Potassium

Potassium (K⁺) is a mineral that is vital to cell metabolism. Potassium is a major intracellular cation (positively charged ion) and a type of electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance ¹, ², ³. Potassium is present in all body tissues and is required for normal cell function because of its role in maintaining intracellular fluid volume and transmembrane electrochemical gradients ⁴, ⁵. Potassium helps transport nutrients into cells and removes waste products out of cells. Potassium is essential for the proper functioning of the heart, kidneys, muscles, nerves, and digestive system. Potassium is also important in muscle function, helping to transmit messages between nerves and muscles ⁴.

Potassium (K⁺) is a positively charged ion (cation), which is present throughout your body in both intracellular and extracellular fluids. The majority of body potassium, > 90%, are intracellular. It moves freely from intracellular fluid (ICF) to extracellular fluid (ECF) and vice versa when adenosine triphosphate (ATP) increases the permeability of the cell membrane. Potassium (K⁺) is mainly replaced inside or outside the cells by another cation, sodium (Na⁺). The movement of potassium into or out of the cells is linked to certain body hormones and also to certain physiological states. Standard laboratory tests measure extracellular fluid (ECF) potassium. Potassium enters the body rapidly during food ingestion. Insulin is produced when a meal is eaten; this causes the temporary movement of potassium from extracellular fluid (ECF) to intracellular fluid (ICF). Over the ensuing hours, the kidneys excrete the ingested potassium and homeostasis is returned. In the critically ill patient, suffering from high potassium level or hyperkalemia, this mechanism can be manipulated beneficially by administering high concentration (50%) intravenous glucose. Insulin can be added to the glucose, but glucose alone will stimulate insulin production and cause movement of potassium from extracellular fluid (ECF) to intracellular fluid (ICF). The stimulation of alpha receptors causes increased movement of potassium from intracellular fluid (ICF) to extracellular fluid (ECF). A noradrenaline infusion can elevate serum potassium levels. An adrenaline infusion, or elevated adrenaline levels, can lower serum potassium levels. Metabolic acidosis causes a rise in extracellular potassium levels (hyperkalemia). In this situation, excess of hydrogen ions (H⁺) are exchanged for intracellular potassium ions, probably as a result of the cellular response to a falling blood pH. Metabolic alkalosis causes the opposite effect, with potassium moving into the cells ⁶.

Potassium (K⁺), along with other electrolytes such as sodium (Na⁺), chloride (Cl^–), and bicarbonate (HCO3^–), helps regulate the amount of fluid in your body and maintains a stable acid-base balance. Potassium is present in all body fluids, but most potassium is found within the cells (intracellularly). Only a small amount is present in fluids outside the cells and in the liquid part of the blood (called serum or plasma).

The total amount of potassium (K⁺) in the adult body is about 45 millimole (mmol)/kg body weight (about 140 g for a 175 pound adult;  1 millimole [mmol] = 1 milliequivalent [mEq] = 39.1 mg of potassium) ⁷. Most potassium are found within the cells (intracellularly) and a small amount is in extracellular fluid. The intracellular concentration of potassium is about 30 times higher than the extracellular concentration, and this difference forms a transmembrane electrochemical gradient that is maintained via the Sodium-Potassium ATPase pumps (Na⁺-K⁺ ATPase ion pumps) ⁸. When activated, the sodium-potassium ATPase pump (Na⁺-K⁺ ATPase ion pumps) exchanges 2 extracellular potassium (K⁺) ions for 3 intracellular sodium (Na⁺) ions, influencing membrane potential based on physiological excitation or inhibition. These sodium-potassium ATPase pumps (Na⁺-K⁺ ATPase ion pumps) are partially responsible, along with the sodium-potassium-chloride (Na⁺-K⁺-2Cl) co-transporter and sodium-calcium (Ca) exchanger, for maintaining the potential difference across the resting cell membrane as well. In addition to maintaining cellular tonicity, this gradient is required for proper nerve transmission, muscle contraction, and kidney function ⁴, ⁹, ¹⁰.

Potassium (K⁺) homeostasis depends on external balance (dietary intake [typically 100 mmol per day] versus excretion [95% via the kidney; 5% via the colon]) and internal balance (the distribution of potassium (K⁺) between intracellular and extracellular fluid compartments). The uneven distribution of potassium (K⁺) across cell membranes means that a mere 1% shift in its distribution can cause a 50% change in plasma potassium (K⁺) concentration ³. Hormonal mechanisms involving insulin, beta-adrenergic agonists and aldosterone modulate potassium (K⁺) distribution by promoting rapid transfer of potassium (K⁺) across the plasma membrane ¹¹. Your body uses what potassium (K⁺) it requires and your kidneys eliminate the rest in the urine. Your body tries to keep the blood potassium level within a very narrow range. Levels are mainly controlled by aldosterone, a hormone produced by the adrenal glands in the kidneys. Extrarenal potassium (K⁺) losses from the body are usually small, but can be marked in individuals with chronic diarrhea, severe burns or prolonged sweating ³, ¹¹. Under normal circumstances, the kidney’s distal nephron secretes potassium (K⁺) and determines final urinary excretion. In patients with low potassium levels or hypokalemia (plasma K+ concentration <3.5 mmol/l), after the exclusion of extrarenal causes, alterations in sodium ion (Na⁺) delivery to the distal nephron, aldosterone status, or a specific inherited or acquired defect in distal nephron function (each of which affects distal nephron K+ secretion), should be considered ³.

Figure 1. Potassium physiology

Because most potassium (K+) ions are found within the cells (a major intracellular cation), it is widely distributed in foods once derived from living tissues. Potassium concentration is higher in fruits and vegetables than in cereals and meat. You get most of the potassium you need from the foods that you eat and most people have an adequate intake of potassium. Recommended adequate intakes for potassium were set by the Food and Nutrition Board of the Institute of Medicine at 4700 mg/day ⁵. However it should be noted that the Food and Nutrition Board of the Institute of Medicine Recommended adequate intakes (AIs) for potassium at 4700 mg/day for adults is substantially higher than the World Health Organization’s (WHO) guidelines, which recommend 3150 mg/day for adults ¹². The National Health and Nutrition Examination Survey (NHANES) data indicates that 99.2% of potassium in the US diet is naturally occurring, with the remaining 0.8% coming from fortified foods ¹³. These naturally occurring potassium sources include milk and other non-alcoholic beverages, as well as potatoes and fruit, which rank highest as sources of potassium intake among American adults ¹⁴. In addition, Western dietary practices with higher consumption of cereal, low nutrient density processed foods and lower consumption of fruits and vegetables has led to a diet lower in potassium and higher in sodium in recent decades ⁵. Salting foods and discarding the liquid induces sodium (Na⁺) for potassium (K⁺) exchange and reduces the potassium content of foods. Few Americans meet the recommended intakes; the average intake is 2591 ± 9 mg/day ¹³. This large gap between potassium intakes and recommended intakes led to potassium being called a shortfall nutrient in the Dietary Guidelines for Americans ¹⁵.

Actual potassium requirements would vary with an individual’s genetics, blood pressure (BP) status, and sodium intake ⁴. Blood pressure is currently the primary criterion for determining potassium requirements, with African Americans being more vulnerable to high blood pressure (hypertension) and more responsive to potassium supplementation than whites; individuals with high blood pressure (hypertension) are more responsive to increasing potassium intakes than individuals with normal blood pressure, and potassium having a greater benefit for those consuming a high salt diet ¹⁶. Other benefits of increasing potassium consumption may include improved blood sugar (glucose) control, glucose intolerance and insulin resistance becoming a concern for individuals with high blood pressure (hypertension) prescribed potassium wasting diuretics (water pills) ¹⁷. These differences support personalized nutrition approaches. Understanding movement of potassium within the body may help to improve these health outcomes.

Potassium is absorbed via passive diffusion, primarily in the small intestine ⁸. About 90% of ingested potassium is absorbed and used to maintain its normal intracellular and extracellular concentrations ¹⁸. There is around 50 mEq/kg of potassium (K⁺) in the body such that total body potassium (K⁺) in a 70-kg person is 3,500 mEq. Around 98% of potassium (K⁺) is found mainly within cells, and about 2% of the bodies’ potassium (K⁺) is in the extracellular fluid. The normal concentration of potassium (K⁺) in the extracellular fluid is 3.5–5.3 mEq/L. Large deviations from these values are not compatible with life.

Approximately 90% of the daily potassium (K⁺) intake is excreted in the urine, whereas a smaller percentage (10%) is excreted by the gastrointestinal tract in the stool and a very small amount is lost in sweat ¹⁹, ¹¹, ²⁰. Therefore, within the body, the kidney is the major organ responsible for potassium (K⁺) homeostasis. The kidneys control potassium excretion in response to changes in dietary intakes, and potassium excretion increases rapidly in healthy people after potassium consumption, unless body stores are depleted ⁴. The kidney facilitates potassium (K⁺) homeostasis by adjusting renal potassium (K⁺) excretion over several hours in response to a potassium load. Initial changes in extracellular potassium (K⁺) concentration are buffered by movement of potassium (K⁺) into or out of skeletal muscle cells. Internal potassium (K⁺) balance is a term used to refer to regulation of potassium (K⁺) distribution between the intracellular and extracellular space. Insulin, catecholamines, and, to a lesser extent, aldosterone are critical factors responsible for maintaining the normal internal distribution of potassium (K⁺) ¹¹, ²⁰.

The kidneys can adapt to variable potassium intakes in healthy individuals even in the setting of high dietary intake, but a minimum of 5 mmol (about 195 mg) potassium is excreted daily in urine ⁷. To demonstrate this, studies have shown potassium (K⁺) levels are kept within the normal range even when there are increases to ~15 g daily of dietary potassium (K⁺) intake sustained for 20 days ²¹, ²². Recent findings have identified the presence of an enteric potassium (K⁺) sensing mechanism that initiates the renal secretory process upon K+ entry into the gastrointestinal tract ²⁰. The distal convoluted tubule has been identified as a site critical for potassium (K⁺) homeostasis, where it acts as a potassium (K⁺) sensor capable of initiating potassium (K⁺) excretion independent of mineralocorticoid activity ²⁰. Combined with other obligatory losses, potassium balance cannot be achieved with intakes less than about 400–800 mg/day ¹¹, ²⁰.

Assessing potassium status is not routinely done in clinical practice, and it is difficult to do because most potassium in the body is inside cells ²³. Although blood potassium levels can provide some indication of potassium status, they often correlate poorly with tissue potassium stores ⁷, ²⁴, ²⁵. Other methods to measure potassium status include collecting balance data (measuring net potassium retention and loss); measuring the total amount of potassium or the total amount of exchangeable potassium in the body; and conducting tissue analyses (e.g., muscle biopsies), but all have limitations ²⁴.

Normal serum concentrations of potassium range from about 3.6 to 5.0 mmol/L and are regulated by a variety of mechanisms ⁷, ²⁶. Diarrhea, vomiting, kidney disease, use of certain medications, and other conditions that alter potassium excretion or cause transcellular potassium shifts can cause low potassium level also called hypokalemia (serum potassium levels below 3.6 mmol/L) or high potassium level also called hyperkalemia (serum potassium levels above 5.0 mmol/L) ²⁶. Otherwise, in healthy individuals with normal kidney function, abnormally low or high blood levels of potassium are rare.

Because the blood concentration of potassium is so small, minor changes can have significant consequences. If potassium levels are too low (serum potassium levels below 3.6 mmol/L) or too high (serum potassium levels above 5.0 mmol/L), there can be serious health consequences; a person may be at risk for developing shock, respiratory failure, or heart rhythm disturbances. An abnormal potassium level can alter the function of the nerves and muscles; for example, the heart muscle may lose its ability to contract.

Your body needs potassium to:

• Build proteins
• Break down and use carbohydrates
• Build muscle
• Maintain normal body growth
• Control the electrical activity of the heart
• Control the acid-base balance

Reduced potassium consumption has been associated with hypertension and cardiovascular diseases, and appropriate consumption levels could be protective against these conditions ²⁷. A recent meta-analysis including 11 cohort studies reported an inverse association between potassium intake and risk of stroke ²⁸. Additionally, two meta-analyses of trials comparing increased potassium to lower potassium intake found that increased potassium intake lowers blood pressure ²⁹, ³⁰. These results were further supported by a systematic review without a meta-analysis, which concluded that increased potassium intake results in decreased blood pressure in adults ³¹. Thus, a public health intervention aimed at increasing potassium intake from food could be a cost-effective strategy to reduce the burden of cardiovascular morbidity and mortality. Moreover, increasing potassium consumption from food in the population is safe; in individuals without renal impairment caused by medical conditions or drug therapy, the body is able to efficiently adapt and excrete excess potassium via the urine when consumption ³².

The American Heart Association recommended potassium intake for an average adult is 4,700 milligrams (mg) per day. Most of us aren’t getting nearly that much. On average, adult males eat almost 3,200 mg/day, and adult females eat about 2,400 mg/day ³³. Remember that potassium is only part of an overall heart-healthy eating pattern. Other dietary factors that may affect blood pressure include amount and type of dietary fat; cholesterol; protein, sugar and fiber; calcium and magnesium, and of course, sodium.

For example, the DASH (Dietary Approaches to Stop Hypertension) diet study found that a diet rich in fruits, vegetables, fat-free or low-fat (1 percent) milk and milk products, whole-grain foods, fish, poultry, beans, seeds and unsalted nuts reduced blood pressure compared to a typical American diet. The DASH eating plan also had less sodium; sweets, added sugars and sugar-containing beverages; saturated and trans fats; and red meats than the typical American diet.

People with kidney problems, especially those on dialysis, should not eat too many potassium-rich foods. Your health care provider will recommend a special diet.

What are normal potassium levels?

Normal serum potassium values are between 3.5 to 5.0 millimoles/L (mmol/L) or 3.5 to 5.0 milliequivalent/L (mEq/L) ¹, ³⁴, ³⁵, ³⁶. However, there can be slight variation between laboratories and for this reason, it is important to look for the specific reference interval listed on your test report. Potassium levels outside this range, 3.5 to 5.0 millimoles/L (mmol/L) or 3.5 to 5.0 milliequivalent/L (mEq/L), are not compatible with life with increased rates of death from several causes ³⁷, ³⁸.

Your health care provider may order a potassium blood test as part of your regular checkup or to monitor an existing condition, such as diabetes, kidney disease, or adrenal gland disorders. You may also need this test if you take medicines that could affect your potassium levels or if you have symptoms of having too much or too little potassium.

Interpretation of a potassium test requires carefully considering the result, the laboratory reference range, and your health situation. Because potassium is frequently measured with other electrolytes, levels may be evaluated together. For a blood test, the report should list the amount of potassium measured in either milliequivalents per liter (mEq/L) or millimoles per liter (mmol/L). The test report will also show a reference range, which the laboratory considers an expected range for potassium levels.

What are high potassium levels?

High potassium levels also known as hyperkalemia is defined as serum potassium level greater than 5 mEq/L or greater than 5 mmol/L (Kim MJ, Valerio C, Knobloch GK. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2023 Jan;107(1):59-70.https://www.aafp.org/pubs/afp/issues/2023/0100/potassium-disorders-hypokalemia-hyperkalemia.html)).

If your potassium levels are too high or hyperkalemia, your symptoms may include ³⁹:

• Arrhythmia (a problem with the rate or rhythm of your heartbeat)
• Fatigue
• Muscle weakness
• Nausea
• Numbness or tingling

Too much potassium in the blood or hyperkalemia is often the result of two or more causes. High potassium levels may be a sign of ³⁹:

• Kidney disease. Your kidneys remove extra potassium from your body. Too much potassium may mean your kidneys aren’t working well.
• Addison disease also called adrenal insufficiency, is a disorder in which your immune system mistakenly attacks your adrenal glands, damaging the adrenal cortex. Other causes include infections and cancer. The damage causes the adrenal glands cortex not to make enough of the hormone cortisol and sometimes the hormone aldosterone.
• Injuries, burns, or surgery that can cause your cells to release extra potassium into your blood
• Type 1 diabetes that is not well controlled
• The side effects of certain medicines, such as diuretics (water pills) or antibiotics
• A diet too high in potassium (not common). Bananas, apricots, green leafy vegetables, avocados and many other foods are good sources of potassium that are part of a healthy diet. But eating very large amounts of potassium-rich foods or taking potassium supplements can lead to health problems.

What are low potassium levels?

Low potassium levels also known as hypokalemia is defined as serum potassium level less than 3.6 mEq/L or less than 3.6 mmol/L (Kim MJ, Valerio C, Knobloch GK. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2023 Jan;107(1):59-70.https://www.aafp.org/pubs/afp/issues/2023/0100/potassium-disorders-hypokalemia-hyperkalemia.html)).

If your potassium levels are too low or hypokalemia, your symptoms may include ³⁹:

• Irregular heartbeat
• Muscle cramps
• Weak or twitching muscles
• Fatigue
• Nausea
• Constipation
• Severe hypokalemia may result in muscular paralysis or abnormal heart rhythms (cardiac arrhythmias) that can be fatal ⁴⁰, ⁴¹
• Chronic low potassium levels (chronic hypokalemia) is associated with high blood pressure (hypertension) and kidney stone formation.

Too little potassium in the blood or hypokalemia may be a sign of ³⁹:

• Use of prescription diuretics (water pills)
• Fluid loss from diarrhea, vomiting, or heavy sweating
• Using too many laxatives
• Adrenal gland disorders, including Cushing’s syndrome and aldosteronism
• Kidney disease
• Alcohol use disorder
• Eating a lot of real licorice, which comes from licorice plants. Most licorice products sold in the U.S. don’t contain any real licorice. Check the package ingredient label to be sure.
• A diet too low in potassium (not common). Bananas, apricots, green leafy vegetables, avocados and many other foods are good sources of potassium that are part of a healthy diet.

Potassium function

Potassium (K⁺) is the principal positively charged ion (cation) in the fluid inside of cells, while sodium (Na⁺) is the principal cation in the extracellular fluid. Potassium (K⁺) concentrations are about 30 times higher inside than outside cells, while sodium (Na⁺) concentrations are more than 10 times lower inside than outside cells ⁴². The concentration differences of these charged particles causes a difference in electric potential between the inside and outside of cells, known as the membrane potential. A cell’s membrane potential is maintained by ion pumps in the cell membrane, especially the Sodium-Potassium ATPase pumps (Na⁺-K⁺ ATPase ion pumps). These sodium-potassium ATPase pumps (Na⁺-K⁺ ATPase ion pumps) use ATP (energy) to pump sodium (Na⁺) of the cell and potassium (K⁺) into the cell, leading to a potassium (K⁺) gradient across the cell membrane [potassium (K⁺) in > potassium (K⁺) out], which is partially responsible for maintaining the cell membrane potential (Figure 2). The sodium-potassium ATPase pumps (Na⁺-K⁺ ATPase ion pumps) activity has been estimated to account for 20%-40% of the resting energy consumption in a typical adult ⁴². The large proportion of energy dedicated to maintaining sodium/potassium concentration gradients emphasizes the importance of this function in sustaining life ⁴². The cell membrane potential created by potassium and sodium ions allows the cell generate an action potential–a “spike” of electrical discharge. The ability of cells to produce electrical discharge is critical for body functions such as nerve impulse transmission, muscle contraction, and heart function ⁴³, ⁴⁴, ⁴⁵.

Potassium is also an essential mineral needed to regulate water balance, blood pressure and levels of acidity ⁴⁶. The more potassium you eat, the more sodium you pass out of the body through urine. Increased potassium intake has no adverse effect on blood lipid concentration, catecholamine concentrations, or renal function in apparently healthy adults without impaired renal handling of potassium ³³. The largest benefit was detected when sodium intake was more than 4 g/day, which is the intake of most populations globally ⁴⁷, so increased potassium intake should benefit most people in most countries. However, the authors also found a statistically significant decrease in blood pressure with increased potassium when sodium intake was 2-4 g/day. Therefore, increased potassium can continue to be beneficial in terms of blood pressure even as individuals and populations decrease their sodium intake. Studies examining both nutrients simultaneously support this concept, showing an increased benefit with simultaneous reduction in sodium and increase in potassium compared with changes in one nutrient individually ⁴⁸, ⁴⁹.

Potassium also helps relax blood vessel walls, which helps lower blood pressure ³³.

World Health Organization recommends an increase in potassium intake from food to reduce blood pressure and risk of cardiovascular disease, stroke and coronary heart disease in adults. World Health Organization suggests a potassium intake of at least 90 mmol/day (3510 mg/day) for adults (conditional recommendation) ³².

Potassium also acts as a cofactor for some enzymes activity. For example, the activation of Na+/K+-ATPase requires the presence of sodium and potassium. The presence of potassium is also required for the activity of pyruvate kinase, an important enzyme in carbohydrate metabolism ⁵⁰.

Figure 2. Sodium-Potassium ATPase pump

How much potassium do you need?

The amount of potassium you need each day depends on your age and sex. Average daily recommended amounts are listed below in milligrams (mg). Table 1 lists the current Adequate Intakes (AIs) for potassium for healthy individuals. Intake recommendations for potassium and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by an expert committee of the Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine ⁵. Dietary Reference Intake (DRI) is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values, which vary by age and sex, include:

• Recommended Dietary Allowance (RDA): Average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals; often used to plan nutritionally adequate diets for individuals.
• Adequate Intake (AI): Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA.
• Estimated Average Requirement (EAR): Average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals.
• Tolerable Upper Intake Level (UL): Maximum daily intake unlikely to cause adverse health effects.

When the Food and Nutrition Board evaluated the available data in 2005, it found the data insufficient to derive an Estimated Average Requirement (average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals) for potassium, so the board established Adequate Intake (intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an Recommended Dietary Allowance) for all ages based on potassium intakes in healthy populations ⁵¹. In 2019, a National Academies of Sciences, Engineering, and Medicine committee updated the Dietary Reference Intake (DRI) for potassium and sodium ⁵. The committee found the data insufficient to derive an Estimated Average Requirement (EAR) for potassium. Therefore, they established Adequate Intakes (AIs) for all ages based on the highest median potassium intakes in healthy children and adults, and on estimates of potassium intakes from breast milk and complementary foods in infats. The National Academies of Sciences, Engineering, and Medicine committee also used an expanded Dietary Reference Intake (DRI) model to include a recommended intake level for a nutrient to reduce the risk of chronic disease, what they termed the chronic disease risk reduction intake ⁵¹. In 2019, a National Academies of Sciences, Engineering, and Medicine committee updated the Dietary Reference Intake (DRI) for potassium and sodium ⁵. According to the model, a chronic disease risk reduction intake might be set for a nutrient like potassium when there is a causal relationship between a certain level of intake and a reduced risk of chronic disease based on evidence of at least moderate strength. However, the committee found the evidence to be insufficient to derive a chronic disease risk reduction intake for potassium ⁵.

[Source ⁵² ]

Table 1. Average daily recommended intake for Potassium

Birth to 6 months	400 mg
Infants 7–12 months	860 mg
Children 1–3 years	2,000 mg
Children 4–8 years	2,300 mg
Children 9–13 years (boys)	2,500 mg
Children 9–13 years (girls)	2,300 mg
Teens 14–18 years (boys)	3,000 mg
Teens 14–18 years (girls)	2,300 mg
Adults 19+ years (men)	3,400 mg
Adults 19+ years (women)	2,600 mg
Pregnant teens	2,600 mg
Pregnant women	2,900 mg
Breastfeeding teens	2,500 mg
Breastfeeding women	2,800 mg

Footnote: *Adequate Intakes (AIs) do not apply to individuals with impaired potassium excretion because of medical conditions (e.g., kidney disease) or the use of medications that impair potassium excretion.

[Source ²³ ]

Potassium Intakes and Status of Americans

Dietary surveys consistently show that people in the United States consume substantially less potassium than recommended, which is why the 2015–2020 Dietary Guidelines for Americans identifies potassium as a “nutrient of public health concern” ⁵³. According to data from the 2013–2014 National Health and Nutrition Examination Survey (NHANES), the average daily potassium intake from foods is 2,423 mg for males aged 2–19, and 1,888 mg for females aged 2–19 ⁵⁴. In adults aged 20 and over, the average daily potassium intake from foods is 3,016 mg for men and 2,320 mg for women.

Average potassium intakes vary by race. Non-Hispanic blacks aged 20 and older consume an average of 2,449 mg potassium per day. Average daily intakes are 2,695 mg for Hispanic whites and 2,697 mg for non-Hispanic whites ⁵⁴.

Use of potassium-containing dietary supplements does not significantly increase total potassium intakes among U.S. adults ⁵⁵, probably because most potassium-containing dietary supplements provide no more than 99 mg potassium per serving ⁵⁶. Data from NHANES 2013–2014 indicate that 12% of children and adults aged 2 and over use supplements containing potassium, and among those who do, supplement use adds a mean of only 87 mg to total daily potassium intakes ⁵⁴.

Foods high in Potassium

Potassium is found in many foods. You can get recommended amounts of potassium by eating a variety of foods, including the following ⁵⁷:

• Fruits, such as dried apricots, prunes, raisins, orange juice, and bananas
• Vegetables, such as acorn squash, potatoes, spinach, tomatoes, and broccoli
• Lentils, kidney beans, soybeans, and nuts
• Milk and yogurt
• Meats, poultry, and fish

Potassium is found in a wide variety of plant and animal foods and in beverages. Many fruits and vegetables are excellent sources, as are some legumes (e.g., soybeans) and potatoes. Meats, poultry, fish, milk, yogurt, and nuts also contain potassium ¹⁸. Among starchy foods, whole-wheat flour and brown rice are much higher in potassium than their refined counterparts, white wheat flour and white rice ⁵⁸. Selected food sources of potassium are listed in Table 2. People with kidney problems, especially those on dialysis, should not eat too many potassium-rich foods. Your health care provider will recommend a special diet low in potassium.

Milk, coffee, tea, other nonalcoholic beverages, and potatoes are the top sources of potassium in the diets of American adults ⁵⁹. Among children in the United States, milk, fruit juice, potatoes, and fruit are the top sources ⁶⁰.

It is estimated that the body absorbs about 85%–90% of dietary potassium ⁴. The forms of potassium in fruits and vegetables include potassium phosphate, sulfate, citrate, and others, but not potassium chloride ⁶¹.

The U.S. Department of Agriculture’s FoodData Central (https://fdc.nal.usda.gov) lists the nutrient content of many foods and provides a comprehensive list of foods containing potassium ordered by nutrient content (https://www.nal.usda.gov/sites/www.nal.usda.gov/files/potassium.pdf). The 2015–2020 Dietary Guidelines for Americans provides a a list of foods containing potassium ⁶².

Table 2. Food Sources of Potassium

Food	Milligrams (mg) per serving	Percent DV*
Apricots, dried, ½ cup	755	16
Lentils, cooked, 1 cup	731	16
Squash, acorn, mashed, 1 cup	644	14
Prunes, dried, ½ cup	635	14
Raisins, ½ cup	618	13
Potato, baked, flesh only, 1 medium	610	13
Kidney beans, canned, 1 cup	607	13
Orange juice, 1 cup	496	11
Soybeans, mature seeds, boiled, ½ cup	443	9
Banana, 1 medium	422	9
Milk, 1%, 1 cup	366	8
Spinach, raw, 2 cups	334	7
Chicken breast, boneless, grilled, 3 ounces	332	7
Yogurt, fruit variety, nonfat, 6 ounces	330	7
Salmon, Atlantic, farmed, cooked, 3 ounces	326	7
Beef, top sirloin, grilled, 3 ounces	315	7
Molasses, 1 tablespoon	308	7
Tomato, raw, 1 medium	292	6
Soymilk, 1 cup	287	6
Yogurt, Greek, plain, nonfat, 6 ounces	240	5
Broccoli, cooked, chopped, ½ cup	229	5
Cantaloupe, cubed, ½ cup	214	5
Turkey breast, roasted, 3 ounces	212	5
Asparagus, cooked, ½ cup	202	4
Apple, with skin, 1 medium	195	4
Cashew nuts, 1 ounce	187	4
Rice, brown, medium-grain, cooked, 1 cup	154	3
Tuna, light, canned in water, drained, 3 ounces	153	3
Coffee, brewed, 1 cup	116	2
Lettuce, iceberg, shredded, 1 cup	102	2
Peanut butter, 1 tablespoon	90	2
Tea, black, brewed, 1 cup	88	2
Flaxseed, whole, 1 tablespoon	84	2
Bread, whole-wheat, 1 slice	81	2
Egg, 1 large	69	1
Rice, white, medium-grain, cooked, 1 cup	54	1
Bread, white, 1 slice	37	1
Cheese, mozzarella, part skim, 1½ ounces	36	1
Oil (olive, corn, canola, or soybean), 1 tablespoon	0	0

Footnote: *DV = Daily Value. The U.S. Food and Drug Administration (FDA) developed DVs (Daily Values) to help consumers compare the nutrient contents of foods and dietary supplements within the context of a total diet. The Daily Value (DV) for potassium is 4,700 mg for adults and children age 4 years and older ⁶³. FDA requires the new food labels to list potassium content. Foods providing 20% or more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.

[Source ⁵⁸ ] [Source ⁶⁴ ]

Potassium supplements

In dietary supplements, potassium is often present as potassium chloride, but many other different supplemental forms including potassium citrate, potassium gluconate, potassium bicarbonate, potassium aspartate, potassium orotate and potassium phosphate are also used ⁶⁵. The Supplement Facts panel on a dietary supplement label declares the amount of elemental potassium in the product, not the weight of the entire potassium-containing compound. Some dietary supplements contain potassium iodide in microgram amounts, but this ingredient serves as a form of the mineral iodine, not potassium. Potassium iodide is used to protect your thyroid gland from taking in radioactive iodine that may be released during a nuclear radiation emergency ⁶⁶. Radioactive iodine can damage your thyroid gland. You should only take potassium iodide if there is a nuclear radiation emergency and public officials tell you that you should take it ⁶⁶. Potassium iodide is in a class of medications called anti-thyroid medications. It works by blocking radioactive iodine from entering your thyroid gland. Potassium iodide is also sometimes used to treat overactive thyroid gland and sporotrichosis (a skin infection caused by a fungus) ⁶⁶. Talk to your doctor about the risks of using potassium iodide for your condition. Many salt substitutes contain potassium chloride, and acesulfame potassium (Ace-K) is an FDA-approved general purpose sweetener.

Not all multivitamin/mineral supplements contain potassium, but those that do typically provide about 80 mg potassium ⁶⁵. Potassium-only supplements are also available, and most contain up to 99 mg potassium ⁶⁷. Information on many dietary supplements that contain potassium is available in the Dietary Supplement Label Database ⁶⁵ from the National Institutes of Health, which contains label information from tens of thousands of dietary supplement products on the market. Because of the potential for serious side effects from potassium supplements, you should seek medical advice before deciding to use a potassium supplement. The best way to increase your potassium intake is by increasing the consumption of potassium-rich food and beverages ⁶⁷.

Many dietary supplement manufacturers and distributors limit the amount of potassium in their products to 99 mg (which is only about 3% of the DV) because of two concerns related to potassium-containing drugs. First, the FDA has ruled that some oral drug products that contain potassium chloride and provide more than 99 mg potassium are not safe because they have been associated with small-bowel lesions ⁶⁸. Second, the FDA requires some potassium salts containing more than 99 mg potassium per tablet to be labeled with a warning about the reports of small-bowel lesions ⁶⁹. In accordance with a ruling by Congress, the FDA may not limit the amount of any nutrient, including potassium, in a dietary supplement, except for safety-related reasons ⁷⁰. However, the FDA has not issued a ruling about whether dietary supplements containing more than 99 mg potassium must carry a warning label ⁶⁹.

Higher doses of supplemental potassium are generally prescribed to prevent and treat potassium depletion and hypokalemia ⁴². The use of more potent potassium supplements in potassium deficiency requires close monitoring of serum potassium concentrations ⁴².

Only a few studies have examined how well the various forms of potassium in dietary supplements are absorbed. A 2016 dose-response trial found that humans absorb about 94% of potassium gluconate in supplements, and this absorption rate is similar to that of potassium from potatoes ⁷¹. According to an older study, liquid forms of potassium chloride (used as drugs to treat conditions such as digitalis intoxication or arrhythmias due to hypokalemia) are absorbed within a few hours ⁷². Enteric coated tablet forms of potassium chloride (designed to prevent dissolution in the stomach but allow it in the small intestine) are not absorbed as rapidly as liquid forms ⁷³.

Salt substitutes

Many salt substitutes contain potassium chloride as a replacement for some or all of the sodium chloride in salt. The potassium content of these products varies widely, from about 440 mg to 2,800 mg potassium per teaspoon ⁵¹. Some people, such as those with kidney disease or who are taking certain medications, should consult their healthcare provider before taking salt substitutes because of the risk of hyperkalemia posed by the high levels of potassium in these products.

Adverse reactions to potassium supplements

Gastrointestinal symptoms are the most common side effects of potassium supplements, including nausea, vomiting, abdominal discomfort, and diarrhea ⁷⁴. Intestinal ulceration has been reported after the use of enteric-coated potassium chloride tablets. The use of potassium salts in certain medications has been associated with small-bowel lesions, causing obstruction, hemorrhage, and perforation ⁶⁹, ⁷⁵. For this reason, the FDA requires some oral drugs providing more than 99 mg of potassium to be labeled with a warning. Taking potassium with meals or taking a microencapsulated form of potassium may reduce gastrointestinal side effects ⁶⁷. Rashes may occasionally occur. The most serious adverse reaction to potassium supplementation is hyperkalemia (elevated serum potassium levels), yet is rare in subjects with normal kidney function (see Potassium Toxicity). Chronic ingestion of doses of potassium supplements (e.g., up to 15,600 mg for 5 days) in healthy people can increase plasma levels of potassium, but not beyond the normal range ⁷⁶. However, very high amounts of potassium supplements or salt substitutes that contain potassium could exceed the kidney’s capacity to excrete potassium, causing acute hyperkalemia even in healthy individuals. Furthermore, individuals with abnormal kidney function and those on potassium-sparing medications should be monitored closely to prevent hyperkalemia ⁶⁷, ⁷⁷.

Drug interactions

Several types of medications have the potential to affect potassium status in ways that could be dangerous. Table 3 lists the classes of medications known to increase the risk of hyperkalemia (elevated serum potassium) in patients who also use potassium supplements ⁶⁷, ⁷⁸, ⁷⁹. People taking these and other medications should discuss their potassium intakes and status with their health care providers.

Several classes of medications are known to induce hypokalemia (low serum potassium) see Table 4 below. In the absence of treatment, hypokalemia can have serious complications and even be fatal (see Potassium Deficiency). Various mechanisms explain how certain medications can lead to potassium depletion. For example, both loop and thiazide diuretics increase the urinary excretion of potassium. Corticoids cause sodium retention that leads to a compensatory increase in urinary potassium excretion. Penicillins formulated as sodium salts also stimulate potassium excretion. Several medications, including aminoglycosides, anti-fungal agents (amphotericin-B, fluconazole), and cisplatin, can damage the renal tubular epithelium and lead to severe potassium loss. Outdated tetracycline antibiotics have been linked to electrolyte disturbances.

Table 3. Medications associated with Hyperkalemia (high potassium levels)

Medication Family	Specific Medications
Angiotensin converting enzyme (ACE) inhibitors	captopril (Capoten), enalapril (Vasotec), fosinopril (Monopril), ramipril (Altace)
Angiotensin receptor blockers	Losartan (Cozaar), valsartan (Diovan), irbesartan (Avapro), candesartan (Atacand)
Anticoagulant	Heparin
Anti-hypertensive agents	Beta-blockers, alpha-blockers
Anti-infective agents	Trimethoprim-sulfamethoxazole, pentamidine
Cardiac glycoside	Digitalis
Nonsteroidal anti-inflammatory agents (NSAID)	Indomethacin, ibuprofen, ketorolac
Potassium-sparing diuretics	Spironolactone (Aldactone), triamterene (Dyrenium), amiloride (Midamor)

ACE inhibitors and angiotensin receptor blockers (ARBs)

ACE inhibitors, such as benazepril (Lotensin®), and ARBs such as losartan (Cozaar®), are used to treat hypertension and heart failure, slow progression of kidney disease in patients with chronic kidney disease and type 2 diabetes, and decrease morbidity and mortality after myocardial infarction ⁸⁰, ⁸¹. These medications reduce urinary potassium excretion, which can lead to hyperkalemia. Experts recommend monitoring potassium status in people taking ACE inhibitors or angiotensin receptor blockers (ARBs), especially if they have other risk factors for hyperkalemia, such as impaired kidney function ⁸⁰.

Potassium sparing diuretics

Potassium-sparing diuretics, such as amiloride (Midamor®) and spironolactone (Aldactone®), reduce the excretion of potassium in the urine and can cause hyperkalemia ⁸². Experts recommend monitoring potassium status in people taking these medications, especially if they have impaired kidney function or other risk factors for hyperkalemia ⁸².

Loop and thiazide diuretics

Treatment with loop diuretics, such as furosemide (Lasix®) and bumetanide (Bumex®), and thiazide diuretics, such as chlorothiazide (Diuril®) and metolazone (Zaroxolyn®), increases urinary potassium excretion and can lead to hypokalemia ⁸². Experts recommend monitoring potassium status in people taking these medications, and initiating potassium supplementation if warranted ⁸².

Table 4. Medications associated with Hypokalemia (low serum potassium)

Medication Family	Specific Medications
Aminoglycosides	amikacin (Amikin), gentamicin (Garamycin), kanamycin (Kantrex), tobramycin (Nebcyn), streptomycin
Antibiotics	Penicillins: penicillin G sodium (Pfizerpen), mezlocillin (Mezlin), carbenicillin (Geocillin), ticarcillin (Ticar) Tetracyclines (when outdated)
Anti-cancer agent	cisplatin (Platinol-AQ)
Anti-fungal agents	amphotericin B (Abelcet, Amphotec, AmBisome, Amphocin, Fungizone), fluconazole (Diflucan)
Beta-adrenergic agonists	albuterol (Salbutamol, Ventolin), bitolterol (Tornalate), metaproterenol (Alupent)
Diuretics	Loop diuretics: bumetanide (Bumex), ethacrynic acid (Edecrin), furosemide (Lasix), torsemide (Demadex) Thiazide diuretics: Acetazolamide, thiazides, chlorthalidone (Hygroton), indapamide (Lozol), metolazone (Zaroxolyn), chlorothiazide (Diuril)
Mineralocorticoids	fludrocortisone (Florinef), hydrocortisone (Cortef), cortisone (Cortone), prednisone (Deltasone) Substances with mineralocorticoid effects: licorice, carbenoxolone, gossypol
Other	methylxanthines (e.g., theophylline), sodium polystyrene sulfonate, sodium phosphates, caffeine

Potassium Toxicity

Abnormally elevated serum potassium concentrations are referred to as hyperkalemia. Hyperkalemia occurs when potassium intake exceeds the capacity of the kidneys to eliminate it. Acute or chronic kidney failure, the use of potassium-sparing diuretics, and insufficient aldosterone secretion (hypoaldosteronism) may result in the accumulation of potassium due to a decreased urinary potassium excretion. Oral doses of potassium >18 g taken at one time in individuals not accustomed to high intakes may lead to severe hyperkalemia, even in those with normal kidney function ⁸³, ⁶⁷. Hyperkalemia may also result from a shift of intracellular potassium into the circulation, which may occur with the rupture of red blood cells (hemolysis) or tissue damage (e.g., trauma or severe burns). Symptoms of hyperkalemia may include tingling of the hands and feet, muscular weakness, and temporary paralysis. The most serious complication of hyperkalemia is the development of an abnormal heart rhythm (cardiac arrhythmia), which can lead to cardiac arrest ⁷⁸. A meta-analysis of randomized controlled studies showed that heart rate in healthy adults was unlikely to be affected by the chronic use of supplemental potassium doses of 2 to 3 g/day ⁸⁴.

Potassium Health Benefits

There is substantial evidence suggesting that a diet high in potassium-rich food and beverages may be associated with lower risks of stroke, hypertension, kidney stones, and possibly osteoporosis ⁴². The relative deficiency of dietary potassium in the modern diet and a higher sodium-to-potassium ratio may contribute to the development of some chronic diseases ⁴². However, currently there is insufficient evidence to establish a causal relationship between potassium intakes and the risk of these chronic conditions ⁸⁵. As a consequence, median potassium intakes observed in apparently healthy people were used to set adequate intakes (AI) by age/life stage in the recent revision of the Dietary Reference Intakes (DRIs) for potassium. The revised adequate intakes (AI) values are 2600 mg/day for women and 3400 mg/day for men ⁵.

Fruit and vegetables are among the richest sources of dietary potassium, and a large body of evidence supports the association of increased fruit and vegetable intakes with reduced risk of cardiovascular disease. Health experts recommends the consumption of a diet high in potassium-rich foods, especially fruit, vegetables, nuts, and dairy products to ensure adequate potassium intakes.

A diet rich in fruit and vegetables that supplies 2600 to 3400 mg/day of potassium should contribute to maintaining a low risk of chronic disease in generally healthy older adults. This recommendation does not apply to individuals who have been advised to limit potassium consumption by a health care professional.

High blood pressure

High blood pressure or hypertension is a major risk factor for heart disease and stroke, affects almost a third of Americans ⁴, ⁸⁶. According to an extensive body of literature, low potassium intakes increase the risk of hypertension, especially when combined with high sodium intakes ⁸⁷. Higher potassium intakes, in contrast, may help decrease blood pressure, in part by widening of blood vessels (vasodilation) and urinary sodium excretion, which in turn reduces plasma volume ⁵¹; this effect may be most pronounced in salt-sensitive individuals ⁴.

Forty-five percent of adult Americans have hypertension (blood pressure levels ≥130/80 mm Hg) ⁸⁸. Chronic hypertension damages the heart, blood vessels, and kidneys, thereby increasing the risk of heart disease and stroke, as well as hypertensive kidney disease ⁸⁹, ⁹⁰. Modern diets, which are high in sodium and low in potassium, are recognized as largely contributing to the high prevalence of hypertension. Unlike 24-hour dietary recalls, 24-hour urine collections provide accurate estimates of dietary intakes of sodium and potassium ⁹¹. An analysis of the 2014 US National Health and Nutrition Examination Survey (NHANES) showed an increase in systolic blood pressure with increasing sodium excretion and increasing sodium-to-potassium ratio in the urine ⁹². In this study, the highest versus lowest quartile of urinary potassium excretion (mid-values, 3,043 mg/day versus 1,484 mg/day) was associated with a 62% lower risk of hypertension ⁹².

The Dietary Approaches to Stop Hypertension (DASH) eating pattern, which emphasizes potassium from fruits, vegetables, modestly higher in protein, and lower in total fat, saturated fat, cholesterol, red meat, sweets, and sugar-containing beverages, lowers systolic blood pressure by an average of 5.5 mmHg and diastolic blood pressure by 3.0 mmHg ⁹³. The DASH eating pattern provides three times more potassium than the average American diet ⁹⁴. Compared to the control diet providing only 3.5 servings/day of fruit and vegetables and 1,700 mg/day of potassium, adherence to the DASH diet that included 8.5 servings/day of fruit and vegetables and 4,100 mg/day of potassium lowered systolic/diastolic blood pressures by an average 11.4/5.5 mm Hg in people with hypertension and 3.5/2.1 mm Hg in those without hypertension ⁹⁴. A 2014 meta-analysis of 17 randomized controlled trials that examined the effect of the DASH diet compared to a control diet in a total of 2,561 adults found overall reductions in systolic and diastolic blood pressure by 6.7 mm Hg and 3.5 mm Hg, respectively ⁹⁵. However effective the DASH diet is, the blood pressure-lowering effects can hardly be solely attributed to potassium intakes, because the DASH diet also increases intakes of other nutrients, such as magnesium and calcium, that are also associated with reductions in blood pressure ⁹⁶.

Results from most clinical trials suggest that potassium supplementation reduces blood pressure. A 2017 meta-analysis of 25 randomized controlled trials in 1,163 participants with hypertension found significant reductions in systolic blood pressure by 4.48 mm Hg and diastolic blood pressure by 2.96 mmHg with potassium supplementation, mostly as potassium chloride at 30–120 mmol/day potassium (1,173–4,692 mg), for 4–15 weeks ⁹⁷. Another meta-analysis of 15 randomized controlled trials found that potassium supplements (mostly containing potassium chloride at 60–65 mEq/day potassium [2,346–2,541 mg]) for 4–24 weeks in 917 patients with normal blood pressure or hypertension who were not taking antihypertensive medications significantly reduced both systolic and diastolic blood pressure ⁹⁸. The supplements had the greatest effect in patients with hypertension, reducing systolic blood pressure by a mean of 6.8 mmHg and diastolic blood pressure by 4.6 mmHg. Two earlier meta-analyses of 19 trials ⁹⁹ and 33 trials ¹⁰⁰ had similar findings. However, a Cochrane review of six of the highest-quality trials found nonsignificant reductions in systolic and diastolic blood pressure with potassium supplementation ¹⁰¹.

In 2018, the Agency for Healthcare Research and Quality (AHRQ) published a systematic review of the effects of sodium and potassium intakes on chronic disease outcomes and their risk factors ⁷⁴. The authors concluded that, based on observational studies, the associations between dietary potassium intakes and lower blood pressure in adults were inconsistent ⁷⁴. They also found no evidence for an association between potassium intakes and the risk of hypertension ⁷⁴. The authors did report, however, that potassium supplements (mostly containing potassium chloride) in doses ranging from 20 to 120 mmol/day (782 to 4,692 mg/day) for 1 to 36 months lowered both systolic and diastolic blood pressure compared to placebo ⁷⁴. A similar analysis conducted by the National Academies of Sciences, Engineering, and Medicine committee that included 16 trials found that potassium supplements significantly lowered systolic blood pressure by a mean of 6.87 mmHg and diastolic blood pressure by 3.57 mmHg ¹⁰². However, the effects were stronger among studies including participants with hypertension; for studies including only participants without hypertension, the effects were not statistically significant ¹⁰². Based on 13 randomized controlled trials that primarily enrolled patients with hypertension, the Agency for Healthcare Research and Quality (AHRQ) review found that the use of potassium-containing salt substitutes in place of sodium chloride significantly reduced systolic blood pressure in adults by a mean of 5.58 mmHg and diastolic blood pressure by 2.88 mmHg ⁷⁴. However, reducing sodium intake decreased both systolic and diastolic blood pressure in adults, and increasing potassium intake via food or supplements did not reduce blood pressure any further. This finding suggests that at least some of the beneficial effects of potassium salt substitutes on blood pressure may be due to the accompanying reduction in sodium intake, rather than the increase in potassium intake ²³.

Supplemental potassium can help lower blood pressure, but potassium supplements should only be used in consultation with a medical provider ⁴². Increasing potassium intake to recommended levels (see Table 1) by consuming a diet rich in fruit and vegetables (see Table 2) can help lower blood pressure and may have additional benefits to health ⁴². Blood pressure is a reliable cardiovascular diseases (CVDs) risk marker ¹⁰³. Yet, although reducing sodium consumption while increasing potassium intake helps with lowering blood pressure ¹⁰⁴, current evidence suggests that dietary advice and support interventions may not be sufficient to deliver long-term cardiovascular benefits in individuals with hypertension ¹⁰⁵.

Stroke

Higher potassium intakes have been associated with a decreased risk of stroke and possibly other cardiovascular diseases (CVDs) ¹⁰⁶. Observational studies have consistently reported an increased risk of cardiovascular disease with elevated dietary sodium intakes ¹⁰⁷, ¹⁰⁸. Several prospective cohort studies have also found an inverse association between potassium intake and risk of stroke. A meta-analysis of 11 prospective cohort studies in 247,510 adults found that a 1,640 mg per day higher potassium intake was associated with a significant 21% lower risk of stroke as well as nonsignificant lower risks of coronary heart disease and total cardiovascular disease ¹⁰⁹. Similarly, the authors of a meta-analysis of 9 cohort studies reported a significant 30% lower risk of stroke with daily potassium intakes ranging between 3,510 mg and 4,680 mg and a nonsignificant reduction in coronary heart disease and cardiovascular disease (CVD) risk ¹¹⁰. However, the Agency for Healthcare Research and Quality (AHRQ) review found inconsistent relationships between potassium intakes and risk of stroke based on 15 observational studies ⁷⁴.

In a more recent meta-analysis of 16 studies, the highest versus lowest dietary potassium intake was found to be associated with a 13% lower risk of stroke after multiple adjustments (including for blood pressure) ¹¹¹. The lowest risk of stroke corresponded to daily potassium intakes around 3,500 mg. Subgroup analyses showed a reduced risk of ischemic stroke, but not hemorrhagic stroke. Finally, in a recent meta-analysis of 16 observational studies, each 1-unit increase in the dietary sodium-to-potassium ratio was found to be associated with a 22% higher risk of stroke ⁸⁶.

Any beneficial effect of potassium on cardiovascular disease (CVD) is likely due to its antihypertensive effects. However, some research shows a benefit even when blood pressure is accounted for. For example, a 2016 meta-analysis of 16 cohort studies with a total of 639,440 participants found that those with the highest potassium intakes (median 103 mmol [4,027 mg] per day) had a 15% lower risk of stroke than those with the lowest potassium intakes (median 52.5 mmol [2,053 mg] per day) ¹¹¹. In addition, participants who consumed 90 mmol potassium/day (approximately 3,500 mg) had the lowest risk of stroke ¹¹¹. However, even when blood pressure was accounted for, higher potassium intakes still produced a significant 13% lower risk of stroke. These findings suggest that other mechanisms (e.g., improved endothelial function and reduced free radical formation) may be involved ⁸⁶.

The FDA has approved the following health claim: “Diets containing foods that are a good source of potassium and that are low in sodium may reduce the risk of high blood pressure and stroke” ¹¹². Overall, the evidence suggests that consuming more potassium might have a favorable effect on blood pressure and stroke, and it might also help prevent other forms of cardiovascular disease. However, more research on both dietary and supplemental potassium is needed before firm conclusions can be drawn.

Kidney stones

Kidney stones are most common in people aged 40 to 60 ¹¹³. Stones containing calcium in the form of calcium oxalate or calcium phosphate are the most common type of kidney stone. Low potassium intakes impair calcium reabsorption within the kidney, increasing urinary calcium excretion and potentially causing abnormally high urinary calcium (hypercalciuria) and kidney stones ⁶¹, ⁸⁶. Low urinary levels of citrate also contribute to kidney stone development.

In individuals with a history of developing calcium-containing kidney stones, increased dietary acid load has been significantly associated with increased urinary calcium excretion ¹¹⁴. Increasing dietary potassium (and alkali) intake by increasing fruit and vegetable intake or by taking potassium bicarbonate (KHCO3) supplements has been found to decrease urinary calcium excretion ¹¹⁵, ¹¹⁶. Conversely, potassium deprivation has been found to increase urinary calcium excretion ¹¹⁵, ¹¹⁶.

Observational studies show inverse associations between dietary potassium intakes and risk of kidney stones. In a cohort of 45,619 men aged 40 to 75 years with no history of kidney stones, those with the highest potassium intakes (≥4,042 mg/day on average) had a 51% lower risk of kidney stones over 4 years of follow-up than those with the lowest intakes (≤2,895 mg/day) ¹¹⁷. Similarly, in over 90,000 women aged 34–59 who participated in the Nurses’ Health Study and had no history of kidney stones, those who consumed an average of over 4,099 mg of potassium per day had a 35% lower risk of kidney stones over a 12-year follow-up period than those who averaged less than 2,407 mg of potassium per day ¹¹⁸.

Three large US prospective cohort studies — the Health Professionals Follow-up Study and the Nurses’ Health Studies I and II — which included 193,676 participants, have examined dietary potassium intake and animal protein-to-potassium ratio (a marker of dietary acid load) in the diet in relation to the risk of developing kidney stones ¹¹⁹. In all three cohorts, dietary potassium intake was derived almost entirely from potassium-rich foods, such as fruit and vegetables. Across the three cohorts, individuals in the highest quintile of potassium intake were found to be 33%-56% less likely to develop symptomatic kidney stones than those in the lowest quintile of intake ¹¹⁹. Additionally, a pooled analysis of the data from all three cohorts showed that those with the highest versus lowest animal protein-to-potassium ratio were 41% more likely to develop kidney stones ¹¹⁹.

Some research suggests that supplementation with potassium citrate reduces hypercalciuria as well as the risk of kidney stone formation and growth ¹¹³. In a clinical trial of 57 patients with at least two kidney stones (either calcium oxalate or calcium oxalate plus calcium phosphate) over the previous 2 years and hypocitraturia (low urinary citrate levels), supplementation with 30–60 mEq potassium citrate (providing 1,173 to 2,346 mg potassium) for 3 years significantly reduced kidney stone formation compared with placebo ¹²⁰. This study was included in a 2015 Cochrane review of seven studies that examined the effects of potassium citrate, potassium-sodium citrate, and potassium-magnesium citrate supplementation on the prevention and treatment of calcium-containing kidney stones in a total of 477 participants, most of whom had calcium oxalate stones ¹¹³. The potassium citrate salts significantly reduced the risk of new stones and reduced stone size. However, the proposed mechanism involves citrate, not potassium per se; citrate forms complexes with urinary calcium and increases urine pH, inhibiting the formation of calcium oxalate crystals ¹¹³, ¹²¹. Urinary alkalinization with supplemental potassium citrate is used in kidney stone formers to reduce the risk of recurrent kidney stone formation ¹²². However, potassium citrate therapy should only be initiated under the supervision of a medical provider.

The authors of the Agency for Healthcare Research and Quality (AHRQ) review concluded that observational studies suggest an association between higher potassium intakes and lower risk of kidney stones ⁷⁴. However, they also found the evidence insufficient to determine whether potassium supplements are effective because only one trial that addressed this question ¹²⁰ met their inclusion criteria.

Additional research is needed to fully understand the potential link between dietary and supplemental potassium and the risk of kidney stones.

Bone health

Observational studies suggest that increased consumption of potassium from fruits and vegetables is associated with increased bone mineral density (BMD) ¹²³. This evidence, combined with evidence from metabolic studies and a few clinical trials, suggests that dietary potassium may improve bone health.

In a 2015 case-cohort study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk study, which included 5,319 individuals, dietary intakes of potassium (alone or combined with intakes of magnesium) were found to be inversely associated with heel bone (calcaneus) broadband ultrasound attenuation (BUA) measurements (a predictor of the risk of incidental fracture) and risk of hip fracture in women but not in men ¹²⁴. More recently, a cross-sectional study in older Korean adults reported higher total hip and femur neck bone mineral density (BMD) in those in the top versus bottom tertile of potassium intakes ¹²⁵. Although these observational studies suggest a link between potassium intakes and bone health, they cannot establish whether there is a cause-and-effect relationship ⁴².

The underlying mechanisms by which potassium might influence bone health are poorly understood, but one hypothesis is that potassium helps protect bone through its effect on acid-base balance ⁸⁶. Western diets tend to be relatively low in sources of alkali (fruit and vegetables) and high in sources of acid (fish, meat, and cheese) ¹²⁶. When the quantity of bicarbonate ions is insufficient to maintain normal pH, the body is capable of mobilizing alkaline calcium salts from bone in order to neutralize acids consumed in the diet or generated by metabolism ¹²⁷. Because fruit and vegetables are rich in both potassium and precursors to bicarbonate ions, increasing their consumption might help reduce the net acid content of the diet and preserve calcium in bones, which might otherwise be mobilized to maintain normal pH.

Diets that are high in acid-forming foods, such as meats and cereal grains, contribute to metabolic acidosis and might have an adverse effect on bone. Alkaline components in the form of potassium salts (potassium bicarbonate or citrate, but not potassium chloride) from food or potassium supplements might counter this effect and help preserve bone tissue. In the Framingham Heart Study for example, higher potassium intake was associated with significantly greater bone mineral density in 628 elderly men and women ¹²⁸. In another study, the DASH eating pattern significantly reduced biochemical markers of bone turnover ¹²⁹. The DASH eating pattern has a lower acid load than typical Western diets and is also high in calcium and magnesium, in addition to potassium, so any independent contribution of potassium cannot be determined ²³.

Only a few clinical trials have examined the effects of potassium supplements on markers of bone health. One trial found that supplementation with potassium citrate at either 60 mmol/day (2,346 mg potassium) or 90 mmol/day (3,519 mg potassium) for 6 months significantly reduced urinary calcium excretion compared with placebo in 52 healthy men and women older than 55 years ¹³⁰. In another clinical trial, 201 healthy adults aged 65 years or older received daily supplementation with 60 mEq potassium citrate (providing 2,346 mg potassium) or placebo as well as 500 mg/day calcium (as calcium carbonate) and 400 IU/day vitamin D3 for 2 years ¹³¹. Potassium supplementation significantly increased bone mineral density at the lumbar spine and bone microarchitecture compared with placebo. In a similar clinical trial among older adults, supplemental potassium bicarbonate (mean doses of 2,893 or 4,340 mg/day potassium) for 84 days significantly reduced biochemical markers of bone turnover and urinary calcium excretion ¹³². Conversely, a clinical trial in 276 postmenopausal women aged 55–65 years found that supplementation with potassium citrate at either 18.5 mEq/day (providing 723 mg potassium) or 55.5 mEq/day (2,170 mg potassium) for 2 years did not significantly reduce bone turnover or increase bone mineral density at the hip or lumbar spine compared with placebo ¹³³.

Overall, higher intakes of potassium from diets that emphasize fruits and vegetables might improve bone health. However, more research is needed to elucidate the underlying mechanisms and tease out potassium’s individual contribution ²³.

Blood glucose control and type 2 diabetes

Type 2 diabetes is a growing public health concern that currently affects almost 12% of U.S. adults ¹³⁴. Although obesity is the primary risk factor for type 2 diabetes, other metabolic factors also play a role. Because potassium is needed for insulin secretion from pancreatic cells, hypokalemia impairs insulin secretion and could lead to glucose intolerance ⁴. This effect has been observed mainly with long-term use of diuretics (particularly those containing thiazides) or hyperaldosteronism (excessive aldosterone production), which both increase urinary potassium losses, but it can occur in healthy individuals as well ⁴, ²⁵, ⁶¹, ¹³⁵.

Numerous observational studies of adults have found associations between lower potassium intakes or lower serum or urinary potassium levels and increased rates of fasting glucose, insulin resistance, and type 2 diabetes ¹³⁶, ¹³⁷, ¹³⁸, ¹³⁹, ¹⁴⁰, ¹⁴¹, ¹⁴². These associations might be stronger in African Americans, who tend to have lower potassium intakes, than in whites ¹³⁸, ¹⁴¹. For example, one study of 1,066 adults aged 18–30 years without diabetes found that those with urinary potassium levels in the lowest quintile were more than twice as likely to develop type 2 diabetes over 15 years of follow-up than those in the highest quintile ¹³⁸. Among 4,754 participants from the same study with potassium intake data, African Americans with lower potassium intakes had a significantly greater risk of type 2 diabetes over 20 years of follow-up than those with higher intakes, but this association was not found in whites ¹³⁸.

In another observational study, which analyzed data from 84,360 women aged 34–59 years participating in the Nurses’ Health Study, those in the highest quintile of potassium intake had a 38% lower risk of developing type 2 diabetes over 6 years of follow-up than those in the lowest quintile ¹³⁶. Serum potassium levels were inversely associated with fasting glucose levels in 5,415 participants aged 45–84 years from the Multi-Ethnic Study of Atherosclerosis, but these levels had no significant association with diabetes risk over 8 years of follow-up ¹⁴⁰.

Although observational studies suggest that potassium status is linked to blood glucose control and type 2 diabetes, this association has not been adequately evaluated in clinical trials. In a small clinical trial in 29 African American adults with prediabetes and low to normal serum potassium levels (3.3–4.0 mmol/L), supplementation with 40 mEq (1,564 mg) potassium (as potassium chloride) for 3 months significantly lowered fasting glucose levels, but it did not affect glucose or insulin measures during an oral glucose tolerance test ¹⁴³.

The findings from studies conducted to date are promising. But more research, including randomized controlled trials, is needed before potassium’s link with blood glucose control and type 2 diabetes can be confirmed ²³.

High Potassium (Hyperkalemia)

Hyperkalemia is the medical term that describes a potassium level in your blood that is greater than 5 mEq/L or greater than 5 mmol/L (Kim MJ, Valerio C, Knobloch GK. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2023 Jan;107(1):59-70.https://www.aafp.org/pubs/afp/issues/2023/0100/potassium-disorders-hypokalemia-hyperkalemia.html)), ¹⁴⁴. Your blood potassium level is normally between 3.5 to 5.0 millimoles per liter (mmol/L) or 3.5 to 5.0 milliequivalent per liter (mEq/L) ¹, ³⁴, ³⁵, ³⁶, ¹⁴⁵.

Potassium is a nutrient that is critical to the function of nerve and muscle cells, including those in your heart ¹⁴⁶.

In healthy people with normal kidney function, high dietary potassium intakes do not pose a health risk because the kidneys eliminate excess potassium in the urine ⁵¹. Although case reports indicate that very large doses of potassium supplements can cause heart abnormalities and death, the National Academies of Sciences, Engineering, and Medicine committee concluded that these reports do not provide sufficient evidence to set a Tolerable Upper Intake Level (UL) ¹⁰². In addition, there is no evidence that high intakes of potassium cause hyperkalemia in adults with normal kidney function or other adverse effects. Therefore, the committee did not set a Tolerable Upper Intake Level (UL) for potassium ¹⁰².

However, in people with impaired urinary potassium excretion due to chronic kidney disease or the use of certain medications, such as angiotensin converting enzyme (ACE) inhibitors or potassium-sparing diuretics, even dietary potassium intakes below the Adequate Intake (see Table 1) can cause hyperkalemia ¹⁰². Hyperkalemia can also occur in people with type 1 diabetes, congestive heart failure, adrenal insufficiency, or liver disease ²⁶, ¹⁴⁷. Individuals at risk of hyperkalemia should consult a physician or registered dietitian about appropriate potassium intakes from all sources.

Often a report of high blood potassium isn’t true hyperkalemia also known as pseudohyperkalemia. Instead, pseudohyperkalemia (false elevation in measured potassium) may be caused by the rupture of blood cells in the blood sample during or shortly after the blood draw  due to specimen collection, handling, or other causes ¹⁴⁸, ¹⁴⁹. The ruptured cells leak their potassium into the sample. This falsely raises the amount of potassium in the blood sample, even though the potassium level in your body is actually normal. When this is suspected, a repeat blood sample is done ¹⁴⁹.

While mild hyperkalemia is usually asymptomatic, very high potassium levels (blood potassium level higher than 6.0 mmol/L) may cause life-threatening cardiac arrhythmias, heart palpitations, muscle weakness, paralysis and paresthesias (a burning or prickling sensation in the extremities) and requires immediate treatment ¹⁴⁸, ²⁶, ¹⁴⁷, ¹⁵⁰. Symptoms usually develop at higher levels, 6.5 mEq/L to 7 mEq/L, but the rate of change is more important than the numerical value ¹⁴⁸.

Patients with chronic hyperkalemia may be asymptomatic at increased levels, while patients with dramatic, acute potassium shifts may develop severe symptoms at lower ones ¹⁴⁸. Infants have higher baseline levels than children and adults ¹⁴⁸.

Talk to your doctor about what your results mean. Hyperkalemia should always be confirmed before aggressive treatment in cases where the serum potassium is elevated without explanation ¹⁴⁸.  True hyperkalemia may be caused by increased potassium intake, transcellular movement of intracellular potassium into the extracellular space, and decreased renal excretion. The urgency of therapy depends on symptoms, serum levels, and causes of hyperkalemia ¹⁵¹, ¹⁵². You may need to change a medication that’s affecting your potassium level, or you may need to treat another medical condition that’s causing your high potassium level. Treatment of high potassium is often directed at the underlying cause. In some instances, you may need emergency medications or dialysis.

High potassium symptoms

There are often no symptoms with a high level of potassium.

High potassium is usually found when your doctor has ordered blood tests to help diagnose a condition you’re already experiencing or to monitor medications you’re taking. It’s usually not discovered by chance.

If you have symptoms of hyperkalemia, particularly if you have kidney disease or are taking medications that raise your potassium level, call your doctor immediately. Hyperkalemia is a serious and potentially life-threatening disorder. It can cause:

• Muscle fatigue
• Weakness
• Paralysis
• Difficulty breathing
• Abnormal heart rhythms (arrhythmias) – slow, weak, or irregular pulse
• Palpitations
• Nausea or vomiting
• Chest pain
• Sudden collapse, when the heartbeat gets too slow or even stops

Talk to your doctor about what your results mean. You may need to change a medication that’s affecting your potassium level, or you may need to treat another medical condition that’s causing your high potassium level ¹⁵³. Treatment of high potassium is often directed at the underlying cause. In some instances, you may need emergency medications or dialysis.

If you have symptoms of hyperkalemia and have reason to think your potassium level might be high, call your doctor immediately.

Hyperkalemia (high potassium) causes

The most common cause of high blood potassium or hyperkalemia is pseudohyperkalemia, which is not reflective of the true serum potassium levels ¹⁴⁸. Instead, it may be caused by the rupture of blood cells in the blood sample (hemolysis of the sample) during or shortly after the blood draw. The ruptured blood cells leak their potassium into the sample. This falsely raises the amount of potassium in the blood sample (pseudohyperkalemia), even though the potassium level in your body is actually normal. When this is suspected, a repeat blood sample is done. Hemolysis is more common when a syringe is used than a vacuum device. Using tourniquets and excessive fist-pumping during the blood draw also increase the risk. Specimens drawn from patients with leukocytosis or thrombocytosis are also frequently associated with falsely elevated potassium concentrations ¹⁴⁸.

The most common cause of genuinely high potassium (hyperkalemia) is related to your kidneys, such as ¹⁵⁴:

• Acute kidney failure also called acute renal failure or acute kidney injury occurs when your kidneys suddenly become unable to filter waste products from your blood. Acute kidney failure can occur when ¹⁵⁵:
  • You have a condition that slows blood flow to your kidneys. Diseases and conditions that may slow blood flow to the kidneys and lead to kidney injury include:
    • Blood or fluid loss
    • Blood pressure medications
    • Heart attack
    • Heart disease
    • Infection
    • Liver failure
    • Use of aspirin, ibuprofen (Advil, Motrin IB, others), naproxen sodium (Aleve, others) or related drugs
    • Severe allergic reaction (anaphylaxis)
    • Severe burns
    • Severe dehydration
  • You experience direct damage to your kidneys. Diseases, conditions and agents that may damage the kidneys and lead to acute kidney failure include:
    • Blood clots in the veins and arteries in and around the kidneys
    • Cholesterol deposits that block blood flow in the kidneys
    • Glomerulonephritis, inflammation of the tiny filters in the kidneys (glomeruli)
    • Hemolytic uremic syndrome, a condition that results from premature destruction of red blood cells
    • Infection, such as with the virus that causes coronavirus disease 2019 (COVID-19)
    • Lupus, an immune system disorder causing glomerulonephritis
    • Medications, such as certain chemotherapy drugs, antibiotics and dyes used during imaging tests
    • Scleroderma, a group of rare diseases affecting the skin and connective tissues
    • Thrombotic thrombocytopenic purpura, a rare blood disorder
    • Toxins, such as alcohol, heavy metals and cocaine
    • Muscle tissue breakdown (rhabdomyolysis) that leads to kidney damage caused by toxins from muscle tissue destruction
    • Breakdown of tumor cells (tumor lysis syndrome), which leads to the release of toxins that can cause kidney injury
  • Your kidneys’ urine drainage tubes (ureters) become blocked and wastes can’t leave your body through your urine. Diseases and conditions that block the passage of urine out of the body (urinary obstructions) and can lead to acute kidney injury include:
    • Bladder cancer
    • Blood clots in the urinary tract
    • Cervical cancer
    • Colon cancer
    • Enlarged prostate
    • Kidney stones
    • Nerve damage involving the nerves that control the bladder
    • Prostate cancer
• Chronic kidney disease also called chronic kidney failure, involves a gradual loss of kidney function. Chronic kidney disease occurs when a disease or condition impairs kidney function, causing kidney damage to worsen over several months or years. Diseases and conditions that cause chronic kidney disease include ¹⁵⁶:
  • Type 1 or type 2 diabetes
  • High blood pressure
  • Glomerulonephritis, an inflammation of the kidney’s filtering units (glomeruli)
  • Interstitial nephritis, an inflammation of the kidney’s tubules and surrounding structures
  • Polycystic kidney disease or other inherited kidney diseases
  • Prolonged obstruction of the urinary tract, from conditions such as enlarged prostate, kidney stones and some cancers
  • Vesicoureteral reflux, a condition that causes urine to back up into your kidneys
  • Recurrent kidney infection, also called pyelonephritis

Glomerular filtration rate (GFR) is a measure of how well your kidneys filter blood and it is equal to the total of the filtration rates of the functioning nephrons in the kidney ¹⁵⁷. Normal GFR varies according to age, sex, and body size; in young adults, it is approximately 120 mL/minute/1.73 m² and declines with age. Acute or chronic kidney disease hyperkalemia is usually not seen until the glomerular filtration rate (GFR) falls below 30 mL/min/1.73 m² ¹⁴⁸. This is commonly due to primary kidney dysfunction but may be due to acute volume depletion from dehydration or bleeding or decreased circulating blood volume due to congestive heart failure or cirrhosis. Tubular dysfunction due to aldosterone deficiency or insensitivity can also cause hyperkalemia.

Other causes of hyperkalemia include:

• Addison’s disease (adrenal failure). Disease in which the adrenal glands do not make enough aldosterone hormone (and cortisol), reducing the kidneys’ ability to remove potassium from the body
• Alcoholism or heavy drug use that causes rhabdomyolysis, a breakdown of muscle fibers that results in the release of potassium into the bloodstream
• Angiotensin-converting enzyme (ACE) inhibitors
• Angiotensin 2 receptor blockers (ARBs)
• Beta blockers
• Dehydration (which is when the body doesn’t have enough water and other fluids to work properly)
• Destruction of red blood cells due to severe injury or burns
• Excessive use of potassium supplements
• Type 1 diabetes

ACE inhibitors and angiotensin receptor blockers (ARBs)

ACE inhibitors, such as benazepril (Lotensin®), and angiotensin 2 receptor blockers (ARBs) such as losartan (Cozaar®), are used to treat hypertension and heart failure, slow progression of kidney disease in patients with chronic kidney disease and type 2 diabetes, and decrease morbidity and mortality after myocardial infarction ⁸⁰. These medications reduce urinary potassium excretion, which can lead to hyperkalemia. Experts recommend monitoring potassium status in people taking ACE inhibitors or angiotensin receptor blockers (ARBs), especially if they have other risk factors for hyperkalemia, such as impaired kidney function ⁸⁰.

Potassium sparing diuretics

Potassium-sparing diuretics, such as amiloride (Midamor®) and spironolactone (Aldactone®), reduce the excretion of potassium in the urine and can cause hyperkalemia ⁸². Experts recommend monitoring potassium status in people taking these medications, especially if they have impaired kidney function or other risk factors for hyperkalemia ⁸².

Loop and thiazide diuretics

Treatment with loop diuretics, such as furosemide (Lasix®) and bumetanide (Bumex®), and thiazide diuretics, such as chlorothiazide (Diuril®) and metolazone (Zaroxolyn®), increases urinary potassium excretion and can lead to hypokalemia ⁸². Experts recommend monitoring potassium status in people taking these medications, and initiating potassium supplementation if warranted.

Intracellular potassium shifts

Cellular injury can release large quantities of intracellular potassium into the extracellular space. This can be due to rhabdomyolysis from a crush injury, excessive exercise, or other hemolytic processes. Metabolic acidosis may cause intracellular potassium to shift into the extracellular space without red cell injury. Metabolic acidosis is most frequently caused by decreased, effective circulating arterial blood volume. Sepsis or dehydration may lead to hypotension and decreased tissue perfusion leading to metabolic acidosis with subsequent potassium elevation.

Insulin deficiency and diabetic ketoacidosis may cause dramatic extracellular shifts causing measured serum potassium to be elevated in the setting of whole-body potassium depletion. Certain medications, such as succinylcholine, may cause severe, acute potassium elevations in patients with up-regulation of receptors, particularly in subacute neuromuscular disease. Tumor lysis syndrome, particularly in patients receiving chemotherapy for hematogenous malignancy, may cause acute hyperkalemia due to massive cancer cell death ¹⁵⁸.

Hyperkalemic periodic paralysis (hyperPP or hyperKPP) is a rare, autosomal dominant condition caused by a mutation in the SCN4A gene that codes for voltage-gated sodium channel causing potassium to shift into the extracellular space due to impaired sodium channel function in skeletal muscle ¹⁵⁹, ¹⁶⁰. Hyperkalemic periodic paralysis (hyperPP) is characterized by attacks of flaccid limb weakness (which may also include weakness of the muscles of the eyes, throat, breathing muscles, and trunk), hyperkalemia (serum potassium concentration greater than 5 mmol/L) or an increase of serum potassium concentration of at least 1.5 mmol/L during an attack of weakness and/or provoking/worsening of an attack by oral potassium intake, normal serum potassium between attacks, and onset before age 20 years ¹⁶¹, ¹⁶⁰. In approximately half of affected individuals, attacks of flaccid muscle weakness begin in the first decade of life, with 25% reporting their first attack at age ten years or older ¹⁶⁰. Initially infrequent, the attacks then increase in frequency and severity over time until approximately age 50 years, after which the frequency of attacks declines considerably ¹⁶⁰. The major attack trigger is eating potassium-rich foods; other triggers include: cold environment; rest after exercise, stress, or fatigue; alcohol; hunger; and changes in activity level. A spontaneous attack commonly starts in the morning before breakfast, lasts for 15 minutes to one hour, and then passes. Individuals with hyperPP frequently have myotonia (muscle stiffness), especially around the time of an episode of weakness. Paramyotonia (muscle stiffness aggravated by cold and exercise) is present in about 45% of affected individuals. More than 80% of individuals with hyperkalemic periodic paralysis (hyperPP) older than age 40 years report permanent muscle weakness and about one third develop a chronic progressive myopathy ¹⁶⁰. Hyperkalemic periodic paralysis (hyperPP) is caused by a mutation in the SCN4A gene that codes for voltage-gated sodium channel Na1.4 ¹⁵⁹. Several diagnostic modalities exist in assisting diagnosis, such as genetic testing, although they are not always definitive. In case of diagnostic uncertainty, a provocative test can be employed, although the availability of genetic testing and electrophysiologic studies largely obviates the need for such dangerous tests. Treatment for hyperkalemic periodic paralysis (hyperPP) is both proactive and reactive, with avoidance of triggers being the mainstay of therapy. At the onset of weakness, attacks may be prevented or aborted with mild exercise and/or oral ingestion of carbohydrates, intravenously injected glucocorticoids, inhalation of salbutamol, or intravenous calcium gluconate ¹⁶⁰. Hyperkalemic attacks of weakness can be prevented by frequent meals rich in carbohydrates; continuous use of a thiazide diuretic or a carbonic anhydrase inhibitor; and avoidance of potassium-rich medications and foods, fasting, strenuous work, and exposure to cold ¹⁶⁰.

Increased potassium intake

Increased potassium intake from food is a very uncommon cause of hyperkalemia in adult patients with normal kidney function but can be an important cause in those with kidney disease. Foods with high potassium content include dried fruits, seaweed, nuts, molasses, avocados, and Lima beans. Many vegetables that are also high in potassium include spinach, potatoes, tomatoes, broccoli, beets, carrots, and squash. High-potassium-containing fruits include kiwis, mangoes, oranges, bananas, and cantaloupe. Red meats are also rich in potassium. While generally safe to consume even in large quantities by patients with normal potassium homeostasis, these foods should be avoided in patients with severe renal disease or other underlying conditions or medications predisposing them to hyperkalemia. Intravenous intake through high potassium-containing fluids, particularly total parenteral nutrition, medications with high potassium content, and massive blood transfusions can significantly elevate serum potassium levels.

Can hyperkalemia be prevented?

Dietary changes can help prevent and treat high potassium levels. Talk to your doctor to understand any risk you might have for hyperkalemia. Your doctor may recommend foods that you may need to limit or avoid. These may include:

• asparagus, avocados, potatoes, tomatoes or tomato sauce, winter squash, pumpkin, cooked spinach
• oranges and orange juice, nectarines, kiwifruit, bananas, cantaloupe, honeydew, prunes and raisins or other dried fruit.

If you are on a low-salt diet, avoid taking salt substitutes ¹⁶².

Hyperkalemia diagnosis

Your health care provider will perform a physical exam and ask about your symptoms. Most patients with mild and even moderate hyperkalemia are relatively asymptomatic ¹⁴⁸. High potassium is often discovered on screening blood tests done in patients with nonspecific complaints, to monitor medications you’re taking or those with suspected electrolyte abnormalities due to infection, dehydration, or hypoperfusion. High potassium is usually not discovered by chance. Causes include renal disease, diabetes, chemotherapy, major trauma, crush injury, or muscle pain suggestive of rhabdomyolysis. Medications that may predispose to the development of hyperkalemia include digoxin, potassium-sparing diuretics, non-steroidal anti-inflammatory drugs, ace-inhibitors or recent intravenous (IV) potassium, total parenteral nutrition, potassium penicillin, or succinylcholine. Patients may complain of weakness, fatigue, palpitations, or syncope.

Physical exam findings may include hypertension and edema in the setting of kidney disease. There may also be signs of hypoperfusion. Muscle tenderness may be present in patients with rhabdomyolysis. Jaundice may be seen in patients with hemolytic conditions. Patients may have muscle weakness, flaccid paralysis, or depressed deep tendon reflexes.

Tests that may be ordered include:

• Electrocardiogram (ECG). The first test that should be ordered in a patient with suspected hyperkalemia is an ECG since the most lethal complication of hyperkalemia is cardiac condition abnormalities which can lead to abnormal heart rhythms (arrhythmias) and death.
• Potassium level

Elevated potassium causes ECG changes in a dose-dependent manner ¹⁴⁸:

• Potassium level = 5.5 to 6.5 mEq/L ECG will show tall, peaked T-waves
• Potassium level = 6.5 to 7.5 mEq/L ECG will show loss of P-waves
• Potassium level = 7 to 8 ECG mEq/L will show widening of the QRS complex
• Potassium level = 8 to 10 mEq/L will produce cardiac arrhythmias, sine wave pattern, and asystole

It should be noted that the rate of rising serum potassium is a greater factor than the potassium level ¹⁴⁸. Patients with chronic hyperkalemia may have relatively normal EGCs even at high levels, and significant ECG changes may be present at much lower levels in patients with sudden spikes in serum potassium ¹⁴⁸.

ECG features of hyperkalemia include ¹⁴⁸:

• Small or absent P wave
• Prolonged PR interval
• Augmented R wave
• Wide QRS
• Peaked T waves

Since pseudohyperkalemia is so common, confirmation should be obtained in asymptomatic patients without typical ECG changes before initiating aggressive therapy ¹⁴⁸.

Your doctor will also likely check your blood potassium level and do kidney blood tests on a regular basis if you:

• Have been prescribed extra potassium
• Have chronic kidney disease
• Take medicines to treat heart disease or high blood pressure
• Use salt substitutes

Additional laboratory testing should include serum blood urea nitrogen (BUN) and creatinine to assess renal function and urinalysis to screen for renal disease. Urine potassium, sodium, and osmolality may also help evaluate the cause. In patients with renal disease, the serum calcium level should also be checked because hypocalcemia may exacerbate the cardiac effects of hyperkalemia. A complete blood count to screen for leukocytosis or thrombocytosis may also be helpful. Serum glucose and blood gas analysis should be ordered in diabetics and patients with suspected acidosis. Lactate dehydrogenase should be ordered in patients with suspected hemolysis. Creatinine phosphokinases and urine myoglobin should be ordered in patients with suspected rhabdomyolysis. Uric acid and phosphorus should be ordered in patients with suspected tumor lysis syndrome. Digoxin toxicity may cause hyperkalemia, so serum levels should be checked in patients on digoxin. If no other cause is found, consider cortisol and aldosterone levels to assess for mineralocorticoid deficiency.

Hyperkalemia treatment

The urgency with which hyperkalemia should be managed depends on how rapidly the condition develops, the absolute serum potassium level, the degree of symptoms, and the cause ¹⁶³, ¹⁶⁴, ¹⁶⁵. If your potassium level is very high (more than 5.5 mEq/L in patients at risk for ongoing hyperkalemia or confirmed hyperkalemia of 6.5 mEq/L), or if there are dangerous indications such as changes in an electrocardiogram (ECG), neuromuscular weakness or paralysis, emergency treatment is needed. That may involve supplying calcium to the body through an intravenous to treat the effects on muscles and the heart or administering glucose and insulin through an intravenous to decrease potassium levels long enough to correct the cause. There are also medicines that help remove the potassium from your intestines and in some cases, a diuretic may be given.

Emergency treatment may also include kidney dialysis if kidney function is deteriorating; medication to help remove potassium from the intestines before absorption; sodium bicarbonate if acidosis is the cause; and water pills, or diuretics.

A doctor may also advise stopping or reducing potassium supplements and stopping or changing the doses of certain medicines for heart disease and high blood pressure. Always follow your health provider’s instructions about taking or stopping medicines.

Hyperkalemia treatment is usually prescribed in the following manner ¹⁴⁸:

1. Exogenous sources of potassium should be immediately discontinued.
2. Treatment of the reversible cause should begin along with the management of hyperkalemia.
3. Calcium given into your veins (IV) to treat the muscle and heart effects of high potassium levels. Calcium therapy will stabilize the cardiac response to hyperkalemia and should be initiated first in the setting of cardiac toxicity. Calcium does not alter the serum concentration of potassium but is a first-line therapy in hyperkalemia-related arrhythmias and ECG changes. Calcium chloride contains three times more elemental calcium than calcium gluconate but is more irritating to peripheral vessels and more likely to cause tissue necrosis with extravasation, so it is usually only given through central venous lines or peripherally in cardiac arrest. Thus, calcium gluconate is the usual initial drug of choice in patients with evidence of cardiac toxicity ¹⁶⁶. As a precaution, calcium should never be given in bicarbonate-containing fluids, as it can cause the precipitation of calcium carbonate.
4. Insulin and glucose given into your veins (IV) to help lower potassium levels long enough to correct the cause or insulin alone in hyperglycemic patients, will drive the potassium back into the cells, effectively lowering serum potassium ¹⁶⁷. A common regimen is ten units of regular insulin given with 50 ml of a 50% dextrose solution (D50). Patients should be monitored closely for the development of hypoglycemia (low blood sugar level). A 10% dextrose infusion at 50 to 75 ml/hour is associated with less hypoglycemia than bolus dosing with 50% dextrose solution (D50).
5. Beta-2 adrenergic agents such as albuterol will also shift potassium intracellularly ¹⁶⁸. To be effective, beta-2 agonists are given in much higher doses than those commonly used for bronchodilation. Intravenous epinephrine, however, should not be used to manage hyperkalemia due to an increased risk of causing angina.
6. Sodium bicarbonate infusion may be helpful in patients with metabolic acidosis. Bolus dosing of sodium bicarbonate is less effective.
7. Loop or thiazide diuretics may help enhance potassium excretion. They may be used in non-oliguric, volume-overloaded patients but should not be used as monotherapy in symptomatic patients. In hypervolemic patients with preserved kidney function (e.g., patients with congestive cardiac failure), 40 mg of intravenous furosemide is administered every 12 hours or may be given as a continuous infusion. In euvolemic or hypovolemic patients with preserved kidney function, an isotonic saline infusion is given before as needed to the patient before administering 40 mg of intravenous furosemide every 12 hours or a continuous furosemide infusion.
8. Medicines that help remove potassium from the intestines before it is absorbed such as patiromer may be helpful, particularly in patients with renal insufficiency who cannot receive immediate dialysis. Sodium polystyrene sulfonate, though commonly used, is falling out of favor due to lack of effectiveness and adverse effects, particularly bowel necrosis in elderly patients. If used due to a lack of alternatives, it should not be given with sorbitol, which increases toxicity ¹⁶⁹.
9. Kidney dialysis should be performed in patients with end-stage renal disease or severe renal impairment.

Complications of hyperkalemia treatment ¹⁴⁸:

• Hypokalemia
• Inability to control hyperkalemia
• Hypocalcemia as a result of bicarbonate infusion
• Hypoglycemia due to insulin
• Metabolic alkalosis from bicarbonate therapy
• Volume depletion from diuresis.

Changes in your diet can help both prevent and treat high potassium levels. You may be asked to:

• Limit or avoid asparagus, avocados, potatoes, tomatoes or tomato sauce, winter squash, pumpkin, and cooked spinach
• Limit or avoid oranges and orange juice, nectarines, kiwifruit, raisins, or other dried fruit, bananas, cantaloupe, honeydew, prunes, and nectarines
• Avoid taking salt substitutes if you are asked to eat a low-salt diet

Your doctor may make the following changes to your medicines:

• Reduce or stop potassium supplements
• Stop or change the doses of medicines you are taking, such as ones for heart disease and high blood pressure
• Take a certain type of water pill to reduce potassium and fluid levels if you have chronic kidney failure

Follow your doctor’s directions when taking your medicines:

• DO NOT stop or start taking medicines without first talking to your provider
• Take your medicines on time
• Tell your provider about any other medicines, vitamins, or supplements you are taking

For people with heart failure

There are some drugs that heart failure patients take that are associated with hyperkalemia. These are: diuretics, beta-blockers and angiotension converting enzyme inhibitors (ACE inhibitors). For patients with heart failure on these drugs, if any symptoms are experienced as above, you should tell your doctor to make sure that the symptoms are not related to hyperkalemia.

If your potassium level is too high, you may need to cut back on certain foods (see Table 5). These tips can also help:

• Soak or boil vegetables and fruits to leach out some of the potassium.
• Avoid foods that list potassium or K, KCl, or K+ — chemical symbols for potassium or related compounds — as ingredients on the label.
• Stay away from salt substitutes. Many are high in potassium. Read the ingredient lists carefully and check with your doctor before using one of these preparations.
• Avoid canned, salted, pickled, corned, spiced, or smoked meat and fish.
• Avoid imitation meat products containing soy or vegetable protein.
• Limit high-potassium fruits such as bananas, citrus fruits, and avocados.
• Avoid baked potatoes and baked acorn and butternut squash.
• Don’t use vegetables or meats prepared with sweet or salted sauces.
• Avoid all types of peas and beans, which are naturally high in potassium.

Table 5. Potassium levels in common foods

Foods	High potassium	Medium potassium	Low potassium	No potassium
Fruits and vegetables	Artichokes, avocados, bananas, broccoli, coconut, dried fruits, leafy greens, kiwis, nectarines, oranges, papayas, potatoes, prunes, spinach, tomatoes, winter squash, yams	Apples, apricots, asparagus, carrots, cherries, corn, eggplant, peaches, pears, peppers, pineapple juice, radishes	Blueberries, cauliflower, cucumbers, grapefruit, grapes, green beans, lettuce, strawberries
Meat and protein	Dried beans and peas, imitation bacon bits, nuts, soy products	Beef, eggs, fish, peanut butter, poultry, pork, veal
Dairy	Milk, yogurt		Sour cream
Grains and processed foods	Plain bagel, plain pasta, oatmeal, white bread, white rice	Bran muffins and cereals, corn tortillas, whole-wheat bread		Fruit punches, jelly beans, nondairy topping, nondairy creamers

[Source ¹⁷⁰ ]

Hyperkalemia prognosis

The prognosis is excellent for patients with mild transient hyperkalemia due to too much potassium in the diet if the inciting cause is addressed and treated. Sudden onset, extreme hyperkalemia can cause cardiac arrhythmias that can be deadly in up to two-thirds of cases if not rapidly treated ¹⁴⁸. Hyperkalemia is an independent risk factor for death in hospitalized patients ¹⁴⁸.

Low Potassium (Hypokalemia)

Low potassium levels also known as hypokalemia is defined as serum potassium level less than 3.6 mEq/L or less than 3.6 mmol/L (Kim MJ, Valerio C, Knobloch GK. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2023 Jan;107(1):59-70.https://www.aafp.org/pubs/afp/issues/2023/0100/potassium-disorders-hypokalemia-hyperkalemia.html)). Severe potassium deficiency or hypokalemia is most common in hospitalized patients, affecting up to 21% of hospitalized patients, usually because of the use of water pills (e.g., loop diuretics and thiazide diuretics) and other medications that cause your body to excrete too much potassium, but it is rare among healthy people with normal kidney function ¹⁷¹, ¹⁷². Because your kidneys work to maintain normal blood levels of potassium by flushing out excess amounts through urine. Potassium can also be lost through stool and sweat. Hypokalemia is also seen in people with inflammatory bowel diseases (Crohn’s disease, ulcerative colitis) that may cause diarrhea and malabsorption of nutrients.

Your body needs potassium for the contraction of muscles (including the heart), and for the functioning of many complicated proteins (enzymes). Potassium is found primarily in the skeletal muscle and bone, and participates with sodium to contribute to the normal flow of body fluids between the cells in the body. Potassium is predominantly intracellular (within a cell) where it is the most abundant cation (positive charged ion) and involved in cell regulation and several cellular processes. The fraction of potassium in the extracellular fluid is small. Therefore, plasma or serum potassium levels are not a reliable indicator of total body potassium stores. The normal concentration of potassium in the body is maintained through a combination of adjustments in acute cellular shifts between the extracellular and intracellular fluid compartments, regulated by your kidneys through the excretion of urine and, to a lesser extent, gastrointestinal losses. When your kidneys are functioning normally, the amount of potassium in your diet is sufficient for use by your body and the excess is usually excreted through urine and sweat. Body chemicals and hormones such as aldosterone also regulate potassium balance. Secretion of the hormone insulin, which is normally stimulated by food, prevents a temporary diet-induced hypokalemia by increasing cell absorption of potassium. When hypokalemia occurs, there is an imbalance resulting from a dysfunction in this normal process, or the rapid loss of urine or sweat without replacement of sufficient potassium.

Potassium deficiency or hypokalemia is rarely caused by low dietary potassium intake alone because potassium is found in so many foods (see Table 2) ²³, ⁴², ¹⁷³. However, insufficient dietary potassium in patients at risk of hypokalemia can precipitate hypokalemia ⁴⁰. In rare cases, habitual consumption of large amounts of black licorice has resulted in hypokalemia ¹⁷⁴, ¹⁷⁵. Licorice contains a compound called glycyrrhizic acid that has similar physiologic effects to those of aldosterone, a hormone that increases urinary excretion of potassium.

Too little potassium in your blood or hypokalemia may be a sign of ³⁹:

• Use of prescription diuretics (water pills)
• Fluid loss from diarrhea, vomiting, or heavy sweating
• Using too many laxatives
• Adrenal gland disorders, including Cushing’s syndrome and aldosteronism
• Kidney disease
• Alcohol use disorder
• Eating a lot of real licorice, which comes from licorice plants. Most licorice products sold in the U.S. don’t contain any real licorice. Check the package ingredient label to be sure.
• A diet too low in potassium (not common). Bananas, apricots, green leafy vegetables, avocados and many other foods are good sources of potassium that are part of a healthy diet.

Potassium deficiency or hypokalemia is most commonly a result of excessive loss of potassium from prolonged vomiting or diarrhea, use of some diuretics, laxative abuse, eating clay (a type of pica), heavy sweating, dialysis, using certain medications, some forms of kidney disease, inflammatory bowel disease (Crohn’s disease or ulcerative colitis)or metabolic disturbances. Hypokalemia can also be caused by refeeding syndrome (the metabolic response to initial refeeding after a starvation period) because of potassium’s movement into cells ⁷, ¹⁸, ²⁶, ¹⁷⁶, ¹⁷⁷.

Magnesium deficiency also known as hypomagnesemia can also contribute to hypokalemia by increasing urinary potassium losses ⁴¹, ¹⁷⁸, ¹⁷⁹. Magnesium deficiency can also increase the risk of cardiac arrhythmias by decreasing intracellular potassium concentrations. More than 50% of individuals with clinically significant hypokalemia might have magnesium deficiency ¹⁷⁹. In people with hypomagnesemia and hypokalemia, both should be treated concurrently ²⁶.

In general, hypokalemia is associated with diagnoses of cardiac disease, kidney failure, malnutrition, and shock ¹⁸⁰. Hypothermia (occurs when your body loses heat faster than it can produce heat and your body temperature falls below 95°F (35°C)) and increased blood cell production (for example, leukemia) are additional risk factors for developing hypokalemia ¹⁸⁰. There are subsets of patients that are susceptible to the development of hypokalemia. For instance, psychiatric patients are at risk for hypokalemia due to their drug therapy ¹⁸⁰. Hypokalemia is also prevalent in hospitalized patients, in particular, children, those who have a fever and those who are critically ill ¹⁸⁰. Additionally, in developing countries, an increased risk of death is observed in children when severe hypokalemia is associated with diarrhea and severe malnutrition ¹⁸⁰.

The symptoms of hypokalemia are related to alterations in membrane potential and cellular metabolism ⁴⁰. Mild hypokalemia (serum potassium level is 3 to 3.4 mmol/L) is characterized by fatigue, muscle weakness and cramps, not feeling well, tiredness, and intestinal paralysis, which may lead to bloating, constipation, and abdominal pain ⁷, ⁴². Moderate to severe hypokalemia (serum potassium level less than about 2.5 mmol/L) can cause increased urination (polyuria or large volume of dilute urine); decreased brain function (encephalopathy) in patients with kidney disease; high blood sugar levels or glucose intolerance; muscle paralysis; difficulty breathing; and cardiac arrhythmias (irregular heartbeats), especially in individuals with underlying heart disease ⁴¹, ⁷, ⁵². Severe hypokalemia (serum potassium level less than about 2.5 mmol/L) may result in muscular paralysis or abnormal heart rhythms (cardiac arrhythmias) that can be life threatening ⁴⁰, ⁴¹.

Getting too little potassium can increase blood pressure (hypertension), deplete calcium in bones, and increase the risk of kidney stones formation ⁴², ²³. In the absence of treatment, hypokalemia can have serious complications and even be fatal.

Treatment of low potassium or hypokalemia is directed at the underlying cause and may include potassium supplements. Don’t start taking potassium supplements without talking to your doctor first. You may need to change a medication that’s affecting your potassium level, or you may need to treat another medical condition that’s causing your low potassium level.

Hypokalemia (low potassium) causes

Low potassium (hypokalemia) has many causes. Hypokalemia is always a symptom of another disorder, rather than a disease that occurs by itself. The most common cause is excessive loss of potassium through the urine (kaliuresis) due to prescription water or fluid pills (diuretics). Water pills or diuretics medications are often prescribed for people who have high blood pressure or heart disease.

The excessive excretion of potassium in the urine (kaliuresis) may also result from a deficiency of magnesium in the blood (hypomagnesemia), excessive mineralocorticoids such as aldosterone in the blood (hyperaldosteronism) which affect the electrolyte and fluid balance in the body (usually caused by endocrine diseases), kidney disorders, or from the use of high doses of penicillin.

Typically, the potassium level becomes low because too much potassium is lost from the digestive tract (gastrointestinal losses) due to prolonged diarrhea or vomiting, chronic laxative abuse, inadequate dietary intake of potassium, intestinal obstruction or infections such as fistulas in the intestines which continually drain intestinal fluids. Additionally, excessive perspiration due to hot weather or exercise can cause hypokalemia. Hypokalemia is rarely caused by consuming too little potassium because many foods (such as beans, dark leafy greens, potatoes, fish, and bananas) contain potassium.

In many adrenal disorders, such as Cushing syndrome, the adrenal glands produce too much aldosterone, a hormone that causes the kidneys to excrete large amounts of potassium.

Certain drugs (such as insulin, albuterol, and terbutaline) cause more potassium to move from blood into cells and can result in hypokalemia. However, these drugs usually cause temporary hypokalemia, unless another condition is also causing potassium to be lost.

Hypokalemia sometimes occurs with or is caused by a low level of magnesium in the blood (hypomagnesemia).

Causes of potassium loss leading to low potassium include:

• Excessive alcohol use
• Chronic kidney disease
• Diabetic ketoacidosis
• Diarrhea (causing anal irritation)
• Diuretics (water retention relievers)
• Excessive laxative use
• Excessive sweating
• Folic acid deficiency
• Prescription water or fluid pills (diuretics) use
• Primary aldosteronism
• Some antibiotic use
• Vomiting

Gastrointestinal tract losses

Gastrointestinal potassium losses are another common cause of hypokalemia, particularly among hospitalized patients ¹⁸¹. Abnormal gastrointestinal potassium losses occur in all of the following ¹⁸²:

• Chronic diarrhea, including chronic laxative abuse and bowel diversion
• Clay (bentonite) ingestion, which binds potassium and greatly decreases absorption
• Rarely, villous adenoma of the colon, which causes massive potassium secretion

As a portion of daily potassium is excreted in the colon, lower gastrointestinal losses in the form of persistent diarrhea can also result in hypokalemia and may be accompanied by hyperchloremic acidosis ⁷⁷.

Protracted vomiting or gastric suction (which removes volume and hydrochloric acid) causes renal potassium losses due to metabolic alkalosis and stimulation of aldosterone due to volume depletion; aldosterone and metabolic alkalosis both cause the kidneys to excrete potassium ¹⁸².

Renal potassium losses

Various disorders can increase renal potassium excretion.

Diuretic use is a common cause of renally mediated hypokalemia ¹⁸³. When given in the same dosage, chlorthalidone is more likely to induce hypokalemia than hydrochlorothiazide, which is more often implicated because of its widespread use ¹⁸⁴, ¹⁸⁵. Diuretic-induced hypokalemia is dose-dependent and tends to be mild (3 to 3.5 mEq per L [3 to 3.5 mmol per L]), although it can be more severe when accompanied by other causes (e.g., gastrointestinal losses) ¹⁸⁶.

Excess mineralocorticoid (ie, aldosterone) effect can directly increase potassium secretion by the distal nephrons and occurs in any of the following ¹⁸²:

• Adrenal steroid excess that is due to Cushing syndrome, primary hyperaldosteronism, rare renin-secreting tumors, glucocorticoid-remediable aldosteronism (a rare inherited disorder involving abnormal aldosterone metabolism), and congenital adrenal hyperplasia.
• Bartter syndrome, an uncommon genetic disorder that is characterized by renal potassium and sodium wasting, excessive production of renin and aldosterone, and normotension. Bartter syndrome is caused by mutations in a loop diuretic–sensitive ion transport mechanism in the loop of Henle.
• Gitelman syndrome is an uncommon genetic disorder characterized by renal potassium and sodium wasting, excessive production of renin and aldosterone, and normotension. Gitelman syndrome is caused by loss of function mutations in a thiazide-sensitive ion transport mechanism in the distal nephron.
• Ingestion of substances such as glycyrrhizin (present in natural licorice and used in the manufacture of chewing tobacco), which inhibits the enzyme 11 beta-hydroxysteroid dehydrogenase (11β-HSDH), preventing the conversion of cortisol, which has some mineralocorticoid activity, to cortisone, which does not, resulting in high circulating concentrations of cortisol and renal potassium wasting.
• Liddle syndrome, a rare autosomal dominant disorder caused by unrestrained sodium reabsorption in the distal nephron due to one of several mutations found in genes encoding for epithelial sodium channel subunits. Inappropriately high reabsorption of sodium results in both severe hypertension and renal potassium wasting, resulting in hypokalemia.

Renal potassium wasting can also be caused by numerous congenital and acquired renal tubular diseases, such as the renal tubular acidoses and Fanconi syndrome, an unusual syndrome resulting in renal wasting of potassium, glucose, phosphate, uric acid, and amino acids ¹⁸².

Hypomagnesemia is a common correlate of hypokalemia. Much of this correlation is attributable to common causes (ie, diuretics, diarrhea), but hypomagnesemia itself may also result in increased renal potassium losses ¹⁸².

Intracellular shift

The transcellular shift of potassium into cells may also cause hypokalemia. This shift can occur in any of the following ¹⁸²:

• After administration of insulin
• Familial periodic paralysis
• Glycogenesis during total parenteral nutrition or enteral hyperalimentation (stimulating insulin release)
• Stimulation of the sympathetic nervous system, particularly with beta 2-agonists (eg, albuterol, terbutaline), which may increase cellular potassium uptake
• Thyrotoxicosis (occasionally) due to excessive beta-sympathetic stimulation (hypokalemic thyrotoxic periodic paralysis)

Familial periodic paralysis is a rare autosomal dominant disorder characterized by transient episodes of profound hypokalemia thought to be due to sudden abnormal shifts of potassium into cells. Episodes frequently involve varying degrees of paralysis. They are typically precipitated by a large carbohydrate meal or strenuous exercise.

Drug interactions

Several classes of medications are known to induce low serum potassium or hypokalemia see Table 1 below.

Diuretics are by far the most commonly used drugs that cause hypokalemia. Potassium-wasting diuretics that block sodium reabsorption proximal to the distal nephron include ¹⁸², ⁸²:

• Loop diuretics, such as furosemide (Lasix®) and bumetanide (Bumex®)
• Osmotic diuretics
• Thiazide diuretics, such as chlorothiazide (Diuril®) and metolazone (Zaroxolyn®)

Experts recommend monitoring potassium status in people taking these medications, and initiating potassium supplementation if warranted ⁸².

By inducing diarrhea, laxatives, especially when abused, can cause hypokalemia. Secret diuretic or laxative use or both is a frequent cause of persistent hypokalemia, particularly among patients preoccupied with weight loss and among health care practitioners with access to prescription drugs ¹⁸².

Other drugs that can cause hypokalemia include ¹⁸²:

• Aminoglycosides
• Anti-fungal agents (amphotericin-B, fluconazole)
• Antipseudomonal penicillins (eg, carbenicillin)
• Cisplatin. Cisplatin can damage the renal tubular epithelium and lead to severe potassium loss.
• Corticoids. Corticoids cause sodium retention that leads to a compensatory increase in urinary potassium excretion ⁴².
• Penicillin in high doses. Penicillins formulated as sodium salts also stimulate potassium excretion ⁴².
• Theophylline (both acute and chronic intoxication)

Outdated tetracycline antibiotics have been linked to electrolyte disturbances ⁴².

Table 4. Medications associated with Hypokalemia (low serum potassium)

Medication Family	Specific Medications
Aminoglycosides	amikacin (Amikin), gentamicin (Garamycin), kanamycin (Kantrex), tobramycin (Nebcyn), streptomycin
Antibiotics	Penicillins: penicillin G sodium (Pfizerpen), mezlocillin (Mezlin), carbenicillin (Geocillin), ticarcillin (Ticar) Tetracyclines (when outdated)
Anti-cancer agent	cisplatin (Platinol-AQ)
Anti-fungal agents	amphotericin B (Abelcet, Amphotec, AmBisome, Amphocin, Fungizone), fluconazole (Diflucan)
Beta-adrenergic agonists	albuterol (Salbutamol, Ventolin), bitolterol (Tornalate), metaproterenol (Alupent)
Diuretics	Loop diuretics: bumetanide (Bumex), ethacrynic acid (Edecrin), furosemide (Lasix), torsemide (Demadex) Thiazide diuretics: Acetazolamide, thiazides, chlorthalidone (Hygroton), indapamide (Lozol), metolazone (Zaroxolyn), chlorothiazide (Diuril)
Mineralocorticoids	fludrocortisone (Florinef), hydrocortisone (Cortef), cortisone (Cortone), prednisone (Deltasone) Substances with mineralocorticoid effects: licorice, carbenoxolone, gossypol
Other	methylxanthines (e.g., theophylline), sodium polystyrene sulfonate, sodium phosphates, caffeine

Groups at Risk of Potassium Deficiency

Potassium deficiency can occur with intakes that are below the Adequate Intake (AI) [intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an Recommended Dietary Allowance (RDA)] but above the amount required to prevent hypokalemia. The following groups are more likely than others to have poor potassium status.

People with inflammatory bowel diseases

Potassium is secreted within the colon, and this process is normally balanced by absorption ¹⁸⁷. However, in inflammatory bowel disease (including Crohn’s disease and ulcerative colitis), potassium secretion increases, which can lead to poor potassium status. Inflammatory bowel diseases are also characterized by chronic diarrhea, which can further increase potassium excretion ¹⁸⁸.

People who use certain medications, including diuretics and laxatives

Certain diuretics (e.g., thiazide diuretics, loop diuretics) that are commonly used to treat high blood pressure increase urinary potassium excretion and can cause hypokalemia ²⁶, ⁷⁷. Potassium- sparing diuretics, however, do not increase potassium excretion and can actually cause hyperkalemia. Large doses of laxatives and repeated use of enemas can also cause hypokalemia because they increase losses of potassium in stool ²³.

People with pica

Pica is the persistent eating of non-nutritive substances, such as clay. When consumed, clay binds potassium in the gastrointestinal tract, which can increase potassium excretion and lead to hypokalemia ¹⁸, ¹⁷⁶, ¹⁷⁷. Cessation of pica combined with potassium supplementation can restore potassium status and resolve symptoms of potassium deficiency.

Potassium deficiency prevention

Routine potassium replacement is not necessary in most patients receiving diuretics. However, serum potassium should be monitored during diuretic use when risk of hypokalemia or of its complications is high. Risk is high in ¹⁸²:

• Patients with decreased left ventricular function
• Patients taking digoxin
• Patients with diabetes (in whom insulin concentrations can fluctuate)
• Patients with asthma who are taking beta 2-agonists

Triamterene 100 mg orally once a day or spironolactone 25 mg orally 4 times a day does not increase potassium excretion and may be useful in patients who become hypokalemic but must use diuretics. When hypokalemia develops, potassium supplementation, usually with oral potassium chloride, is indicated.

Hypokalemia may also be minimized by dietary restriction of salt (sodium) since high rates of sodium excretion promote urinary potassium losses. People who participate in vigorous sports or exercise in warm weather should be sure to replace potassium that is lost through excessive sweating. This can be accomplished through dietary planning.

Hypokalemia (low potassium) symptoms

Most often, a slight decrease in the potassium level in blood or mild hypokalemia (serum potassium 3 to 3.5 mEq/L [3 to 3.5 mmol/L]) usually causes no symptoms or asymptomatic. In most cases, low potassium is found by a blood test that is done because of an illness, or because you are taking diuretics (water pills). Hypokalemia affects up to 21% of hospitalized patients, usually because of the use of diuretics and other medications ¹⁷¹, ¹⁷², ¹⁸⁹. It is rare for low potassium to cause isolated symptoms such as muscle cramps if you are feeling well in other respects.

Low potassium symptoms may include ³⁹:

• Muscle weakness
• Weak or twitching muscles
• Nausea and vomiting
• Fatigue
• Muscle cramps
• Constipation
• Feeling of skipped heart beats or palpitations
• Tingling or numbness

Serum potassium less than 3 mEq/L (less than 3 mmol/L) generally causes muscle weakness and may lead to muscular paralysis and possibly respiratory failure. Other muscular dysfunction includes cramping, muscle twitches (fasciculations), paralysis of the bowel (paralytic ileus), hypoventilation, low blood pressure (hypotension), tetany (involuntary contraction of muscles), and rhabdomyolysis. Severe hypokalemia may also lead to disruption of skeletal muscle cells, particularly during exercise. The normal physical response to exercise requires the local release of potassium from muscle. In potassium depleted muscle, the lack of potassium prevents adequate widening of blood vessels, resulting in decreased muscle blood flow, cramps and the destruction of skeletal muscle. Other symptoms may include loss of appetite, nausea and vomiting, confusion, distention of the abdomen and a decrease in mental activity.

Persistent hypokalemia may also impair the ability of the kidneys to concentrate urine, resulting in excessive urination (polyuria) with secondary excessive thirst (polydipsia).

A large drop in potassium level (serum potassium level less than about 2.5 mmol/L) may lead to abnormal heart rhythms (arrhythmias), especially in people with underlying heart disease that can be fatal and requires urgent medical attention ⁴⁰, ⁴¹. This can cause you to feel lightheaded or faint. Abnormal heart rhythms (arrhythmias) are the most worrisome complication of very low potassium levels, particularly in people with underlying heart disease. A very low potassium level can even cause your heart to stop.

Chronic low potassium levels (chronic hypokalemia) is associated with high blood pressure (hypertension), kidney stone formation, increased bone turnover, urinary calcium excretion, and salt sensitivity (meaning that changes in sodium intakes affect blood pressure to a greater than normal extent).

Potassium deficiency diagnosis

Hypokalemia is often asymptomatic. The diagnosis of hypokalemia (serum potassium < 3.5 mEq/L [< 3.5 mmol/L]) may be found during routine serum electrolyte measurement. Doctors then try to identify what is causing the potassium level to decrease (see Figure 3) ¹⁹⁰, ¹⁹¹. The cause may be clear based on your symptoms (such as vomiting) or use of drugs or other substances. If the cause is not clear, further investigation is warranted and doctors measure how much potassium is excreted in urine to determine whether excess excretion is the cause. Because low potassium levels can cause abnormal heart rhythms, doctors usually do electrocardiography (ECG) to check for abnormal heart rhythms.

Evaluation begins with a search for warning signs or symptoms warranting urgent treatment ²⁶. These include weakness or palpitations, changes on electrocardiography (ECG), severe hypokalemia (less than 2.5 mEq per L [2.5 mmol per L]), rapid-onset hypokalemia, or underlying heart disease or cirrhosis ¹⁹⁰, ¹⁹². Most cases of hypokalemia-induced rhythm disturbances occur in individuals with underlying heart disease ¹⁸³. Early identification of potassium transcellular shifts is important because management may differ. Identification and treatment of concurrent hypomagnesemia are also important because magnesium depletion impedes potassium repletion and can exacerbate hypokalemia-induced rhythm disturbances ¹⁹³, ¹⁹⁴.

It should be suspected in patients with typical changes on an ECG or who have muscular symptoms and risk factors and confirmed by blood testing.

Figure 3. Potassium deficiency diagnostic algorithm

[Source ²⁶ ]

History and physical examination

A focused history includes evaluation for possible gastrointestinal losses, review of medications, and assessment for underlying cardiac comorbidities ²⁶. A history of paralysis, hyperthyroidism, or use of insulin or beta agonists suggests possible transcellular shifts leading to redistributive hypokalemia. The physical examination should focus on identifying cardiac arrhythmias and neurologic manifestations, which range from generalized weakness to ascending paralysis.

Electrocardiography (ECG)

Electrocardiography (ECG) should be done on patients with hypokalemia. Cardiac effects of hypokalemia are usually minimal until serum potassium concentrations are less than 3 mEq/L (< 3 mmol/L). Hypokalemia causes sagging of the ST segment, depression of the T wave (decreased T-wave amplitude), and elevation of the U wave (see Figure 4) ¹⁸². With marked hypokalemia can lead to PR-interval prolongation, ST-interval depression, the T wave becomes progressively smaller or T-wave inversions and the U wave becomes increasingly larger ¹⁸². Sometimes, a flat or positive T wave merges with a positive U wave, which may be confused with QT prolongation (see figure ECG patterns in hypokalemia). Hypokalemia may cause sinus bradycardia, premature ventricular beats and premature atrial contractions, ventricular tachycardia or fibrillation and supraventricular tachyarrhythmias, torsade de pointes and 2nd- or 3rd-degree atrioventricular block ¹⁹⁵, ¹⁸². Such arrhythmias become more severe with increasingly severe hypokalemia; eventually, ventricular fibrillation may occur ¹⁸². Although the risk of ECG changes and arrhythmias increases as serum potassium concentration decreases, these findings are not reliable because some patients with severe hypokalemia do not have ECG changes ¹⁹⁶. Patients with significant preexisting heart disease and patients receiving digoxin are at risk of cardiac conduction abnormalities as a result of even mild hypokalemia.

Figure 4. ECG patterns in hypokalemia

[Source ¹⁸² ]

Laboratory and urine tests

Potassium deficiency or hypokalemia diagnosis should be confirmed with a repeat serum potassium measurement. Other laboratory tests include serum glucose and magnesium levels, urine electrolyte and creatinine levels, and acid-base balance. After acidosis and other causes of intracellular potassium shift (increased beta-adrenergic effect, hyperinsulinemia) have been eliminated, 24-hour urinary potassium and serum magnesium concentrations are measured.

The most accurate method for evaluating urinary potassium excretion is a 24-hour timed urine potassium collection; normal kidneys excrete no more than 15 to 30 mEq per L (15 to 30 mmol per L) of potassium per day in response to hypokalemia. In hypokalemia, potassium secretion is normally less than 15 mEq/L (< 15 mmol/L) ¹⁸². Extrarenal gastrointestinal potassium loss or decreased potassium ingestion is suspected in chronic unexplained hypokalemia when renal potassium secretion is less than 15 mEq/L (< 15 mmol/L). Secretion of more than 15 mEq/L (> 15 mmol/L) suggests a renal cause for potassium loss ¹⁸². A more practical approach is calculation of the urine potassium-to-creatinine ratio from a spot urine specimen; a ratio greater than 1.5 mEq per mmol (13 mEq per g) of creatinine is indicative of renal potassium wasting ¹⁹⁷, ¹⁸⁰.

Unexplained hypokalemia with increased renal potassium secretion and hypertension suggests an aldosterone-secreting tumor or Liddle syndrome ¹⁸². Unexplained hypokalemia with increased renal potassium loss and normal blood pressure suggests Bartter syndrome or Gitelman syndrome, but hypomagnesemia, surreptitious vomiting, and diuretic abuse are more common and should also be considered ¹⁸².

If no cause is identified with the initial workup, assessment of thyroid and adrenal function should be considered.

Hypokalemia Treatment

Treatment of low potassium is directed at the underlying cause and may include potassium supplements. If your condition is mild, your doctor will likely prescribe oral potassium pills. If your condition is severe, you may need to get potassium through a vein (IV). Treatment urgency depends on the severity of your hypokalemia, the existence of comorbid conditions and the rate of decline of serum potassium levels ¹⁸⁰. Rapid correction is possible with oral potassium; the fastest results are likely best achieved by combining oral (e.g., 20 to 40 mmol) and intravenous administration ¹⁹⁸.

The goal of potassium replacement in the context of kidney or gastrointestinal losses is to immediately raise serum potassium concentration to a safe level and then replace the remaining deficit over days to weeks. A potassium-sparing diuretic should also be considered when the cause of hypokalemia involves renal potassium wasting as potassium replacement therapy alone may not be enough.

The immediate goal of treatment is the prevention of potentially life-threatening cardiac conduction disturbances and neuromuscular dysfunction by raising serum potassium to a safe level ²⁶. Further replenishment can proceed more slowly, and attention can turn to the diagnosis and management of the underlying disorder ¹⁹². Patients with a history of congestive heart failure or heart attack (myocardial infarction) should maintain a serum potassium concentration of at least 4 mEq per L (4 mmol per L), based on expert opinion ¹⁹².

For hypokalemia associated with diuretic use, stopping the diuretic or reducing its dosage may be effective ¹⁹². Another strategy, if otherwise indicated to treat a comorbid condition, is use of an angiotensin-converting enzyme (ACE) inhibitor, angiotensin receptor blocker (ARB), beta blocker, or potassium-sparing diuretic because each of these drugs is associated with an elevation in serum potassium ²⁶.

It is appropriate to increase dietary potassium in patients with low-normal and mild hypokalemia, particularly in those with a history of hypertension or heart disease ¹⁹². The effectiveness of increased dietary potassium is limited, however, because most of the potassium contained in foods is coupled with phosphate, whereas most cases of hypokalemia involve chloride depletion and respond best to supplemental potassium chloride ¹⁹², ⁷⁷.

Eating foods rich in potassium can help treat and prevent low level of potassium. These foods include:

• Avocados
• Baked potato
• Bananas
• Bran
• Carrots
• Cooked lean beef
• Milk
• Oranges
• Peanut butter
• Peas and beans
• Salmon
• Seaweed
• Spinach
• Tomatoes
• Wheat germ

Many oral potassium supplements are available. Nonurgent hypokalemia is treated with 40 to 100 mmol of oral potassium per day over days to weeks. For the prevention of hypokalemia in patients with persistent losses, as with ongoing diuretic therapy or hyperaldosteronism, 20 mmol per day is usually sufficient ¹⁹⁹. Because high single doses can cause gastrointestinal irritation and occasional bleeding, potassium deficiency are usually replaced in divided doses. Liquid potassium chloride given orally elevates concentrations within 1 to 2 hours but has a bitter taste and is tolerated particularly poorly in doses greater than 25 to 50 mEq. (> 25 to 50 mmol) ¹⁸². Wax-impregnated potassium chloride preparations are safe and better tolerated. GI bleeding may be even less common with microencapsulated potassium chloride preparations. Several of these preparations contain 8 or 10 mEq/capsule. Because a decrease in serum potassium of 1 mEq/L (1 mmol/L) correlates with about a 200- to 400-mEq (200 to 400 mmol) deficit in total body potassium stores, total deficit can be estimated and replaced over a number of days at 20 to 80 mEq (20 to 80 mmol)/day.

When hypokalemia is severe (eg, with ECG changes or severe symptoms), is unresponsive to oral therapy, or occurs in hospitalized patients who are taking digoxin or who have significant heart disease or ongoing losses, potassium must be replaced intravenously (IV) ¹⁸². Because use of intravenous (IV) potassium increases the risk of hyperkalemia (a serum or plasma potassium level above the upper limits of normal, usually greater than 5.0 mEq/L to 5.5 mEq/L) and can cause pain and vein inflammation (phlebitis), intravenous potassium should be reserved for patients with severe hypokalemia, hypokalemic ECG changes, or physical signs or symptoms of hypokalemia, or for those unable to tolerate the oral form ²⁶.

When intravenous (IV) potassium is used, standard administration is 20 to 40 mmol of potassium in 1 L of normal saline [the concentration should not exceed 40 mEq/L (40 mmol/L)] ²⁶. Correction typically should not exceed 20 mmol per hour, although higher rates using central venous catheters have been successful in emergency situations ¹⁹⁸. Continuous cardiac monitoring is indicated if the rate exceeds 10 mmol per hour. In children, dosing is 0.5 to 1.0 mmol per L per kg over one hour (maximum of 40 mmol) ²⁰⁰. Potassium should not be given in dextrose-containing solutions because dextrose-stimulated insulin secretion can exacerbate hypokalemia ²⁶.

In hypokalemia-induced arrhythmia, intravenous (IV) potassium chloride must be given more rapidly, usually through a central vein or using multiple peripheral veins simultaneously. Infusion of 40 mEq (40 mmol) potassium chloride/hour can be undertaken but only with continuous cardiac monitoring and hourly serum potassium determinations. Glucose solutions are avoided because elevation in the serum insulin concentrations could result in transient worsening of hypokalemia.

Even when potassium deficits are severe, it is rarely necessary to give > 100 to 120 mEq (> 100 to 120 mmol) of potassium in a 24-hour period unless potassium loss is ongoing. In potassium deficit with high serum potassium concentration, as in diabetic ketoacidosis, intravenous (IV) potassium is deferred until the serum potassium starts to fall. When hypokalemia occurs with hypomagnesemia, both the potassium and magnesium deficiencies must be corrected to stop ongoing renal potassium wasting.

Careful monitoring during treatment is essential because supplemental potassium is a common cause of hyperkalemia (a serum or plasma potassium level above the upper limits of normal, usually greater than 5.0 mEq/L to 5.5 mEq/L) in hospitalized patients ²⁰¹. The risk of rebound hyperkalemia is higher when treating redistributive hypokalemia. Because serum potassium concentration drops approximately 0.3 mEq per L (0.3 mmol per L) for every 100-mEq (100-mmol) reduction in total body potassium, the approximate potassium deficit can be estimated in patients with abnormal losses and decreased intake ²⁶. For example, a decline in serum potassium from 3.8 to 2.9 mEq per L (3.8 to 2.9 mmol per L) roughly corresponds to a 300-mEq (300-mmol) reduction in total body potassium ²⁶. Additional potassium will be required if losses are ongoing. Concomitant hypomagnesemia should be treated concurrently.

Potassium deficiency prognosis

The prognosis for patients with hypokalemia depends entirely on the underlying cause of hypokalemia ²⁰². For example, a patient with an acute episode of hypokalemia resulting from diarrhea has an excellent prognosis. Hypokalemia due to a congenital disorder such as Bartter syndrome has a poor to nonexistent potential for resolution ²⁰².

Hypokalemia is associated with increased mortality for patients with diabetes, chronic kidney disease, myocardial infarction, heart failure and COVID-19 pneumonia ²⁰³, ²⁰⁴, ²⁰⁵, ²⁰⁶.

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