text:
by Health Jade Team 12.9K views
What is Potassium
Mechanism of Action of Potassium
What is the recommended dietary potassium intake?
Table 1: Adequate Intakes (AIs) for Potassium*
Potassium Intakes and Status of Americans
Potassium supplements
Salt substitutes
Table 2. Selected Food Sources of Potassium
Benefits of Potassium
Hypertension and stroke
Blood glucose control and type 2 diabetes
High Potassium (Hyperkalemia)
Causes of Hyperkalemia (high potassium)
High potassium symptoms
Hyperkalemia prevention
Hyperkalemia diagnosis
Treatment of Hyperkalemia
Urgent treatment
Lowering total body potassium
For people with heart failure
Low Potassium (Hypokalemia)
Hypokalemia signs and symptoms
Causes of Hypokalemia (low potassium)
Groups at Risk of Potassium Inadequacy
Hypokalemia diagnosis
Hypokalemia Treatment
Hypokalemia Outlook (Prognosis)
Potassium is a mineral that is vital to cell metabolism. Potassium is a type of electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance 1. 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 2. Potassium helps transport nutrients into cells and removes waste products out of cells. Potassium is also important in muscle function, helping to transmit messages between nerves and muscles.
Potassium, along with other electrolytes such as sodium, chloride, and bicarbonate (total CO2), helps regulate the amount of fluid in the body and maintains a stable acid-base balance. Potassium is present in all body fluids, but most potassium is found within the cells (intracellular), where it is the most abundant cation and involved in cell regulation and several cellular processes. Only a small amount of potassium is present in fluids outside the cells (extracellular) and in the liquid part of the blood (called serum or plasma). Therefore, plasma or serum levels are not a reliable indicator of total body potassium stores. Potassium homeostasis is maintained through a combination of adjustments in acute cellular shifts between the extracellular and intracellular fluid compartments, renal excretion and, to a lesser extent, gastrointestinal losses 3.
The total amount of potassium in the adult body is about 45 millimole (mmol)/kg body weight (about 140 g for a 175 pound adult; 1 mmol = 1 milliequivalent [mEq] or 39.1 mg potassium) 4. Most potassium resides 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 (Na+/K+) ATPase transporter 5. In addition to maintaining cellular tonicity, this gradient is required for proper nerve transmission, muscle contraction, and kidney function.
Foods and beverages are the primary source of potassium, with the highest potassium content found in fruits, vegetables, and meats 6. Current dietary guidelines from the US Food and Nutrition Board of the Institute of Medicine recommend potassium intake of 3,400 mg/day in adult men and 2,600 mg/day in adult women with normal kidney function 7. Whereas, the World Health Organization (WHO) recommends a dietary potassium intake of 3,900 mg (100 mmol) per day or at least 90 mmol/day (3510 mg/day), to reduce blood pressure and the risk of cardiovascular damage, stroke and coronary heart disease 8. These recommendations take into account the health and heart protective benefits of a high-potassium diet 9. You get most of the potassium you need from the foods that you eat and most people have an adequate intake of potassium. The body uses what it requires and the kidneys eliminate the rest in the urine. The 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.
In patients with non-dialysis dependent chronic kidney disease (CKD) stages 1–5, the National Kidney Foundation suggests an unrestricted potassium intake unless the serum potassium level is elevated. In hemodialysis patients, potassium intake should be up to 2.7–3.1 g/day and in peritoneal dialysis patients close to 3–4 g/day; in both cases, adjustments based on serum potassium levels are crucial 10. A recent comprehensive review paper on nutritional management of chronic kidney disease (CKD) by Kalantar-Zadeh and Fouque 11 has suggested an intake of 4.7 g/day in the early stages of CKD without risk of high blood potassium (also known as hyperkalemia), but a dietary potassium restriction of less than 3 g (less than 77 mmol) per day in CKD patients who tend to develop hyperkalemia (serum potassium levels >5.3 mEq/L).
Potassium is absorbed via passive diffusion, primarily in the small intestine 5. About 90% of ingested potassium is absorbed and used to maintain its normal intracellular and extracellular concentrations 12. Potassium is excreted primarily in the urine, some is excreted in the stool, and a very small amount is lost in sweat. 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 2. The kidneys can adapt to variable potassium intakes in healthy individuals, but a minimum of 5 mmol (about 195 mg) potassium is excreted daily in urine 4. This, combined with other obligatory losses, suggests that potassium balance cannot be achieved with intakes less than about 400–800 mg/day.
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. Although blood potassium levels can provide some indication of potassium status, they often correlate poorly with tissue potassium stores 4. 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 13.
Normal serum concentrations of potassium range from about 3.6 to 5.0 mmol/L and are regulated by a variety of mechanisms 4. Diarrhea, vomiting, kidney disease, use of certain medications, and other conditions that alter potassium excretion or cause transcellular potassium shifts can cause hypokalemia (serum levels below 3.6 mmol/L) or hyperkalemia (serum levels above 5.0 mmol/L) 14. 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 or too high, 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
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 15. A recent meta-analysis including 11 cohort studies reported an inverse association between potassium intake and risk of stroke 16. Additionally, two meta-analyses of trials comparing increased potassium to lower potassium intake found that increased potassium intake lowers blood pressure
17, 18. 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 19. 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 20.
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 21. 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. The health care provider will recommend a special diet.
Potassium is the major cation (positive ion) inside animal cells, while sodium is the major cation outside animal cells. 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. The balance between potassium and sodium is maintained by ion pumps in the cell membrane. 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 neurotransmission, muscle contraction, and heart function. Potassium is also an essential mineral needed to regulate water balance, blood pressure and levels of acidity 22. 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 21. The largest benefit was detected when sodium intake was more than 4 g/day, which is the intake of most populations globally 23, 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 24, 25.
Potassium also helps relax blood vessel walls, which helps lower blood pressure 21.
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) 20.
Physiologically, potassium exists as an ion in the body. Potassium (K+) is a positively charged electrolyte, cation, which is present throughout the 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. It 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 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 ECF to ICF. Over the ensuing hours, the kidneys excrete the ingested potassium and homeostasis is returned. In the critically ill patient, suffering from hyperkalaemia, 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 ECF to ICF. The stimulation of alpha receptors causes increased movement of potassium from ICF to 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. 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 26.
The amount of potassium you need each day depends on your age and sex. Average daily recommended amounts are listed below in milligrams (mg). 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 27. 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.
In 2019, the National Academies of Sciences, Engineering, and Medicine committee updated the Dietary Reference Intakes (DRIs) for potassium (and sodium) 27. 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 infants. Table 1 lists the current Adequate Intakes (AIs) for potassium for healthy individuals.
The National Academies of Sciences, Engineering, and Medicine committee also used an expanded 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 (CDRR) 27. According to the model, a chronic disease risk reduction intake (CDRR) 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 (CDRR) for potassium
Age Male Female Pregnancy Lactation
Birth to 6 months 400 mg 400 mg
7–12 months 860 mg 860 mg
1–3 years 2,000 mg 2,000 mg
9–13 years 2,500 mg 2,300 mg
14–18 years 3,000 mg 2,300 mg 2,600 mg 2,500 mg
51+ years 3,400 mg 2,600 mg
Footnote: *The Adequate Intake (AI) 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 27 ]
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" 28. 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 29. 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 29.
Use of potassium-containing dietary supplements does not significantly increase total potassium intakes among U.S. adults 30, probably because most potassium-containing dietary supplements provide no more than 99 mg potassium per serving 31. 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 29.
In dietary supplements, potassium is often present as potassium chloride, but many other forms—including potassium citrate, phosphate, aspartate, bicarbonate, and gluconate—are also used 32. 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.
Not all multivitamin/mineral supplements contain potassium, but those that do typically provide about 80 mg potassium 32. Potassium-only supplements are also available, and most contain up to 99 mg potassium. Information on many dietary supplements that contain potassium is available in the Dietary Supplement Label Database 32 from the National Institutes of Health, which contains label information from tens of thousands of dietary supplement products on the market.
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 33. 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 34. 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 35. However, the FDA has not issued a ruling about whether dietary supplements containing more than 99 mg potassium must carry a warning label 34.
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 36. 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 37. 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 38.
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 39. 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.
Potassium is present in a large variety of foods, both from animal and plant sources 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 12. Among starchy foods, whole-wheat flour and brown rice are much higher in potassium than their refined counterparts, white wheat flour and white rice 40.
You can get recommended amounts of potassium by eating a variety of foods, including the following:
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
Milk, coffee, tea, other nonalcoholic beverages, and potatoes are the top sources of potassium in the diets of U.S. adults 41. Among children in the United States, milk, fruit juice, potatoes, and fruit are the top sources 42.
It is estimated that the body absorbs about 85%–90% of dietary potassium 2. The forms of potassium in fruits and vegetables include potassium phosphate, sulfate, citrate, and others, but not potassium chloride 43.
The U.S. Department of Agriculture's Nutrient Database (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 also provides a list of foods containing potassium (https://health.gov/our-work/food-nutrition/previous-dietary-guidelines/2015).
Selected food sources of potassium are listed in Table 2.
Food Milligrams (mg) per serving Percent DV*
Apricots, dried, ½ cup 1101 23
Lentils, cooked, 1 cup 731 16
Prunes, dried, ½ cup 699 15
Squash, acorn, mashed, 1 cup 644 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
Footnotes: *DV = Daily Value. DVs were developed by the U.S. Food and Drug Administration (FDA) to help consumers compare the nutrient contents of products within the context of a total diet. The DV for potassium used as the basis for the values in Table 2 is 3,500 mg for adults and children aged 4 and older, but the DV will increase to 4,700 mg when the updated Nutrition and Supplement Facts labels are implemented 44. The updated labels and DVs must appear on food products and dietary supplements beginning in January 2020, but they can be used now 45. Foods providing 20% or more of the DV are considered to be high sources of a nutrient.
[Source 40]
(Source 46).
Because of potassium's wide-ranging roles in the body, low intakes can increase the risk of illness. This section focuses on four diseases and disorders in which potassium might be involved: hypertension and stroke; kidney stones; bone health; and blood glucose control and type 2 diabetes.
Hypertension, a major risk factor for heart disease and stroke, affects almost a third of Americans. According to an extensive body of literature, low potassium intakes increase the risk of hypertension, especially when combined with high sodium intakes 43. Higher potassium intakes, in contrast, may help decrease blood pressure, in part by increasing vasodilation and urinary sodium excretion, which in turn reduces plasma volume 39; this effect may be most pronounced in salt-sensitive individuals 2.
The Dietary Approaches to Stop Hypertension (DASH) eating pattern, which emphasizes potassium from fruits, vegetables, and low-fat dairy products, lowers systolic blood pressure by an average of 5.5 mmHg and diastolic blood pressure by 3.0 mmHg 47. The DASH eating pattern provides three times more potassium than the average American diet. However, it also increases intakes of other nutrients, such as magnesium and calcium, that are also associated with reductions in blood pressure, so potassium's independent contribution cannot be determined.
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 48. 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 49. 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 50 and 33 trials 51 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 52.
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 53. The authors concluded that, based on observational studies, the associations between dietary potassium intakes and lower blood pressure in adults were inconsistent 53. They also found no evidence for an association between potassium intakes and the risk of hypertension. 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 53. 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 27. However, the effects were stronger among studies including participants with hypertension; for studies including only participants without hypertension, the effects were not statistically significant. Based on 13 randomized controlled trials that primarily enrolled patients with hypertension, the Agency for Healthcare Research and Quality 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 53. 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.
Higher potassium intakes have been associated with a decreased risk of stroke and possibly other cardiovascular diseases (CVDs) 54. 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 CVD 55. Similarly, the authors of a meta-analysis of 9 cohort studies reported a significant 24% lower risk of stroke with higher potassium intakes and a nonsignificant reduction in coronary heart disease and cardiovascular disease (CVD) risk 56. However, a draft Agency for Healthcare Research and Quality report found inconsistent relationships between dietary potassium intakes and risk of stroke based on 1 case-cohort and 10 prospective cohort studies 57.
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). In addition, participants who consumed 90 mmol potassium/day (approximately 3,500 mg) had the lowest risk of stroke 58. 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 59.
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" 45. 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 are most common in people aged 40 to 60 60. 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 hypercalciuria and kidney stones 59. Low urinary levels of citrate also contribute to kidney stone development.
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) 61. 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 62.
Some research suggests that supplementation with potassium citrate reduces hypercalciuria as well as the risk of kidney stone formation and growth 60. 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 63. 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 60. 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 60. The authors of a draft Agency for Healthcare Research and Quality report 57 concluded that observational studies suggest an association between higher potassium intakes and lower risk of kidney stones. However, they also found the evidence insufficient to determine whether potassium supplements are effective because only one trial that addressed this question 63 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.
Observational studies suggest that increased consumption of potassium from fruits and vegetables is associated with increased bone mineral density 64. This evidence, combined with evidence from metabolic studies and a few clinical trials, suggests that dietary potassium may improve bone health.
The underlying mechanisms are unclear, but one hypothesis is that potassium helps protect bone through its effect on acid-base balance 59. 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 65. In another study, the DASH eating pattern significantly reduced biochemical markers of bone turnover 66. This 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.
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 67. 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 68. 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 69. 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 70.
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.
Type 2 diabetes is a growing public health concern that currently affects almost 12% of U.S. adults 71. 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 2. 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 2.
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 72. These associations might be stronger in African Americans, who tend to have lower potassium intakes, than in whites 73. 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 73. 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.
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 74. 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 72.
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 75.
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.
In healthy people with normal kidney function, high dietary potassium intakes do not pose a health risk because the kidneys eliminate excess amounts in the urine 39. In addition, there is no evidence that high intakes of dietary potassium have adverse effects. Therefore, the Food and Nutrition Board did not set a Tolerable Upper Intake Level (UL) for potassium.
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 (AI) can cause hyperkalemia 39. Hyperkalemia can also occur in people with type 1 diabetes, congestive heart failure, adrenal insufficiency, or liver disease 14. Individuals at risk of hyperkalemia should consult a physician or registered dietitian about appropriate potassium intakes from all sources.
Although hyperkalemia can be asymptomatic, severe cases can cause muscle weakness, paralysis, heart palpitations, paresthesias (a burning or prickling sensation in the extremities), and cardiac arrhythmias that could be life threatening 14.
Hyperkalemia is the medical term that describes a potassium level in your blood that's higher than normal 76. Potassium is a nutrient that is critical to the function of nerve and muscle cells, including those in your heart 77.
Your blood potassium level is normally 3.6 to 5.2 millimoles per liter (mmol/L) 78. Hyperkalemia is a potassium level of greater than 5.5 mmol/L. Patients with hyperkalemia may have a normal electrocardiogram (ECG) or only subtle changes. Having a blood potassium level higher than 7.0 mmol/L can be dangerous and requires immediate treatment.
Severe hyperkalemia (more than 6.5 mEq per L [6.5 mmol/L]) can cause muscle weakness, ascending paralysis, heart palpitations, and paresthesias. Chronic kidney disease, diabetes, heart failure, and liver disease all increase the risk of hyperkalemia. Clinicians should review patients' medications to identify those known to cause hyperkalemia, and ask patients about the use of salt substitutes that contain potassium. The physical examination should include assessment of blood pressure and intravascular volume status to identify potential causes of kidney hypoperfusion, which can lead to hyperkalemia. Neurologic signs of hypokalemia include generalized weakness and decreased deep tendon reflexes 79.
Often, a report of high blood potassium isn't true hyperkalemia. Instead, it may be caused by the rupture of blood cells in the blood sample during or shortly after the blood draw. 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.
The most common cause of genuinely high potassium (hyperkalemia) is related to your kidneys 80, such as:
Acute kidney failure
Other causes of hyperkalemia include:
Addison's disease (adrenal failure)
Alcoholism or heavy drug use that causes rhabdomyolysis, a breakdown of muscle fibers that results in the release of potassium into the bloodstream
Destruction of red blood cells due to severe injury or burns
Excessive use of potassium supplements
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 81. These medications reduce urinary potassium excretion, which can lead to hyperkalemia. Experts recommend monitoring potassium status in people taking ACE inhibitors or ARBs, especially if they have other risk factors for hyperkalemia, such as impaired kidney function 81.
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.
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:
Abnormal heart rhythms (arrhythmias) – slow, weak, or irregular pulse
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 83. 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.
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 84.
The health care provider will perform a physical exam and ask about your symptoms.
Tests that may be ordered include:
Electrocardiogram (ECG)
Potassium level
Your provider will 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
Repeat measurement of serum potassium can help identify pseudohyperkalemia, which is common and typically results from potassium moving out of cells during or after sample collection 85. Other laboratory studies include measurement of serum blood urea nitrogen (BUN) and creatinine, measurement of urine electrolytes and creatinine, and assessment of acid-base status. Further evaluation may include measurement of serum glucose to evaluate for hyperglycemia, and measurement of serum renin, aldosterone, and cortisol to further investigate kidney and adrenal function.
ECG should be considered if the potassium level is greater than 6 mEq per L; if there are symptoms of hyperkalemia; if there is suspicion of rapid-onset hyperkalemia; or among patients with underlying kidney disease, heart disease, or cirrhosis who have a new case of hyperkalemia. Findings on ECG are neither sensitive nor specific for hyperkalemia. Therefore, although ECG changes should trigger urgent treatment, treatment decisions should not be based solely on the presence or absence of ECG changes 86.
Peaked T waves are the prototypical, and generally the earliest, ECG sign of hyperkalemia. Other ECG changes include P-wave flattening, PR-interval prolongation, widening of the QRS complex, and sine waves 87. Hyperkalemia-induced arrhythmias include sinus bradycardia, sinus arrest, ventricular tachycardia, ventricular fibrillation, and asystole 87.
If your potassium level is very high, or if there are dangerous indications such as changes in an electrocardiogram, 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.
Indications for prompt intervention are symptoms of hyperkalemia, changes on ECG, severe hyperkalemia (greater than 6.5 mEq per L), rapid-onset hyperkalemia, or underlying heart disease, cirrhosis, or kidney disease 88. Potassium should be monitored often because patients are at risk of redeveloping hyperkalemia until the underlying disorder is corrected and excess potassium is eliminated.
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.
Emergency treatment may include:
Calcium given into your veins (IV) to treat the muscle and heart effects of high potassium levels
Glucose and insulin given into your veins (IV) to help lower potassium levels long enough to correct the cause
Kidney dialysis if your kidney function is poor
Medicines that help remove potassium from the intestines before it is absorbed
Sodium bicarbonate if the problem is caused by acidosis
Some water pills (diuretics)
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 provider 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 provider'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
Intravenous Calcium. Intravenous calcium, which helps prevent life-threatening conduction disturbances by stabilizing the cardiac muscle cell membrane, should be administered if ECG changes are present 89. Intravenous calcium has no effect on plasma potassium concentration. If after five minutes, follow-up ECG continues to show signs of hyperkalemia, the dose should be repeated 90. Clinicians should be aware that intravenous calcium has a short duration, ranging from 30 to 60 minutes.
Insulin and Glucose. The most reliable method for shifting potassium intracellularly is administration of glucose and insulin. Typically, 10 units of insulin are administered, followed by 25 g of glucose to prevent hypoglycemia 90. Because hypoglycemia is a common adverse effect even with the provision of glucose, serum glucose levels should be monitored regularly. Patients with a serum glucose level of more than 250 mg/dL (13.9 mmol/L) typically do not require coadministration of glucose.
Inhaled Beta Agonists. Albuterol, a beta2 agonist, is an underutilized adjuvant for shifting potassium intracellularly 90. All forms of administration (i.e., inhaled, nebulized, and intravenous where available) are effective. It should be noted that the recommended dose of nebulized albuterol (10 to 20 mg) is four to eight times greater than the typical respiratory dose. There is an additive effect when albuterol is combined with insulin 91. Albuterol's potassium-lowering effect is mitigated in some patients, particularly those with end-stage kidney disease; therefore, albuterol should not be used as monotherapy 88.
Sodium Bicarbonate. Although sodium bicarbonate is often used to treat hyperkalemia, the evidence to support this use is equivocal, showing minimal to no benefit 92. Therefore, sodium bicarbonate should not be used as monotherapy. It may have a role as adjuvant therapy, particularly among patients with concurrent metabolic acidosis 92.
Potassium can be removed via the gastrointestinal tract or the kidneys, or directly from the blood with dialysis. Dialysis should be considered in patients with kidney failure or life-threatening hyperkalemia, or when other treatment strategies fail 90. Other modalities are not rapid enough for urgent treatment of hyperkalemia 92.
Currently available cation exchange resins, typically sodium polystyrene sulfonate (Kayexalate) in the United States, are not beneficial for the acute treatment of hyperkalemia but may be effective in lowering total body potassium in the subacute setting 89. Because sodium polystyrene sulfonate can be constipating, many formulations include sorbitol for its laxative effects. However, case reports linking the concomitant use of sodium polystyrene sulfonate and sorbitol to gastrointestinal injury prompted a U.S. Food and Drug Administration boxed warning 93. More recent reports implicate sodium polystyrene sulfonate alone 94. Therefore, use of the drug with or without sorbitol should be avoided in patients with or at risk of abnormal bowel function, such as postoperative patients and those with constipation or inflammatory bowel disease 95.
There is no evidence supporting the use of diuretics for the acute treatment of hyperkalemia. However, diuretics, particularly loop diuretics, may play a role in the treatment of some forms of chronic hyperkalemia, such as that caused by hyporeninemic hypoaldosteronism 92. Fludrocortisone is an option for hyperkalemia associated with mineralocorticoid deficiency, including hyporeninemic hypoaldosteronism 96.
Strategies to prevent chronic hyperkalemia include instructing patients to eat a low-potassium diet, discontinuing or adjusting medications, avoiding nonsteroidal anti-inflammatory drugs, and adding a diuretic if the patient has sufficient renal function.
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 the table). 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.
Potassium levels in common 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
Insufficient potassium intakes can increase blood pressure, kidney stone risk, bone turnover, urinary calcium excretion, and salt sensitivity (meaning that changes in sodium intakes affect blood pressure to a greater than normal extent). Low potassium (hypokalemia) refers to a lower than normal potassium level in your bloodstream. Potassium is a chemical (electrolyte) that is critical to the proper functioning of nerve and muscles cells, particularly heart muscle cells. Hypokalemia is more prevalent than hyperkalemia, and most cases are mild. Hypokalemia affects up to 21% of hospitalized patients, usually because of the use of diuretics and other medications, but it is rare among healthy people with normal kidney function.
Normally, your blood potassium level is 3.6 to 5.2 millimoles per liter (mmol/L). Severe potassium deficiency can cause hypokalemia, (serum potassium level less than about 3.6 mmol/L). A very low potassium level (less than 2.5 mmol/L) can be life-threatening and requires urgent medical attention.
Hypokalemia severity is categorized as mild when the serum potassium level is 3 to 3.4 mmol/L, moderate when the serum potassium level is 2.5 to 3 mmol/L, and severe when the serum potassium level is less than 2.5 mmol/L 3. Values obtained from plasma and serum may differ. Therefore, it is important to know the sampling source. Compared to plasma levels, serum levels are usually slightly higher due to delays in processing and/or the effect of clotting 98.
Mild hypokalemia is characterized by constipation, fatigue, muscle weakness, and malaise 4. Moderate to severe hypokalemia (serum potassium level less than about 2.5 mmol/L) can cause polyuria (large volume of dilute urine); encephalopathy in patients with kidney disease; glucose intolerance; muscular paralysis; poor respiration; and cardiac arrhythmias, especially in individuals with underlying heart disease 4. Severe hypokalemia can be life threatening because of its effects on muscle contraction and, hence, cardiac function 12.
Hypokalemia can occur as a result of decreased potassium intake, transcellular shifts (increased intracellular uptake) or increased potassium loss (skin, gastrointestinal and renal losses). Cellular uptake of potassium is promoted by alkalemia, insulin, beta-adrenergic stimulation, aldosterone and xanthines, such as caffeine. Most cases of hypokalemia result from gastrointestinal (GI) or renal losses 99, 100, 101. Hypokalemia is rarely caused by low dietary potassium intake alone, but it can result from diarrhea due to potassium losses in the stool. However, reduced intake can be a contributor to hypokalemia in the presence of other causes, such as malnutrition or diuretic therapy. Hypokalemia can also result from vomiting, which produces metabolic alkalosis, leading to potassium losses in the kidneys. 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; laxative abuse; diuretic use; eating clay (a type of pica); heavy sweating; or dialysis 102.
Renal potassium losses are associated with increased mineralocorticoid-receptor stimulation such as occurs with primary hyperreninism and primary aldosteronism. Increased delivery of sodium and/or non-absorbable ions (diuretic therapy, magnesium deficiency, genetic syndromes) to the distal nephron can also result in renal potassium wasting.
Magnesium depletion (hypomagnesemia) can contribute to hypokalemia by increasing urinary potassium losses 103. Hypomagnesemia often occurs with and may worsen hypokalemia especially in the presence of chronic diarrhea, alcoholism, genetic disorders, diuretic use and chemotherapy. Both (hypomagnesemia + hypokalemia) can also increase the risk of cardiac arrhythmias by decreasing intracellular potassium concentrations. The combination of hypokalemia and hypomagnesemia are associated with an increased risk of torsades de pointes, particularly in individuals receiving QT-prolonging medications. Additionally, hypomagnesemia can increase urinary potassium losses thus lowering the serum potassium level, as well as, prevent urinary potassium reabsorption thereby impeding potassium repletion. More than 50% of individuals with clinically significant hypokalemia might have magnesium deficiency 104. In people with hypomagnesemia and hypokalemia, both should be treated concurrently 14.
Low potassium symptoms may include:
In severe cases, life-threatening paralysis may develop, such as with hypokalemic periodic paralysis.
Abnormal heart rhythms (arrhythmias) are the most worrisome complication of very low potassium levels, particularly in people with underlying heart disease.
In most cases, low potassium is found by a blood test that is done because of an illness, or because you are taking diuretics. It is rare for low potassium to cause isolated symptoms such as muscle cramps if you are feeling well in other respects.
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 low potassium level.
Treatment of low potassium is directed at the underlying cause and may include potassium supplements. Don't start taking potassium supplements without talking to your doctor first.
Clinical symptoms of hypokalemia do not become evident until the serum potassium level is less than 3 mmol/L unless there is a precipitous fall or the patient has a process that is potentiated by hypokalemia 3. The severity of symptoms also tends to be proportional to the degree and duration of hypokalemia. Symptoms resolve with correction of the hypokalemia.
Significant muscle weakness occurs at serum potassium levels below 2.5 mmol/L but can occur at higher levels if the onset is acute. Similar to the weakness associated with hyperkalemia, the pattern is ascending in nature affecting the lower extremities, progressing to involve the trunk and upper extremities and potentially advancing to paralysis. Affected muscles can include the muscles of respiration which can lead to respiratory failure and death. Involvement of GI muscles can cause an ileus with associated symptoms of nausea, vomiting, and abdominal distension. Severe hypokalemia can also lead to muscle cramps, rhabdomyolysis, and resultant myoglobinuria. Periodic paralysis is a rare neuromuscular disorder, which is inherited or acquired, that is caused by an acute transcellular shift of potassium into the cells. It is characterized by potentially fatal episodes of muscle weakness or paralysis that can affect the respiratory muscles.
Hypokalemia can result in a variety of cardiac dysrhythmias. Although cardiac dysrhythmias or ECG changes are more likely to be associated with moderate to severe hypokalemia, there is a high degree of individual variability and can occur with even mild decreases in serum levels. This variability is dependent on concomitant factors such as magnesium depletion, digitalis therapy, among others. Moreover, characteristic ECG changes do not manifest in all patients. The ECG changes that occur are T-wave flattening initially, followed by ST depression and the appearance of a U wave that can be difficult to distinguish from the T wave. The U wave is often seen in the lateral precordial leads of V4 to V6. Prolongation of the PR and QT interval can also occur. Risk of arrhythmias is highest in older patients, those with heart disease and those receiving digoxin or antiarrhythmic drugs. Administration of anesthesia in the setting of hypokalemia is also a risk for dysrhythmias and impaired cardiac contractility but more so with acute rather than chronic hypokalemia.
Lastly, prolonged hypokalemia can cause structural and functional changes in the kidney that include impairing concentrating ability, increased ammonia production, altered sodium reabsorption and increased bicarbonate absorption 3. Hypokalemia can also result in glucose intolerance by reducing insulin secretion.
Low potassium (hypokalemia) has many causes. The most common cause is excessive potassium loss in urine due to prescription water or fluid pills (diuretics). Vomiting or diarrhea or both can result in excessive potassium loss from the digestive tract. Only rarely is low potassium caused by not getting enough potassium in your diet.
Causes of potassium loss leading to low potassium include:
Diarrhea (causing anal irritation)
Excessive laxative use
Prescription water or fluid pills (diuretics) use
Primary aldosteronism
Some antibiotic use
In general, hypokalemia is associated with diagnoses of cardiac disease, renal failure, malnutrition, and shock 3. Hypothermia and increased blood cell production (for example, leukemia) are additional risk factors for developing hypokalemia. 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. Hypokalemia is also prevalent in hospitalized patients, in particular, pediatric patients, those who have a fever and those who are critically ill. Additionally, in developing countries, an increased risk of mortality is observed in children when severe hypokalemia is associated with diarrhea and severe malnutrition.
Potassium inadequacy 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 105. 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 106.
People who use certain medications, including diuretics and laxatives
Certain diuretics (e.g., thiazide diuretics) that are commonly used to treat high blood pressure increase urinary potassium excretion and can cause hypokalemia 14. 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.
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 12. Cessation of pica combined with potassium supplementation can restore potassium status and resolve symptoms of potassium deficiency.
Hypokalemia is often asymptomatic. Evaluation begins with a search for warning signs or symptoms warranting urgent treatment (Figure 1) 107. 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 108. Most cases of hypokalemia-induced rhythm disturbances occur in individuals with underlying heart disease 109. Early identification of 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 110.
The 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. Assessment of urinary potassium excretion can help distinguish renal losses from other causes of hypokalemia. 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. Excretion of more than 30 mEq of potassium per day indicates inappropriate renal potassium loss. A more practical approach include a spot urine potassium concentration or urine potassium-to-creatinine ratio; a urine potassium concentration of greater than 15 mmol/L or a ratio greater than 13 mEq/mmol of creatinine, respectively, also indicates inappropriate renal potassium loss 111. If no cause is identified with the initial workup, assessment of thyroid and adrenal function should be considered.
After determining the presence or lack of renal potassium wasting, assessment of acid-base status should then be determined. The existence of metabolic acidosis or alkalosis with or without renal potassium wasting can further narrow the differential diagnosis. Aside from diagnostic evaluation, assessment of serum magnesium level, muscle strength, and electrocardiographic changes is warranted as the latter two would warrant immediate intervention.
Typically, the first ECG manifestation of hypokalemia is decreased T-wave amplitude. Further progression can lead to ST-interval depression, T-wave inversions, PR-interval prolongation, and U waves. Arrhythmias associated with hypokalemia include sinus bradycardia, ventricular tachycardia or fibrillation, and torsade de pointes 87. 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 112.
Figure 1. Hypokalemia diagnostic algorithm
Footnote: Suggested algorithm for the evaluation of hypokalemia.
[Source 113 ]
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. Further replenishment can proceed more slowly, and attention can turn to the diagnosis and management of the underlying disorder 108. 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 108.
If your condition is mild, your provider will likely prescribe oral potassium pills. If your condition is severe, you may need to get potassium through a vein (IV).
If you need diuretics, your provider may:
Switch you to a form that keeps potassium in the body. This type of diuretic is called potassium-sparing.
Prescribe extra potassium for you to take every day.
Careful monitoring during treatment is essential because supplemental potassium is a common cause of hyperkalemia in hospitalized patients 114. 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. 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. Additional potassium will be required if losses are ongoing. Concomitant hypomagnesemia should be treated concurrently.
For hypokalemia associated with diuretic use, stopping the diuretic or reducing its dosage may be effective 108. 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.
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 108. 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 108.
Eating foods rich in potassium can help treat and prevent low level of potassium. These foods include:
Cooked lean beef
Because use of intravenous (IV) potassium increases the risk of hyperkalemia and can cause pain and 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. 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 115.
When intravenous potassium is used, standard administration is 20 to 40 mmol of potassium in 1 L of normal saline. Correction typically should not exceed 20 mmol per hour, although higher rates using central venous catheters have been successful in emergency situations.22 Continuous cardiac monitoring is indicated if the rate exceeds 10 mmol per hour. In children, dosing is 0.5 to 1.0 mmol/L per kg over one hour (maximum of 40 mmol) 116. Potassium should not be given in dextrose-containing solutions because dextrose-stimulated insulin secretion can exacerbate hypokalemia.
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 108.
Taking potassium supplements can usually correct the problem. In severe cases, without proper treatment, a severe drop in potassium level can lead to serious heart rhythm problems that can be fatal.
PubChem, Open Chemistry Database. Potassium. https://pubchem.ncbi.nlm.nih.gov/compound/potassium#section=Top
Stone MS, Martyn L, Weaver CM. Potassium intake, bioavailability, hypertension, and glucose control. Nutrients 2016;8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4963920/
Castro D, Sharma S. Hypokalemia. [Updated 2021 May 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482465
Preuss HG, Clouatre DL. Sodium, chloride, and potassium. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:475-92.
Hinderling PH. The pharmacokinetics of potassium in humans is unusual. J Clin Pharmacol 2016;56:1212-20 https://www.ncbi.nlm.nih.gov/pubmed/26854277
Rosano GMC, Tamargo J, Kjeldsen KP, Lainscak M, Agewall S, Anker SD, Ceconi C, Coats AJS, Drexel H, Filippatos G, Kaski JC, Lund L, Niessner A, Ponikowski P, Savarese G, Schmidt TA, Seferovic P, Wassmann S, Walther T, Lewis BS. Expert consensus document on the management of hyperkalaemia in patients with cardiovascular disease treated with renin angiotensin aldosterone system inhibitors: coordinated by the Working Group on Cardiovascular Pharmacotherapy of the European Society of Cardiology. Eur Heart J Cardiovasc Pharmacother. 2018 Jul 1;4(3):180-188. doi: 10.1093/ehjcvp/pvy015
Dietary Reference Intakes for Sodium and Potassium (2019). Consensus Study Report. https://www.nap.edu/read/25353/chapter/1
World Health Organization (WHO) Guideline: Potassium Intake for Adults and Children. WHO; Geneva, Switzerland: 2012.
Aaron, K. J., & Sanders, P. W. (2013). Role of dietary salt and potassium intake in cardiovascular health and disease: a review of the evidence. Mayo Clinic proceedings, 88(9), 987–995. https://doi.org/10.1016/j.mayocp.2013.06.005
Clinical practice guidelines for nutrition in chronic renal failure. K/DOQI, National Kidney Foundation. Am J Kidney Dis. 2000 Jun;35(6 Suppl 2):S17-S104. doi: 10.1053/ajkd.2000.v35.aajkd03517. Erratum in: Am J Kidney Dis 2001 Oct;38(4):917.
Kalantar-Zadeh K, Fouque D. Nutritional Management of Chronic Kidney Disease. N Engl J Med. 2017 Nov 2;377(18):1765-1776. doi: 10.1056/NEJMra1700312
Bailey JL, Sands JM, Franch HA. Water, electrolytes, and acid-based metabolism. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:102-32.
Patrick J. Assessment of body potassium stores. Kidney Int 1977;11:476-90. https://www.kidney-international.org/article/S0085-2538(15)31757-9/pdf
Viera AJ, Wouk N. Potassium disorders: Hypokalemia and hyperkalemia. Am Fam Physician 2015;92:487-95. https://www.aafp.org/afp/2015/0915/p487.html
WHO. Diet, nutrition and the prevention of chronic disease. Report of a Joint WHO/FAO Expert Consultation. Geneva, World Health Organization (WHO), 2003. http://whqlibdoc.who.int/trs/WHO_TRS_916.pdf
D'Elia L, Barba G, Cappuccio FP et al. Potassium intake, stroke, and cardiovascular disease a meta-analysis of prospective studies. Journal of the American College of Cardiology, 2011, 57(10):1210–1219. http://www.ncbi.nlm.nih.gov/pubmed/21371638
Whelton PK, He J, Cutler JA et al. Effects of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical trials. Journal of the American Medical Association, 1997, 277(20):1624–1632. http://www.ncbi.nlm.nih.gov/pubmed/9168293
Geleijnse JM, Kok FJ, Grobbee DE. Blood pressure response to changes in sodium and potassium intake: a metaregression analysis of randomised trials. Journal of Human Hypertension, 2003, 17(7):471–480. http://www.ncbi.nlm.nih.gov/pubmed/12821954
Dietary Guidelines Advisory Committee. The report of the Dietary Guidelines Advisory Committee on Dietary Guidelines for Americans. Washington, D.C., Department of Health and Human Services and Department of Agriculture, 2005. http://www.health.gov/dietaryguidelines/dga2005/report/default.htm
World Health Organization. Guideline: Potassium intake for adults and children. http://apps.who.int/iris/bitstream/10665/77986/1/9789241504829_eng.pdf
American Heart Association. A Primer on Potassium. https://sodiumbreakup.heart.org/a_primer_on_potassium?utm_source=SRI&utm_medium=HeartOrg&utm_term=Website&utm_content=SodiumAndSalt&utm_campaign=SodiumBreakup
DrugBank. Potassium. http://www.drugbank.ca/drugs/DB01345
Brown IJ, Tzoulaki I, Candeias V, Elliott P. Salt intakes around the world: implications for public health. Int J Epidemiol2009;38:791-813.
Kawasaki T, Itoh K, Kawasaki M. Reduction in blood pressure with a sodium-reduced, potassium- and magnesium-enriched mineral salt in subjects with mild essential hypertension. Hypertens Res1998;21:235-43. https://www.ncbi.nlm.nih.gov/pubmed/9877516?access_num=9877516&link_type=MED&dopt=Abstract
Chang HY, Hu YW, Yue CS, Wen YW, Yeh WT, Hsu LS, et al. Effect of potassium-enriched salt on cardiovascular mortality and medical expenses of elderly men. Am J Clin Nutr2006;83:1289-96. http://ajcn.nutrition.org/content/83/6/1289?ijkey=52dc92efe22c9a7ff1bd4e7366b4fcecb7f45e7e&keytype2=tf_ipsecsha
Nurs Crit Care. 2006 Nov-Dec;11(6):273-80. Potassium additive algorithm for use in continuous renal replacement therapy. https://www.ncbi.nlm.nih.gov/pubmed/17883675
National Academies of Sciences, Engineering, and Medicine. Dietary Reference Intakes for Sodium and Potassium. Washington, DC; The National Academies Press; 2019.
U.S. Department of Health and Human Services, U.S. Department of Agriculture. https://health.gov/dietaryguidelines/2015/guidelines/
U.S. Department of Agriculture, Agricultural Research Service. What We Eat in America, 2013-2014. https://www.ars.usda.gov/northeast-area/beltsville-md-bhnrc/beltsville-human-nutrition-research-center/food-surveys-research-group/docs/wweia-data-tables/
Bailey RL, Fulgoni VL, 3rd, Keast DR, Dwyer JT. Dietary supplement use is associated with higher intakes of minerals from food sources. Am J Clin Nutr 2011;94:1376-81. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3192481/
Council for Responsible Nutrition. Re: Docket No. FDA-2012-N-1210; Food Labeling: Revision of the Nutrition and Supplement Facts Labels. https://www.crnusa.org/sites/default/files/pdfs/comments-pdfs/CRN_Comments_FDA_ProposedRule-RevisionNutritionSupplementFactsLabels080114.pdf
National Institutes of Health. Dietary Supplement Label Database. http://www.dsld.nlm.nih.gov/dsld/
U.S. Food and Drug Administration. List of Drug Products That Have Been Withdrawn or Removed from the Market for Reasons of Safety or Effectiveness. https://www.gpo.gov/fdsys/pkg/FR-1999-03-08/pdf/99-5517.pdf
U.S. Food and Drug Administration. Code of Federal Regulations Title 21. 21CFR201.306. Potassium salt preparations intended for oral ingestion by man. https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=201.306
Commission on Dietary Supplement Labels. Report of the Commission 0n Dietary Supplement Labels. https://health.gov/dietsupp/cover.htm
Macdonald-Clarke CJ, Martin BR, McCabe LD, McCabe GP, Lachcik PJ, Wastney M, et al. Bioavailability of potassium from potatoes and potassium gluconate: a randomized dose response trial. Am J Clin Nutr 2016;104:346-53. https://www.ncbi.nlm.nih.gov/pubmed/27413123
Levene DL. Potassium chloride: absorption and excretion. Can Med Assoc J 1973;108:853-5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1941311/pdf/canmedaj01665-0044.pdf
Levene DL. The absorption of potassium chloride–liquid vs. tablet. Can Med Assoc J 1973;108:1480 passim. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1941543/pdf/canmedaj01670-0017.pdf
Institute of Medicine. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC; 2005.
U.S. Department of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard Reference, Release 28. https://ndb.nal.usda.gov/ndb/
O'Neil CE, Keast DR, Fulgoni VL, Nicklas TA. Food sources of energy and nutrients among adults in the US: NHANES 2003-2006. Nutrients 2012;4:2097-120. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546624/
Keast DR, Fulgoni VL, 3rd, Nicklas TA, O'Neil CE. Food sources of energy and nutrients among children in the United States: National Health and Nutrition Examination Survey 2003-2006. Nutrients 2013;5:283-301. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3571649/
He FJ, MacGregor GA. Beneficial effects of potassium on human health. Physiol Plant 2008;133:725-35. https://www.ncbi.nlm.nih.gov/pubmed/18724413
U.S. Food and Drug Administration. Food Labeling: Revision of the Nutrition and Supplement Facts Labels.external link disclaimer Federal Register 81(103):33894-33895. 2016.
Food Labeling: Revision of the Nutrition and Supplement Facts Labels and Serving Sizes of Foods That Can Reasonably Be Consumed at One Eating Occasion; Dual-Column Labeling; Updating, Modifying, and Establishing Certain Reference Amounts Customarily Consumed; Serving Size for Breath Mints; and Technical Amendments; Proposed Extension of Compliance Dates. https://www.federalregister.gov/documents/2017/10/02/2017-21019/food-labeling-revision-of-the-nutrition-and-supplement-facts-labels-and-serving-sizes-of-foods-that
United States Department of Agriculture (USDA). Foods rich in potassium. https://www.ars.usda.gov/is/br/potassium/potassium.pdf
Champagne CM. Dietary interventions on blood pressure: the Dietary Approaches to Stop Hypertension (DASH) trials. Nutr Rev 2006;64:S53-6. https://www.ncbi.nlm.nih.gov/pubmed/16532899
Filippini T, Violi F, D'Amico R, Vinceti M. The effect of potassium supplementation on blood pressure in hypertensive subjects: A systematic review and meta-analysis. Int J Cardiol 2017;230:127-35. https://www.ncbi.nlm.nih.gov/pubmed/28024910
Binia A, Jaeger J, Hu Y, Singh A, Zimmermann D. Daily potassium intake and sodium-to-potassium ratio in the reduction of blood pressure: a meta-analysis of randomized controlled trials. J Hypertens 2015;33:1509-20. https://www.ncbi.nlm.nih.gov/pubmed/26039623
Cappuccio FP, MacGregor GA. Does potassium supplementation lower blood pressure? A meta-analysis of published trials. J Hypertens 1991;9:465-73. https://www.ncbi.nlm.nih.gov/pubmed/1649867
Whelton PK, He J, Cutler JA, Brancati FL, Appel LJ, Follmann D, et al. Effects of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical trials. JAMA 1997;277:1624-32. https://www.ncbi.nlm.nih.gov/pubmed/9168293
Dickinson HO, Nicolson DJ, Campbell F, Beyer FR, Mason J. Potassium supplementation for the management of primary hypertension in adults. Cochrane Database Syst Rev 2006:CD004641. http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD004641.pub2/full
Agency for Healthcare Research and Quality. Sodium and Potassium Intake: Effects on Chronic Disease Outcomes and Risks. Rockville, MD; 2018. https://effectivehealthcare.ahrq.gov/sites/default/files/pdf/cer-206-report-sodium-potassium-update.pdf
Aaron KJ, Sanders PW. Role of dietary salt and potassium intake in cardiovascular health and disease: a review of the evidence. Mayo Clin Proc 2013;88:987-95. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3833247/
D'Elia L, Barba G, Cappuccio FP, Strazzullo P. Potassium intake, stroke, and cardiovascular disease a meta-analysis of prospective studies. J Am Coll Cardiol 2011;57:1210-9. https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0049398/
Aburto NJ, Hanson S, Gutierrez H, Hooper L, Elliott P, Cappuccio FP. Effect of increased potassium intake on cardiovascular risk factors and disease: systematic review and meta-analyses. BMJ 2013;346:f1378. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4816263/
Agency for Healthcare Research and Quality. Effects of Dietary Sodium and Potassium Intake on Chronic Disease Outcomes and Related Risk Factors. https://effectivehealthcare.ahrq.gov/topics/sodium-potassium/research-protocol
Vinceti M, Filippini T, Crippa A, de Sesmaisons A, Wise LA, Orsini N. Meta-Analysis of Potassium Intake and the Risk of Stroke. J Am Heart Assoc 2016;5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5121516/
Weaver CM. Potassium and health. Adv Nutr 2013;4:368S-77S. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650509/
Phillips R, Hanchanale VS, Myatt A, Somani B, Nabi G, Biyani CS. Citrate salts for preventing and treating calcium containing kidney stones in adults. Cochrane Database Syst Rev 2015:CD010057. http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD010057.pub2/full
Curhan GC, Willett WC, Rimm EB, Stampfer MJ. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med 1993;328:833-8. https://www.nejm.org/doi/10.1056/NEJM199303253281203
Curhan GC, Willett WC, Speizer FE, Spiegelman D, Stampfer MJ. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med 1997;126:497-504. https://www.ncbi.nlm.nih.gov/pubmed/9092314
Barcelo P, Wuhl O, Servitge E, Rousaud A, Pak CY. Randomized double-blind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis. J Urol 1993;150:1761-4. https://www.ncbi.nlm.nih.gov/pubmed/8230497
Hanley DA, Whiting SJ. Does a high dietary acid content cause bone loss, and can bone loss be prevented with an alkaline diet? J Clin Densitom 2013;16:420-5. https://www.ncbi.nlm.nih.gov/pubmed/24094472
Tucker KL, Hannan MT, Chen H, Cupples LA, Wilson PW, Kiel DP. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999;69:727-36. https://www.ncbi.nlm.nih.gov/pubmed/10197575
Lin PH, Ginty F, Appel LJ, Aickin M, Bohannon A, Garnero P, et al. The DASH diet and sodium reduction improve markers of bone turnover and calcium metabolism in adults. J Nutr 2003;133:3130-6. https://www.ncbi.nlm.nih.gov/pubmed/14519796
Moseley KF, Weaver CM, Appel L, Sebastian A, Sellmeyer DE. Potassium citrate supplementation results in sustained improvement in calcium balance in older men and women. J Bone Miner Res 2013;28:497-504. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578058/
Jehle S, Hulter HN, Krapf R. Effect of potassium citrate on bone density, microarchitecture, and fracture risk in healthy older adults without osteoporosis: a randomized controlled trial. J Clin Endocrinol Metab 2013;98:207-17. https://academic.oup.com/jcem/article/98/1/207/2823184
Dawson-Hughes B, Harris SS, Palermo NJ, Gilhooly CH, Shea MK, Fielding RA, et al. Potassium bicarbonate supplementation lowers bone turnover and calcium excretion in older men and women: A randomized dose-finding trial. J Bone Miner Res 2015;30:2103-11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817273/
Macdonald HM, Black AJ, Aucott L, Duthie G, Duthie S, Sandison R, et al. Effect of potassium citrate supplementation or increased fruit and vegetable intake on bone metabolism in healthy postmenopausal women: a randomized controlled trial. Am J Clin Nutr 2008;88:465-74. https://www.ncbi.nlm.nih.gov/pubmed/18689384
Centers for Disease Control and Prevention. National Diabetes Statistics Report. https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf
Chatterjee R, Davenport CA, Svetkey LP, Batch BC, Lin PH, Ramachandran VS, et al. Serum potassium is a predictor of incident diabetes in African Americans with normal aldosterone: the Jackson Heart Study. Am J Clin Nutr 2017;105:442-9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5267306/
Chatterjee R, Colangelo LA, Yeh HC, Anderson CA, Daviglus ML, Liu K, et al. Potassium intake and risk of incident type 2 diabetes mellitus: the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Diabetologia 2012;55:1295-303 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3934349/
Colditz GA, Manson JE, Stampfer MJ, Rosner B, Willett WC, Speizer FE. Diet and risk of clinical diabetes in women. Am J Clin Nutr 1992;55:1018-23. https://www.ncbi.nlm.nih.gov/pubmed/1315120
Chatterjee R, Slentz C, Davenport CA, Johnson J, Lin PH, Muehlbauer M, et al. Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial. Am J Clin Nutr 2017;106:1431-8. https://www.ncbi.nlm.nih.gov/pubmed/29092881
Hyperkalemia. University of Maryland Medical Center. http://umm.edu/health/medical/altmed/condition/hyperkalemia. Accessed Oct. 1, 2014.
Mayo Foundation for Medical Education and Research, MayoClinic. High potassium (hyperkalemia) Symptoms. http://www.mayoclinic.org/symptoms/hyperkalemia/basics/definition/SYM-20050776?p=1
Potassium, serum. Mayo Medical Laboratories. http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/81390. Accessed Oct. 1, 2014.
Greenberg A. Diuretic complications. Am J Med Sci. 2000;319(1):10–24.
MayoClinic. Causes of Hyperkalemia. http://www.mayoclinic.org/symptoms/hyperkalemia/basics/causes/sym-20050776
Raebel MA. Hyperkalemia associated with use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Cardiovasc Ther 2012;30:e156-66. https://www.ncbi.nlm.nih.gov/pubmed/21883995
Sarafidis PA, Georgianos PI, Lasaridis AN. Diuretics in clinical practice. Part II: electrolyte and acid-base disorders complicating diuretic therapy. Expert Opin Drug Saf 2010;9:259-73. https://www.ncbi.nlm.nih.gov/pubmed/20095916
Rose BD. Causes of hyperkalemia. http://www.uptodate.com/home. Accessed Oct. 1, 2014.
American Heart Association. Hyperkalemia (High Potassium). http://www.heart.org/HEARTORG/Conditions/HeartFailure/TreatmentOptionsForHeartFailure/Hyperkalemia-High-Potassium_UCM_488806_Article.jsp
Smellie WS. Spurious hyperkalaemia. BMJ. 2007;334(7595):693–695.
Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3(2):324–330.
Diercks DB, Shumaik GM, Harrigan RA, Brady WJ, Chan TC. Electrocardiographic manifestations: electrolyte abnormalities. J Emerg Med. 2004;27(2):153–160.
Alfonzo A, Soar J, MacTier R, et al. Treatment of acute hyperkalaemia in adults. March 1, 2014. https://ukkidney.org/sites/renal.org/files/RENAL%20ASSOCIATION%20HYPERKALAEMIA%20GUIDELINE%202020.pdf
Fordjour KN, Walton T, Doran JJ. Management of hyperkalemia in hospitalized patients. Am J Med Sci. 2014;347(2):93–100.
Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246–3251.
Lens XM, Montoliu J, Cases A, Campistol JM, Revert L. Treatment of hyperkalaemia in renal failure: salbutamol v. insulin. Nephrol Dial Transplant. 1989;4(3):228–232.
Mahoney BA, Smith WA, Lo DS, Tsoi K, Tonelli M, Clase CM. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005;(2):CD003235.
Lillemoe KD, Romolo JL, Hamilton SR, Pennington LR, Burdick JF, Williams GM. Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: clinical and experimental support for the hypothesis. Surgery. 1987;101(3):267–272.
Harel Z, Harel S, Shah PS, Wald R, Perl J, Bell CM. Gastrointestinal adverse events with sodium polystyrene sulfonate (Kayexalate) use: a systematic review. Am J Med. 2013;126(3):264.e9–e24.
FDA Drug Safety Communication. https://www.fda.gov/media/105008/download
Gross P, Pistrosch F. Hyperkalaemia: again. Nephrol Dial Transplant. 2004;19(9):2163–2166.
Harvard University. Harvard Health Publications. Heart failure and potassium. http://www.health.harvard.edu/heart-health/heart-failure-and-potassium
Hay, P. J., Touyz, S., Claudino, A. M., Lujic, S., Smith, C. A., & Madden, S. (2019). Inpatient versus outpatient care, partial hospitalisation and waiting list for people with eating disorders. The Cochrane database of systematic reviews, 1(1), CD010827. https://doi.org/10.1002/14651858.CD010827.pub2
Brown, H. D., Tran, R. H., & Patka, J. H. (2018). Effect of Bolus Insulin Administration Followed by a Continuous Insulin Infusion on Diabetic Ketoacidosis Management. Pharmacy (Basel, Switzerland), 6(4), 129. https://doi.org/10.3390/pharmacy6040129
Shao W, Ayub S, Drutel R, Heise WC, Gerkin R. QTc Prolongation Associated With Psychiatric Medications: A Retrospective Cross-Sectional Study of Adult Inpatients. J Clin Psychopharmacol. 2019 Jan/Feb;39(1):72-77. doi: 10.1097/JCP.0000000000000992
Cunha, T., & Heilberg, I. P. (2018). Bartter syndrome: causes, diagnosis, and treatment. International journal of nephrology and renovascular disease, 11, 291–301. https://doi.org/10.2147/IJNRD.S155397
McKenna D. Myopathy, hypokalaemia and pica (geophagia) in pregnancy. Ulster Med J 2006;75:159-60. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891740/
Rude RK. Magnesium. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:527-37.
Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol 2007;18:2649-52. http://jasn.asnjournals.org/content/18/10/2649.long
Barkas F, Liberopoulos E, Kei A, Elisaf M. Electrolyte and acid-base disorders in inflammatory bowel disease. Ann Gastroenterol 2013;26:23-8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959504/
Musto D, Rispo A, Testa A, Sasso F, Castiglione F. Hypokalemic myopathy in inflammatory bowel diseases. J Crohns Colitis 2013;7:680. https://www.ncbi.nlm.nih.gov/pubmed/23339931
Weiner ID, Wingo CS. Hypokalemia—consequences, causes, and correction. J Am Soc Nephrol. 1997;8(7):1179–1188.
Macdonald JE, Struthers AD. What is the optimal serum potassium level in cardiovascular patients? J Am Coll Cardiol. 2004;43(2):155–161.
Schulman M, Narins RG. Hypokalemia and cardiovascular disease. Am J Cardiol. 1990;65(10):4E–9E.
Millane TA, Ward DE, Camm AJ. Is hypomagnesemia arrhythmogenic? Clin Cardiol. 1992;15(2):103–108.
Kamel KS, Ethier JH, Richardson RM, Bear RA, Halperin ML. Urine electrolytes and osmolality: when and how to use them. Am J Nephrol. 1990;10(2):89–102.
Weaver WF, Burchell HB. Serum potassium and the electrocardiogram in hypokalemia. Circulation. 1960;21:505–521.
Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2015 Sep 15;92(6):487-495. https://www.aafp.org/afp/2015/0915/p487.html
Crop MJ, Hoorn EJ, Lindemans J, Zietse R. Hypokalaemia and subsequent hyperkalaemia in hospitalized patients. Nephrol Dial Transplant. 2007;22(12):3471–3477.
Kim GH, Han JS. Therapeutic approach to hypokalemia. Nephron. 2002;92(suppl 1):28–32.
Ingram TC, Olsson JM. In brief: hypokalemia. Pediatr Rev. 2008;29(9):e50–e51.
Keto while pregnant
What is lectin ?
What are food additives ?
Biotin and Pantothenic Acid