic, and environmental stresses. In: Bajusz E, Rona G, eds. Myocardiology. Vol I. Baltimore: University Park Press; 1970:707-713.
  • 134.Mathe V, Kassay G, Tuske M. [Results of glucose tolerance tests and changes in inorganic serum phosphate and potassium levels in schizophrenic patients responding to treatment with psychotropic drugs]. Int Pharmacopsychiatry 1971;6:111-130.View Abstract
  • 135.Aunsholt NA. Prolonged Q-T interval and hypokalemia caused by haloperidol. Acta Psychiatr Scand 1989;79:411-412.View Abstract
  • 136.Blood modifiers, anticoagulants, heparin. In: Threlkeld DS, ed. Facts and Comparisons Drug Information. St. Louis: Facts and Comparisons; June 1997:87a-87f.
  • 137.Matsumura M, Nakashima A, Tofuku Y. Electrolyte disorders following massive insulin overdose in a patient with type 2 diabetes. Intern Med 2000;39:55-57.View Abstract
  • 138.Kobler E, Nuesch HJ, Buhler H et al. [Drug-induced esophageal ulcers]. Schweiz Med Wochenschr 1979;109:1180-1182.View Abstract
  • 139.Mavromatis F. Tetracycline nephropathy: case report with renal biopsy. JAMA 1965;193:191-194.View Abstract
  • 140.Smith SR, Kendall MJ. Metabolic responses to beta 2 stimulants. J R Coll Physicians Lond 1984;18:190-194.View Abstract
  • 141.Cayton RM. Beta agonists and potassium. Lancet 1985;325:1395.
  • 142.Haalboom JR, Deenstra M, Struyvenberg A. Hypokalaemia induced by inhalation of fenoterol. Lancet 1985;1:1125-1127.View Abstract
  • 143.Deacon SP. Salbutamol and hypokalaemia. Lancet 1976;1:1302.View Abstract
  • 144.Wager J, Fredholm BB, Lunell NO, Persson B. Development of tolerance to oral salbutamol in the third trimester of pregnancy: a study of circulatory and metabolic effects. Br J Clin Pharmacol 1981;12:489-495.View Abstract
  • 145.Smith SR, Gove I, Kendall MJ et al. Beta agonists and potassium. Lancet 1985;325:1394-1395.
  • 146.Sydney MA. Ventricular arrhythmias associated with use of thioridazine hydrochloride in alcohol withdrawal. BMJ 1973;4:467.View Abstract
  • 147.Ryan MP. Interrelationships of magnesium and potassium homeostasis. Miner Electrolyte Metab 1993;19:290-295.View Abstract
  • 148.Dorup I, Skajaa K, Thybo NK. Oral magnesium supplementation restores the concentrations of magnesium, potassium and sodium-potassium pumps in skeletal muscle of patients receiving diuretic treatment. J Intern Med 1993;233:117-123.View Abstract
  • 149.Sansone RA. Complications of hazardous weight-loss methods. Am Fam Physician 1984;30:141-146.View Abstract
  • 150.Blumenthal M, Busse W, Goldberg A et al. The Complete German Commission E Monographs. Austin, Texas: American Botanical Council: Integrative Medicine Communications; 1998.
  • .[No authors listed.] Drug evaluation annual. Vol 3. Milwaukee: American Medical Association; 1993.
  • .Adu D, Michael J, Turney J, McMaster P. Hyperkalemia in cyclosporine-treated renal allograft recipients. Lancet 1983;2(8346):370.
  • .Agarwal R, Afzalpurkar R, et al. Pathophysiology of potassium absorption and secretion by the human intestine. Gastroenterology 1994;107(2):548-571. (Review)
  • .Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Semin Dial 2001;14(5):348-456. (Review)
  • .Akbarpour F, Afrasiabi A, Vaziri ND. Severe hyperkalemia caused by indomethacin and potassium supplementation. South Med J 1985;78(6):756-757.
  • .Aker S, Heering P, Kinne-Saffran E, et al. Different effects of cyclosporine a and FK506 on potassium transport systems in MDCK cells. Exp Nephrol 2001;9(5):332-340.
  • .Alpern RJ, Sakhaee K. The clinical spectrum of chronic metabolic acidosis: homeostatic mechanisms produce significant morbidity. Am J Kidney Dis 1997;29:291-302.
  • .Ames BN. Micronutrient deficiencies: a major cause of DNA damage. Ann N Y Acad Sci 2000;889:87-106.
  • .Andersson B, Behnam-Motlagh P, Henriksson R, et al. Pharmacological modulation of lung cancer cells for potassium ion depletion. Anticancer Res 2005;25(4):2609-2616.
  • .Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure: DASH Collaborative Research Group. N Engl J Med 1997;336(16):1117-1124.
  • .Apstein C. Glucose-insulin-potassium for acute myocardial infraction: remarkable results from a new prospective, randomized trial. Circulation 1998;98:2223-2226.
  • .Apstein CS, Opie Lh. Glucose-insulin-potassium (GIK) for acute myocardial infarction: a negative study with a positive value. Cardiovasc Drugs Ther 1999;13(3):185-189.
  • .Arnett, T. Regulation of bone cell function by acid-base balance. Proc Nutr Soc 2002;62:511-520.
  • .Ascherio A, Rimm EB, Hernan MA, et al. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men. Circulation 1998;98(12):1198-1204.
  • .Bakris GL, Siomos M, Richardson D, et al. ACE inhibition or angiotensin receptor blockade: impact on potassium in renal failure: VAL-K Study Group. Kidney Int 2000;58:2084-2092.
  • .Bandyopadhyay S, Banerjee S. Severe hyperkalaemia with normal electrocardiogram. Int J Clin Pract 2001;55:486-487.
  • .Barden A, Beilin LJ, Vandongen R, et al. A double-blind placebo-controlled trial of the effects of short-term potassium supplementation on blood pressure and atrial natriuretic peptide in normotensive women. Am J Hypertens 1991;4(3 Pt 1):206-213.
  • .Barri YM, Wingo CS. The effects of potassium depletion and supplementation on blood pressure: a clinical review. Am J Med Sci 1997;314(1):37-40.
  • .Bauer JH, Reams G. Short- and long-term effects of calcium entry blockers on the kidney. Am J Cardiol 1987;59(2):66A-71A. (Review)
  • .Bazzano LA, He J, Ogden LG, et al. Dietary potassium intake and risk of stroke in US men and women: National Health and Nutrition Examination Survey I epidemiologic follow-up study. Stroke 2001;32(7):1473-1480.
  • .Berul CI, Morad M. Regulation of potassium channels by nonsedating antihistamines. Circulation 1995;91(8):2220-2225.
  • .Beyer FR, Dickinson HO, Nicolson DJ, et al. Combined calcium, magnesium and potassium supplementation for the management of primary hypertension in adults. Cochrane Database Syst Rev 2006;3:CD004805. (Review)
  • .Bowyer JF, Masserano JM, Weiner N. Inhibitory effects of amphetamine on potassium-stimulated release of [3H]dopamine from striatal slices and synaptosomes. J Pharmacol Exp Ther 1987;240(1):177-186.
  • .Bradberry SM, Vale JA. Disturbances of potassium homeostasis in poisoning. J Toxicol Clin Toxicol 1995;33(4):295-310. (Review)
  • .Brancati FL, Appel LJ, Seidler AJ, et al. Effect of potassium supplementation on blood pressure in African Americans on a low-potassium diet: a randomized, double-blind, placebo-controlled trial. Arch Intern Med 1996;156:61-67.
  • .Brater DC. Effects of nonsteroidal anti-inflammatory drugs on renal function: focus on cyclooxygenase-2-selective inhibition. Am J Med 1999;107(6A):65S-70S.
  • .Brody T. Nutritional biochemistry. 2nd ed. San Diego: Academic Press; 1999. (Review)
  • .Bugge JF. Severe hyperkalaemia induced by trimethoprim in combination with an angiotensin-converting enzyme inhibitor in a patient with transplanted lungs. J Intern Med 1996;240(4):249-251.
  • .Buist RA. Drug-nutrient interactions: an overview. Int Clin Nutr Rev 1984;4(3):114. (Review)
  • .Burgess E, Lewanczuk R, Bolli P, et al. Lifestyle modifications to prevent and control hypertension:6: recommendations on potassium, magnesium and calcium: Canadian Hypertension Society, Canadian Coalition for High Blood Pressure Prevention and Control, Laboratory Centre for Disease Control at Health Canada, Heart and Stroke Foundation of Canada. CMAJ 1999;160(9 Suppl):S35-S45.
  • .Bushinsky DA, Gavrilov K, Chabala JM, et al. Effect of metabolic acidosis on the potassium content of bone. J Bone Miner Res 1997;12:1664-1671.
  • .Cappuccio FP, MacGregor DA. Does potassium supplementation lower blood pressure? A meta-analysis of published trials. J Hypertens 1991;9:465-473. (Meta-analysis)
  • .Caudarella R, Vescini F, Buffa A, et al. Citrate and mineral metabolism: kidney stones and bone disease. Front Biosci 2003;8:1085-1106.
  • .Chakko SC, Frutchey J, Gheorghiade M. Life-threatening hyperkalemia in severe heart failure. Am Heart J 1989;117(5):1083-1091.
  • .Chang HY, Hu YW, Yue CS, et al. Effect of potassium-enriched salt on cardiovascular mortality and medical expenses of elderly men. Am J Clin Nutr 2006;83(6):1289-1296.
  • .Chau L, Ratnaike RN. Drug-associated nutritional problems in older persons. Rev Clin Gerontol 2003;13:183-193. (Review)
  • .Choi CS, Lee FN, McDonough AA, et al. Independent regulation of in vivo insulin action on glucose versus K+ uptake by dietary fat and K+ content. Diabetes 2002;51:915-920.
  • .Clark BA, Brown RS. Potassium homeostasis and hyperkalemic syndromes. Endocrinol Metab Clin North Am 1995;24(3):573-591. (Review)
  • .Cohen L. Potassium replacement associated with the development of tetany in a patient with hypomagnesaemia. Magnes Res 1993;6(1):43-45.
  • .Cox M. Potassium homeostasis. Med Clin North Am 1981;65(2):363-384. (Review)
  • .Cruz CS, Cruz AA, Marcilio de Souza CA. Hyperkalaemia in congestive heart failure patients using ACE inhibitors and spironolactone. Nephrol Dial Transplant 2003;18:1814-1819.
  • .Curhan GC, Willett WC, Rimm EB, et al. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med 1993;328(12):833-838.
  • .Curhan GC, Willett WC, Speizer FE, et al. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med 1997;126(7):497-504.
  • .Davis BR, Oberman A, Blaufox MD, et al. Lack of effectiveness of a low-sodium/high-potassium diet in reducing antihypertensive medication requirements in overweight persons with mild hypertension:TAIM Research Group:Trial of Antihypertensive Interventions and Management. Am J Hypertens 1994;7:926-932.
  • .Demigné C, Sabboh H, Puel C, et al. Organic anions and potassium salts in nutrition and metabolism. Nutr Res Rev 2004;17(2):249-258.
  • .Demigné C, Sabboh H, Rémésy C, et al. Protective effects of high dietary potassium: nutritional and metabolic aspects. J Nutr 2004;134(11):2903-2906. (Review)
  • .Deutsch C. Potassium channel ontogeny. Annu Rev Physiol 2002;64:19-46. (Review)
  • .Dickey RA, Janick JJ. Lifestyle modifications in the prevention and treatment of hypertension. Endocr Pract 2001;7(5):392-399. (Review)
  • .Dickinson HO, Nicolson DJ, Campbell F, et al. Potassium supplementation for the management of primary hypertension in adults. Cochrane Database Syst Rev 2006;3:CD004641. (Review)
  • .Djurhuus MS, Vaag A, Klitgard NA. Muscle sodium, potassium, and [(3H)]ouabain binding in identical twins, discordant for type 2 diabetes. J Clin Endocrinol Metab 2001;86:859-866.
  • .Domrongkitchaiporn S, Stitchantrakul W, Kochakarn W. Causes of hypocitraturia in recurrent calcium stone formers: focusing on urinary potassium excretion. Am J Kidney Dis 2006;48(4):546-554.
  • .Dorph S, Oigaard A. [Effect of triamterene on serum potassium and serum creatinine in long-term treatment with thiazides.] Nord Med 1968;79(16):516-518. [Danish]
  • .Dos Santos P, Kowaltowski AJ, Laclau MN, et al. Mechanisms by which opening the mitochondrial ATP- sensitive K(+) channel protects the ischemic heart. Am J Physiol Heart Circ Physiol 2002;283(1):H284-295.
  • .Dyckner T, Wester PO. Ventricular extrasystoles and intracellular electrolytes before and after potassium and magnesium infusions in patients on diuretic treatment. Am Heart J 1979;97(1):12-18.
  • .Dyckner T, Wester PO. Ventricular extrasystoles and intracellular electrolytes in hypokalemic patients before and after correction of the hypokalemia. Acta Med Scand 1978;204(5):375-379.
  • .Elisaf M, Milionis H, Siamopoulos KC. Hypomagnesemic hypokalemia and hypocalcemia: clinical and laboratory characteristics. Miner Electrolyte Metab 1997;23(2):105-112.
  • .Epstein W. The roles and regulation of potassium in bacteria. Prog Nucleic Acid Res Mol Biol 2003;75:293-320.
  • .Evans KJ, Greenberg A. Hyperkalemia: a review. J Intensive Care Med 2005;20(5):272-290. (Review)
  • .Evans KJ, Reddan DN, Szczech LA. Nondialytic management of hyperkalemia and pulmonary edema among end-stage renal disease patients: an evaluation of the evidence. Semin Dial 2004;17(1):22-29. (Review)
  • .Ewe K. Influence of diphenolic laxatives on water and electrolyte permeation in man. Monograph 1977:420-426.
  • .Fang J, Madhavan S, Alderman MH. Dietary potassium intake and stroke mortality. Stroke 2000;31(7):1532-1537.
  • .Féraille E, Mordasini D, Gonin S, et al. Mechanism of control of Na,K-ATPase in principal cells of the mammalian collecting duct. Ann N Y Acad Sci 2003;986:1-9.
  • .Floris-Moore MA, Amodio-Groton MI, Catalano MT. Adverse reactions to trimethoprim/sulfamethoxazole in AIDS. Ann Pharmacother 2003;37(12):1810-1813.
  • .Flynn JT, Bunchman TE, Sherbotie JR. Indications, results, and complications of tacrolimus conversion in pediatric renal transplantation. Pediatr Transplant 2001;5(6):439-446.
  • .Follmer CH, Colatsky TJ. Block of delayed rectifier potassium current, IK, by flecainide and E-4031 in cat ventricular myocytes. Circulation 1990;82(1):289-293.
  • .Food and Nutrition Board, Institute of Medicine. Potassium:dietary reference intakes for water, potassium, sodium, chloride, and sulfate. Washington, DC: National Academies Press; 2004:173-246.
  • .Fotherby MD, Potter JF. Potassium supplementation reduces clinic and ambulatory blood pressure in elderly hypertensive patients. J Hypertens 1992;10:1403-1408.
  • .Frassetto LA, Morris RC, Sellmeyer DE, et al. Diet, evolution and aging: the physiopathologic effects of post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. Eur J Nutr 2001;40:200-213.
  • .Garland HO, Phipps DJ, Harpur ES. Gentamicin-induced hypercalciuria in the rat: assessment of nephron site involved. J Pharmacol Exp Ther 1992;263(1):293-297.
  • .Garlid KD, Dos Santos P, Xie ZJ, et al. Mitochondrial potassium transport: the role of the mitochondrial ATP-sensitive K(+) channel in cardiac function and cardioprotection. Biochim Biophys Acta 2003;1606(1-3):1-21. (Review)
  • .Garlid KD, Paucek P. Mitochondrial potassium transport: the K(+) cycle. Biochim Biophys Acta 2003;1606(1-3):23-41. (Review)
  • .Gennari FJ. Disorders of potassium homeostasis: hypokalemia and hyperkalemia. Crit Care Clin 2002;18(2):273-288,vi. (Review)
  • .Gennari FJ. Hypokalemia. N Engl J Med 1998;339(7):451-458.
  • .Giebisch G. A trail of research on potassium. Kidney Int 2002;62:1498-1512.
  • .Giebisch G. Renal potassium transport: mechanisms and regulation. Am J Physiol 1998;274:F817-F833.
  • .Gilliland FD, Berhane KT, Li YF, et al. Dietary magnesium, potassium, sodium, and children’s lung funtion. Am J Epidemiol 2002;155(2):125-131.
  • .Goldszer RC, Coodley EL, Rosner MJ, et al. Hyperkalemia associated with indomethacin. Arch Intern Med 1981;141(6):802-804.
  • .Good CB, McDermott L, McCloskey B. Diet and serum potassium in patients on ACE inhibitors. JAMA 1995;274(7):538. (Letter)
  • .Gosmanov AR, Thomason DB. Insulin and isoproterenol differentially regulate mitogen-activated protein kinase-dependent Na+-K+-2Cl- cotransporter activity in skeletal muscle. Diabetes 2002;51:615-623.
  • .Greenberg A. Hyperkalemia: treatment options. Semin Nephrol 1998;18(1):46-57. (Review)
  • .Grobbee DE, Hofman A, Roelandt JT, et al. Sodium restriction and potassium supplementation in young people with mildly elevated blood pressure. J Hypertens 1987;5:115-119.
  • .Gu D, He J, Wu X, et al. Effect of potassium supplementation on blood pressure in Chinese: a randomized, placebo-controlled trial. J Hypertens 2001;19(7):1325-1331.
  • .Guven M, Onaran I, Ulutin T, et al. Effect of acute hyperglycemia on potassium (86Rb+) permeability and plasma lipid peroxidation in subjects with normal glucose tolerance. J Endocrinol Investig 2001;24:231-235.
  • .Hajjar IM, Grim CE, George V, et al. Impact of diet on blood pressure and age-related changes in blood pressure in the US population: analysis of NHANES III. Arch Intern Med 2001;161(4):589-593.
  • .Harrington M, Cashman KD. High salt intake appears to increase bone resorption in postmenopausal women but high potassium intake ameliorates this adverse effect. Nutr Rev 2003;61:179-183.
  • .Hartmann RC, Auditore JV, Jackson DP. Hyperkalemia due to release of potassium from platelets during coagulation. J Clin Invest 1958;37:699.
  • .Heering P, Grabensee B. Influence of ciclosporin A on renal tubular function after kidney transplantation. Nephron 1991;59(1):66-70.
  • .Hendler SS, Rorvik DR, eds. PDR for nutritional supplements. Montvale, NJ: Medical Economics Company, Inc; 2001. (Review)
  • .Herman E, Rado J. Fatal hyperkalemic paralysis associated with spironalactone: observation on a patient with severe renal disease and refractory edema. Arch Neurol 1966;15(1):74-77.
  • .Herman E, Rado J. [Hyperkalemia with fatal paralysis in a diabetic patient treated with aldactone.] Orv Hetil 1967;108(2):74-76. [Hungarian]
  • .Hermansen K. Diet, blood pressure and hypertension. Br J Nutr 2000:83(Suppl 1):S113-119.
  • .Higgins R, Ramaiyan K, Dasgupta T, et al. Hyponatraemia and hyperkalaemia are more frequent in renal transplant recipients treated with tacrolimus than with cyclosporin: further evidence for differences between cyclosporin and tacrolimus nephrotoxicities. Nephrol Dial Transplant 2004;19(2):444-450.
  • .Hijazi N, Abalkhail B, Seaton A. Diet and childhood asthma in a society in transition: a study in urban and rural Saudi Arabia. Thorax 2000;55:775-779.
  • .Holbrook JT, Cottrell SL, Smith JC Jr. Correlations of changes in dietary potassium and sodium with blood pressure during a one-year study. Am J Clin Nutr 1984;40(6 Suppl):1390-1392.
  • .Holbrook JT, Patterson KY, Bodner JE, et al. Sodium and potassium intake and balance in adults consuming self-selected diets. Am J Clin Nutr 1984;40(4):786-793.
  • .Hollander-Rodriguez JC, Calvert JF Jr. Hyperkalemia. Am Fam Physician 2006;73(2):283-290. (Review)
  • .Holt GA. Food and drug interactions. Chicago: Precept Press;1998.
  • .Howes LG. Which drugs affect potassium? Drug Saf 1995;12(4):240-244.
  • .Hylander B. Survival of extreme hyperkalemia. Acta Med Scand 1987;221(1):121-123.
  • .Iso H, Stampfer MJ, Manson JE, et al. Prospective study of calcium, potassium, and magnesium intake and risk of stroke in women. Stroke 1999;30(9):1772-1779.
  • .Joint National Committee. Sixth report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. Arch Int Med 1997;157:2413-2446.
  • .Jones G, Riley MD, Whiting S. Association between urinary potassium, urinary sodium, current diet, and bone density in prepubertal children. Am J Clin Nutr 2001;73:839-844.
  • .Joshipura KJ, Ascherio A, Manson JE, et al. Fruit and vegetable intake in relation to risk of ischemic stroke. JAMA 1999;282(13):1233-1239.
  • .Juurlink DN, Mamdani M, Kopp A, et al. Drug-drug interactions among elderly patients hospitalized for drug toxicity. JAMA 2003;289:1652-1658.
  • .Juurlink DN, Mamdani MM, Lee DS, et al. Rates of hyperkalemia after publication of the Randomized Aldactone Evaluation Study. N Engl J Med 2004;351:543-551.
  • .Kang D, et al. Lemonade-based dietary manipulation in patients with hypocitraturic nephrolithiasis. Abstract 1038. American Urological Association 101st Annual Meeting.Atlanta, May 25, 2006.
  • .Kendler BS. Recent nutritional approaches to the prevention and therapy of cardiovascular disease. Prog Cardiovasc Nurs 1997;12(3):3-23.
  • .Kerr DJ, McAlpine LG, Dagg JH. Pseudohyperkalaemia. BMJ 1985;291:890-891.
  • .Khaw KT, Thom S. Randomized double-blind crossover trial of potassium on blood pressure in normal subjects. Lancet 1982;2:1127-1129.
  • .Kim HC, Hwang EA, Han SY, et al. Primary immunosuppression with tacrolimus in kidney transplantation: three-year follow-up in a single center. Transplant Proc 2004;36(7):2082-2083.
  • .Kosek JC, Mazze RI, Cousins MJ. Nephrotoxicity of gentamicin. Lab Invest 1974;30(1):48-57.
  • .Krauss RM, Eckel RH, Howard B, et al. AHA dietary guidelines: revision 2000: a statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation 2000;102:2284-2299.
  • .Lemann J Jr, Pleuss JA, Gray RW. Potassium causes calcium retention in healthy adults. J Nutr 1993;123(9):1623-1626.
  • .Lenz T, Becker B, Bergner R. [Potassium in renal disease.] Med Klin (Munich) 2004;99(7):355-361. [German]
  • .Liu S, Manson JE, Lee IM, et al. Fruit and vegetable intake and risk of cardiovascular disease: the Women’s Health Study. Am J Clin Nutr 2000;72(4):922-928.
  • .Lotz M, Zisman E, Bartter FC. Evidence for a phosphorus-depletion syndrome in man. N Eng J Med 1968;278:409.
  • .MacCarthy EP, Frost GW, Strokes GS. Indomethacin-induced hyperkalaemia. Med J Aust 1979;1(12):550.
  • .Mactier RA, Khanna R. Hyperkalemia induced by indomethacin and naproxen and reversed by fludrocortisone. South Med J 1988;81(6):799-801.
  • .Mandal AK. Hypokalemia and hyperkalemia. Med Clin North Am 1997;81(3):611-639.
  • .Marinella MA. Trimethoprim-induced hyperkalemia: an analysis of reported cases. Gerontology 1999;45(4):209-212.
  • .Markovich D, Wang H, Puttaparthi K, et al. Chronic K depletion inhibits renal brush border membrane Na/sulfate cotransport. Kidney Int 1999;55:244-251.
  • .Marz R. Medical nutrition from Marz. 2nded. Portland, OR: Omni Press; 1997.
  • .McCarron DA, Reussner ME. Are low intakes of calcium and potassium important causes of cardiovascular disease? Am J Hypertens 2001;14:206S-212S.
  • .Macdonald JE, Struthers AD. What is the optimal serum potassium level in cardiovascular patients? J Am Coll Cardiol 2004;43(2):155-161. (Review)
  • .McDonough AA, Thompson CB, Youn JH. Skeletal muscle regulates extracellular potassium. Am J Physiol 2002;282:F967-F974.
  • .McKenna MJ, Harmer AR, Fraser SF, et al. Effects of training on potassium, calcium and hydrogen ion regulation in skeletal muscle and blood during exercise. Acta Physiol Scand 1996;156(3):335-346. (Review)
  • .McLean, R. Magnesium and its therapeutic uses: a review. Am J Med 1994;96(1):63-76. (Review)
  • .Meneton P, Loffing J, Warnock DG. Sodium and potassium handling by the aldosterone-sensitive distal nephron: the pivotal role of the distal and connecting tubule. Am J Physiol 2004;287:F593-F601.
  • .Meneton P, Schultheis PJ, Greeb J, et al. Increased sensitivity to K+ deprivation in colonic H,K-ATPase-deficient mice. J Clin Investig 1998;101:536-542.
  • .Mironova GD, Negoda AE, Marinov BS, et al. Functional distinctions between the mitochondrial ATP-dependent K+ channel (mitoKATP) and its inward rectifier subunit (mitoKIR). J Biol Chem 2004;279(31):32562-32568.
  • .Miyachi Y, Niwa Y. Effects of potassium iodide, colchicine and dapsone on the generation of polymorphonuclear leukocyte-derived oxygen intermediates. Br J Dermatol 1982;107(2):209-214.
  • .Montie T, Patamasucon P. Aminoglycosides: the complex problem of antibiotic mechanisms and clinical applications. Eur J Clin Microbiol Infect Dis 1995;14:85-87. (Editorial)
  • .Morganti A. Should a diuretic always be the first choice in patients with essential hypertension? The case for no. J Am Soc Nephrol 2005;16(3 Suppl 1):S70-S73.
  • .Morita H, Fujiki N, Miyahara T, et al. Hepatoportal bumetanide-sensitive K+-sensor mechanism controls urinary K+ excretion. Am J Physiol 2000;278:R1134-R1139.
  • .Morris RC, Frassetto LA, Schmidlin O, et al. Expression of osteoporosis as determined by diet-disordered electrolyte and acid-base metabolism. In: Burkhardt P, Dawson-Hughes B, Heaney R, eds. Nutritional aspects of osteoporosis. San Diego: Academic Press; 2001:357-378.
  • .Morris RC, Jr, Schmidlin O, Tanaka M, et al. Differing effects of supplemental KCl and KHCO3: pathophysiological and clinical implications. Semin Nephrol 1999;19(5):487-493.
  • .Nakada S, et al. Medical management of calcium oxalate stone formers with lemonade results in therapeutic urinary citrate and higher urine volumes than those on potassium citrate. Abstract 1537. American Urological Association 101st Annual Meeting.Atlanta, May 25, 2006.
  • .New SA. Intake of fruit and vegetables: implications for bone health. Proc Nutr Soc 2003;62:859-899.
  • .New SA, Bolton-Smith C, Grubb DA, et al. Nutritional influences on bone mineral density: a cross-sectional study in premenopausal women. Am J Clin Nutr 1997;65(6):1831-1839.
  • .New SA, Robins SP, Campbell MK, et al. Dietary influences on bone mass and bone metabolism: further evidence of a positive link between fruit and vegetable consumption and bone health? Am J Clin Nutr 2000;71(1):142-151.
  • .Nielsen H, Landbo K. [Hypokalemia, myopathy with myoglobinuria after prolonged ingestion of licorice.] Ugeskr Laeger 1970;132(38):1778-1780. [Danish]
  • .Nieves JW. Osteoporosis: the role of micronutrients. Am J Clin Nutr 2005;81(5):1232S-1239S. (Review)
  • .Nishizaka MK, Zaman MA, Calhoun DA. Efficacy of low-dose spironolactone in subjects with resistant hypertension. Am J Hypertens 2003;16:925-930.
  • .Olukoga A, Donaldson D. Liquorice and its health implications. J R Soc Health 2000;120(2):83-89.
  • .Overlack A, Maus B, Ruppert M, et al. Potassium citrate versus potassium chloride in essential hypertension: effects on hemodynamic, hormonal and metabolic parameters. Dtsch Med Wochenschr 1995;120:631-635. [German; English abstract]
  • .Pajor AM. Sodium-coupled transporters for Krebs cycle intermediates. Annu Rev Physiol 1999;61:663-682.
  • .Pamnati MB, Bryant HJ, Clough DL, et al. Increased dietary potassium and magnesium attenuate experimental volume dependent hypertension possibly through endogenous sodium-potassium pump inhibitor. Clin Exp Hypertens 2003;25:103-115.
  • .Patki PS, Singh J, Gokhale SV, et al. Efficacy of potassium and magnesium in essential hypertension: a double-blind, placebo controlled, crossover study. BMJ 1990;301(6751):521-523.
  • .Paucek P, Jaburek M. Kinetics and ion specificity of Na(+)/Ca(2+) exchange mediated by the reconstituted beef heart mitochondrial Na(+)/Ca(2+) antiporter. Biochim Biophys Acta 2004;1659(1):83-91.
  • .Perazella MA. Hyperkalemia in the elderly: a group at high risk. Conn Med 1996;60(4):195-198.
  • .Perazella MA, Mahnensmith RL. Hyperkalemia in the elderly: drugs exacerbate impaired potassium homeostasis. J Gen Intern Med 1997;12(10):646-656. (Review)
  • .Perazella MA, Mahnensmith RL. Trimethoprim-sulfamethoxazole: hyperkalemia is an important complication regardless of dose. Clin Nephrol 1996;46(3):187-192. (Review)
  • .Perlmutter EP, Sweeney D, Herskovits G, et al. Case report: severe hyperkalemia in a geriatric patient receiving standard doses of trimethoprim-sulfamethoxazole. Am J Med Sci 1996;311(2):84-85.
  • .Peterson LN. Potassium in nutrition. In: O’Dell BL, Sunde RA, eds. Handbook of nutritionally essential minerals. New York: Marcel Dekker, Inc; 1997:153-183.
  • .Preston RA, Hirsh MJ, Oster JR, et al. University of Miami Division of Clinical Pharmacology therapeutic rounds: drug-induced hyperkalemia. Am J Ther 1998;5(2):125-132.
  • .Prevot A, Martini S, Guignard JP. In utero exposure to immunosuppressive drugs. Biol Neonate 2002;81(2):73-81. (Review)
  • .Pronsky Z. Powers and Moore’s food-medications interactions. 9thed. Pottstown, PA: Food-Medication Interactions; 1991. (Review)
  • .Rabinowitz L, Sarason RL, Yamauchi H, et al. Time course of adaptation to altered K intake in rats and sheep. Am J Physiol 1984;247:F607-F617.
  • .Rabinowitz L. Homeostatic regulation of potassium excretion. J Hypertens 1989;7:433-442.
  • .Ray K, Dorman S, Watson R. Severe hyperkalemia due to the concomitant use of salt substitutes and ACE inhibitors in hypertension: a potentially life threatening interaction. J Hum Hypertens 1999;13(10):717-720.
  • .Reif S, Klein I, Lubin F, et al. Pre-illness dietary factors in inflammatory bowel disease. Gut 1997;40:754-760.
  • .Remer T, Manz F. Potential renal acid load of foods and its influence on urine pH. J Am Diet Assoc 1995;95:791-797.
  • .Remer T. Influence of diet on acid-base balance. Semin Dial 2000;13:221-226.
  • .Reiser IW, Chou SY, Brown MI, et al. Reversal of trimethoprim-induced antikaliuresis. Kidney Int 1996;50(6):2063-2069.
  • .Resnick LM. Cellular ions in hypertension, insulin resistance, obesity and diabetes: an unifying theme. J Am Soc Nephrol 1992;3:S78-S85.
  • .Robinson C, Weigly E. Basic nutrition and diet therapy. New York: MacMillan; 1984. (Review)
  • .Roe DA. Diet and drug interactions. New York: Van Nostrand Reinhold;1989. (Review)
  • .Roe DA. Drug-induced nutritional deficiencies. 2nd ed. Westport, CT: Avi Publishing;1985. (Review)
  • .Roe DA. Risk factors in drug-induced nutritional deficiencies. In: Roe DA, Campbell T, eds. Drugs and nutrients: the interactive effects. New York: Marcel Decker;1984:505-523. (Review)
  • .Rosenkranz RP, McClelland DL, Roszkowski AP. Effects of nicardipine, nifedipine, verapamil, and diltiazem on urine volume, sodium and potassium excretion and plasma aldosterone levels in the rat. Proc West Pharmac ol Soc 1984;27:67-72.
  • .Ryan MP. Interrelationships of magnesium and potassium homeostasis. Miner Electrolyte Metab 1993;19(4-5):290-295.
  • .Sabboh H, Besson C, Tressol JC, et al. Organic potassium salts or fibers effects on mineral balance and digestive fermentations in rats adapted to an acidogenic diet. Eur J Nutr 2006;45(6):342-348.
  • .Sacks FM, Brown LE, Appel L, et al. Combinations of potassium, calcium, and magnesium supplements in hypertension. Hypertension 1995;26(6 Pt 1):950-956.
  • .Sacks FM, Obarzanek E, Windhauser MM, et al. Rationale and design of the Dietary Approaches to Stop Hypertension trial (DASH): amulticenter controlled-feeding study of dietary patterns to lower blood pressure. Ann Epidemiol 1995;5(2):108-118.
  • .Sacks FM, Willett WC, Smith A, et al. Effect on blood pressure of potassium, calcium, and magnesium in women with low habitual intake. Hypertension 1998;31(1):131-138.
  • .Saito N, Kuchiba A. The changes of magnesium under high salt diets and by administration of antihypertensive diuretics. Magnes Bull 1987;9:53.
  • .Salem MM, Rosa RM, Batlle DC. Extrarenal potassium tolerance in chronic renal failure: implications for the treatment of acute hyperkalemia. Am J Kidney Dis 1991;18(4):421-440. (Review)
  • .Schaefer M, Link J, Hannemann L, et al. Excessive hypokalemia and hyperkalemia following head injury. Intensive Care Med 1995;21(3):235-237.
  • .Schaefer TJ, Wolford RW. Disorders of potassium. Emerg Med Clin North Am 2005;23(3):723-747,viii-ix. (Review)
  • .Schlanger LE, Kleyman TR, Ling BN. K(+)-sparing diuretic actions of trimethoprim: inhibition of Na+ channels in A6 distal nephron cells. Kidney Int 1994;45:1070-1076.
  • .Schmidt A, Gruber U, Bohmig G, et al. The effect of ACE inhibitor and angiotensin II receptor antagonist therapy on serum uric acid levels and potassium homeostasis in hypertensive renal transplant recipients treated with CsA. Nephrol Dial Transplant 2001;16(5):1034-1037.
  • .Schwartz AB. Potassium-related cardiac arrhythmias and their treatment. Angiology. 1978;29(3):194-205.
  • .Seah TG, Lew TW, Chin NM. A case of pseudohyperkalaemia and thrombocytosis. Ann Acad Med Singapore 1998;27:442-443.
  • .Sebastian A, Harris ST, Ottaway JH, et al. Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. N Engl J Med 1994;330(25):1776-1781.
  • .Sheng H-W. Sodium, chloride and potassium. In: Stipanuk M, ed. Biochemical and physiological aspects of human nutrition. Philadelphia: WB Saunders; 2000:686-710.
  • .Sica DA. Antihypertensive therapy and its effects on potassium homeostasis. J Clin Hypertens (Greenwich) 2006;8(1):67-73. (Review)
  • .Sica DA. Eplerenone and serum potassium change: relationship to renal function. Am J Hypertens 2003;16(Suppl 1):A100.
  • .Sica DA, Hess M. Pharmacotherapy in congestive heart failure: aldosterone receptor antagonism: interface with hyperkalemia in heart failure. Congest Heart Fail 2004;10:259-264.
  • .Singer GG, Brenner BM. Fluid and electrolyte disturbances. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison’s principles of internal medicine. 14th ed. New York: McGraw-Hill; 1998:269.
  • .Singh RB, Singh NK, Niaz MA, et al. Effect of treatment with magnesium and potassium on mortality and reinfarction rate of patients with suspected acute myocardial infarction. Int J Clin Pharmacol Ther 1996;34:219-225.
  • .Skinner SL. A cause of erroneous potassium levels. Lancet 1961;i:478-480.
  • .Sugarman A, Kahn T. Calcium channel blockers enhance extrarenal potassium disposal in the rat. Am J Physiol 1986;250(4 Pt 2):F695-701.
  • .Suter PM. Potassium and hypertension. Nutr Rev 1998;56:151-133. (Review)
  • .Sweeney G, Klip A. Mechanisms and consequences of Na+,K+-pump regulation by insulin and leptin. Cell Mol Biol 2001;47:363-372.
  • .Tamirisa KP, Aaronson KD, Koelling TM. Spironolactone-induced renal insufficiency and hyperkalemia in patients with heart failure. Am Heart J 2004;148:971-978.
  • .Tan SY, Burton M. Hyporeninemic hypoaldosteronism: an overlooked cause of hyperkalemia. Arch Intern Med 1981;141(1):30-33.
  • .Taylor DO, Barr ML, Radovancevic B, et al. A randomized, multicenter comparison of tacrolimus and cyclosporine immunosuppressive regimens in cardiac transplantation: decreased hyperlipidemia and hypertension with tacrolimus. J Heart Lung Transplant 1999;18(4):336-345.
  • .Textor SC, Bravo EL, Fouad FM, Tarazi RC. Hyperkalemia in azotemic patients during angiotensin-converting enzyme inhibition and aldosterone reduction with captopril. Am J Med 1982;73(5):719-725.
  • .Threlkeld DS, ed. Anti-infectives, tetracyclines. In: Facts and comparisons drug information. St Louis: Facts and Comparisons;1989.
  • .Threlkeld DS, ed. Diuretics and cardiovasculars, antihyperlipidemic agents, HMG-CoA reductase inhibitors. In: Facts and comparisons drug information. St Louis: Facts and Comparisons;1998.
  • .Threlkeld DS, ed. Hormones, adrenal cortical steroids, glucocorticoids. In: Facts and comparisons drug information. St Louis: Facts and Comparisons;1991.
  • .Threlkeld DS, ed. Respiratory drugs, bronchodilators, sympathomimetics. In Facts and comparisons drug information. St Louis: Facts and Comparisons;1994:174a-175.
  • .Toffaletti J. Electrolytes, divalent cations, and blood gases (magnesium). Anal Chem 1991;63(12):192R-194R.
  • .Trinchieri A, Zanetti G, Curro A, et al. Effect of potential renal acid load of foods on calcium metabolism of renal calcium stone formers. Eur Urol 2001;39(Suppl 2):33-36.
  • .Trovato A, Nuhlicek DN, Midtling JE. Drug-nutrient interactions. Am Fam Physician 1991;44(5):1651-1658.(Review)
  • .Tsuruoka S, Schwartz GJ, Ioka T, et al. Citrate reverses cyclosporin A-induced metabolic acidosis and bone resorption in rats. Am J Nephrol 2005;25(3):233-239.
  • .Tucker KL, Hannan MT, Chen H, et al. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999;69(4):727-736.
  • .USDA. Composition of foods: USDA handbook #8. Washington, DC:ARS, USDA;1976-1986.
  • .Wang DW, Sato T, Arita M. Voltage dependent inhibition of ATP sensitive potassium channels by flecainide in guinea pig ventricular cells. Cardiovasc Res 1995;29(4):520-525.
  • .Wasan KM, Wong JC, Corr T, et al. Role of plasma lipids and lipoproteins in predicting amphotericin B-induced nephrotoxicity in pediatric oncology patients. Cancer Chemother Pharmacol 2006;57(1):120-124.
  • .Weisberg LS, Szerlip HM, Cox M. Disorders of potassium homeostasis in critically ill patients. Crit Care Clin 1987;3(4):835-854. (Review)
  • .Werbach MR. Foundations of nutritional medicine. Tarzana, CA: Third Line Press;1997. (Review)
  • .Whang R, Whang DD, Ryan MP. Refractory potassium repletion: a consequence of magnesium deficiency. Arch Intern Med 1992;152:40-45. (Review)
  • .Whelton PK, He J. Potassium in preventing and treating high blood pressure. Semin Nephrol 1999;19(5):494-499. (Meta-analysis)
  • .Whelton PK, He J, Cutler JA, et al. Effects of oral potassium on blood pressure: meta-analysis of randomized controlled clinical trials. JAMA 1997;277(20):1624-1632.
  • .Witt JM, Koo JM, Danielson BD. Effect of standard-dose trimethoprim/sulfamethoxazole on the serum potassium concentration in elderly men. Ann Pharmacother 1996;30(4):347-350.
  • .Wright LF, DuVal JW Jr. Renal injury associated with laxative abuse. South Med J 1987;80(10):1304-1306.
  • .Yang LE, Leong PKK, Guzman JP, et al. Modest K+ restriction provokes insulin resistance of cellular K+ uptake without decrease in plasma K+. Ann N Y Acad Sci 2003;986:625-627.
  • .Yeh JK, Aloia JF, Semla HM. Interrelation of cortisone and 1,25 dihydroxycholecalciferol on intestinal calcium and phosphate absorption. Calcif Tissue Int 1984;36(5):608-614.
  • .Young DB, Lin H, McCabe RD. Potassium’s cardiovascular protective mechanisms. Am J Physiol 1995;268(4 Part 2):R825-R837.
  • .Young DB, Ma G. Vascular protective effects of potassium. Semin Nephrol 1999;19:477-486.
  • .Young IS, Goh EM, McKillop UH, et al. Magnesium status and digoxin toxicity. Br J Clin Pharmacol 1991;32(6):717-721.
  • .Zaman R, Wilkins MR, Kendall MJ, et al. The effect of food and alcohol on the pharmacokinetics of acebutolol and its metabolite, diacetolol. Biopharm Drug Dispos 1984;5:91-95.
  • .Zanabli AR, Yango A, Dworkin L. Incidence of hyperkalemia in high risk patients during treatment with an angiotensin converting enzyme inhibitor (Lisinopril) versus an angiotensin II receptor blocker (Losartan). SDJ Med 2004;57(6):227-231.
  • .Zull DN. Disorders of potassium metabolism. Emerg Med Clin North Am 1989;7(4):771-94. (Review)