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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
Drug/Class Interaction TypeMechanism and SignificanceManagement
Albuterol, rimiterol
Beta-2-adrenoceptor agonist bronchodilators
Oral or intravenous albuterol, rimiterol, and related beta-2-adrenoceptor agonists can deplete potassium and other nutrients, possibly to a clinically significant degree. Hypokalemia due to these drugs, particularly in combination with steroids or digoxin, may contribute to arrhythmias or aggravate asthma. Evidence is lacking to determine frequency of occurrence or confirm benefits of potassium coadministration.
Monitor regularly. Coadministration of potassium (and magnesium) may prevent or correct nutrient depletion.
Antikaliuretic-diuretic agent
/ /
As a potassium-sparing diuretic, amiloride carries implicit risk of hyperkalemia when combined with significant increase in potassium intake, especially with compromised renal function and concomitant ACE inhibitor therapy. Probability of adverse events with concurrent use of potassium supplements, salt substitutes, or food sources generally recognized; risk of acute and severe event with rapid increase in intake.
Limit potassium intake, and avoid rapid and significantly increased intake, outside professional supervision. Closely monitor high-risk patients.
Aminoglycoside antibiotics
Aminoglycosides can cause renal tubular damage and induce hypokalemia; renal failure is also potentiated by potassium depletion. Case reports and animal studies available; small but recognized risk for elderly and compromised persons. Evidence from clinical trials lacking to confirm benefits of concomitant potassium.
Concurrent potassium may prevent or correct adverse effects with long-term or repeated drug therapy. Monitor.
Amphotericin B
Amphotericin can cause potassium depletion, especially with steroids; hypokalemia is possible, particularly with drug-induced renal damage or rapid infusion. Not common but widely recognized.
Concurrent potassium may prevent or correct adverse effects with long-term or repeated drug therapy. Monitor.
Angiotensin-converting enzyme (ACE) inhibitors
/ /
Significant risk of hyperkalemia when potassium intake increased during ACE inhibitor therapy, especially with compromised renal function or diabetes. Probability of acute and severe adverse events with concurrent use of potassium supplements, salt substitutes, or food sources generally recognized, particularly with rapid increase in intake.
Limit potassium intake, and avoid rapid and significantly increased intake, outside professional supervision. Closely monitor high-risk patients.
Beta-adrenoceptor antagonists
Beta blockers can elevate potassium levels and may cause hyperkalemia. A variety of mechanisms may be involved, but not fully elucidated. Frequency unknown, but potentially severe consequences.
Potassium generally contraindicated but may be indicated in certain circumstances. Monitor potassium closely with beta blockers.
Carbonic anhydrase inhibitors

Carbonic anhydrase inhibitors generally decrease renal blood flow and glomerular filtration rate. However, other than furosemide and acetazolamide, limited evidence indicates they do not appear to affect potassium status adversely in most individuals. Potential for significant disequilibrium in carbon dioxide transport; low probability but high risk.
Concurrent potassium may prevent or correct adverse effects with long-term or repeated drug therapy. Monitor, especially for acidosis.
/ /
Renotubular damage is common with cisplatin and may cause wasting of potassium and other minerals. Resulting hypokalemia may be refractory without concomitant administration of potassium and magnesium. Risk of clinically significant adverse effects widely recognized.
Concurrent potassium and magnesium may prevent or correct depletion. Protect renal function. Closely monitor electrolyte status.

Colchicine can impair absorption and increase loss of potassium (and other nutrients). Coadministration of potassium may prevent or correct clinically significant adverse effects. Minimal research but widely accepted as possible or probable.
Coadministration of potassium and other nutrients may prevent or correct adverse effects with long-term or repeated drug therapy. Monitor.
Corticosteroids, oral
Oral corticosteroids can deplete potassium and other nutrients, possibly to clinically significant degree. Hypokalemia due to these drugs, particularly in combination with other agents affecting potassium status, may contribute to edema, arrhythmias, or aggravate asthma. Widely recognized, but minimal evidence and lack of consensus as to clinical significance. Benefits of potassium coadministration unproven.
Consider coadministration of potassium and other nutrients, may prevent or correct adverse effects with long-term therapy. Monitor, especially with renal impairment.

Cyclosporine-induced nephrotoxicity and other mechanisms can cause hyperkalemia, most often in patients with compromised renal function. Onset of effects can be rapid or gradual. Varied attempts at reducing drug toxicity and its effects on renal function and potassium metabolism, but mixed results and no consensus as to effective corrective measures.
Close monitoring of allograft patients is always essential. Potassium generally contraindicated, but coadministration may be indicated; caution imperative. END_
Cardiac glycosides
Hypokalemia increases risk of digoxin toxicity, but digoxin impairs potassium function, and overdose can cause hyperkalemia. Increased risk in patients taking diuretics. Interplay with magnesium; increased risks with dual depletion.
Consider coadministration of potassium, magnesium, and other nutrients, especially through food sources; may prevent or correct adverse effects. Monitor, especially with diuretics and renal impairment.
Diuretics, potassium depleting
Loop and thiazide diuretics
Potassium-wasting diuretics inherently increase risk of potassium depletion and hypokalemia. Generally accepted as inherent risk of clinically significant adverse effects. Concomitant ACE inhibitor therapy or other polypharmacy often used to mitigate depletion.
Coadministration of potassium and other nutrients, as food or supplements, can prevent or correct depletion and sequelae. Monitor.
Stool softeners
Through various mechanisms, laxatives or stool softeners can deplete potassium and other nutrients, more often with repeated use. However, hypokalemia occasionally possible with short-term cathartic use, as in procedure preparation. Generally recognized as possible risk, but corrective measures inconsistently applied. Increased risk of adverse effects in cardiac patients, especially with concomitant diuretics or other potassium-depleting drugs.
Review diet and exercise; advise improvements as indicated. Coadministration of potassium and other nutrients may prevent or correct adverse effects with long-term or repeated drug therapy. Monitor.
Angiotensin II receptor antagonists
/ /
All angiotensin II receptor antagonists inherently carry risk of hyperkalemia. Through effects on renin-angiotensin system and aldosterone, losartan may cause clinically significant elevations in potassium levels. Effect on potassium is universal and widely recognized. However, severity may vary, and clinically significant events are uncommon.
Avoid extra potassium, especially rapid and significantly increased intake, outside professional supervision. Monitor regularly.
Nonsteroidal anti-inflammatory drugs (NSAIDs)
/ /
Various NSAIDs alter potassium metabolism through a range of mechanisms, many only partially understood, but many resulting from drug-induced nephrotoxicity. Severe potassium-related adverse effects with NSAIDs are uncommon but not rare; they may be acute and reversible, but chronic renal failure possible.
Limit potassium intake, and avoid rapid or significantly increased intake; professional supervision indicated. Closely monitor high-risk patients.
Antiarrhythmic drugs
Hypokalemia of various origins can significantly increase risk of acute cardiac irregularities and adverse reactions to antiarrhythmic drugs, especially when accompanied by hypomagnesemia.
Closely monitor; restore electrolyte balance, particularly magnesium and potassium, whenever disturbed or depleted by diuretics, vomiting, diarrhea, or other causes.
Spironolactone, triamterene
Potassium-sparing diuretics (spironolactone, triamterene) carry implicit risk of hyperkalemia if potassium intake significantly increased, especially with compromised renal function or concomitant ACE inhibitor. Probability of acute and severe adverse events with concurrent use of potassium supplements, salt substitutes, or food sources generally recognized. Frequently coadministered with potassium-depleting diuretics based on known activity.
Limit potassium intake, and avoid rapid and significantly increased intake; professional supervision indicated. Closely monitor high-risk patients.
/ /
Trimethoprim, alone or with sulfamethoxazole, can elevate potassium levels, sometimes causing hyperkalemia, through one or more mechanisms involving renal function. Severe adverse effects are uncommon but not rare; they may be acute and reversible, but chronic renal failure possible. Risk minimal to moderate for most patients but increased in AIDS patients or others with compromised physiological function or polypharmacy affecting renal function.
Limit potassium intake, and avoid rapid or significantly increased intake, outside professional supervision. Closely monitor high-risk patients.
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


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


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.


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
Aminoglycoside Antibiotics, Including Gentamicin, Neomycin, and Tobramycin
Amphotericin B (AMB; Fungizone)
Angiotensin-Converting Enzyme (ACE) Inhibitors
Beta-Adrenoceptor Antagonists (Beta-Adrenergic Blocking Agents)
Carbenoxolone (CBX)
Carbonic Anhydrase Inhibitors, Potassium Depleting
Corticosteroids, Oral
Cotrimoxazole (Sulfamethoxazole and Trimethoprim)
Digoxin and Related Cardiac Glycosides
Diuretics, Potassium Depleting, Including Loop and Thiazide Diuretics
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
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)
Pseudoephedrine, Phenylpropanolamine, and Related Decongestants
Tetracycline Antibiotics
Theophylline/Aminophylline and Related Beta-2 Sympathomimetics (Oral and Inhalant)
nutrient-nutrient interactions
Magnesium and Magnesium-Containing Antacids
herb-nutrient interactions
Diuretic Herbs
Licorice Root
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