The most abundant exchangeable cation in the body.

Crucial for physiological function, such as preserving intracellular fluid volume and maintaining nerve and muscle function.

Significant variability and inaccuracy in plasma potassium measured in whole blood.

The blood potassium level is related to ingestion, internal recirculation, and elimination in the gastrointestinal and renal  systems.

Because of active potassium uptake by the sodium-potassium pump (Na+/K+-ATPase) across cell membranes, approximately 98% of total body potassium is intracellular.

Serum plasma potassium is only a small fraction of total body potassium.

2% of potassium, approximately 60 mmol, constitutes the extracellular pool.

In a 70kg adult, the total body potassium concentration is approximately 3010 mEq, about 43mEq/ kg, but only 2% , or approximately 60 mEq, is extrcellular.

The gradient between intra and extracellular potassium concentrations essential for muscle contraction and nerve conduction.

K+ contributes to the regulation of vascular tone through alterations in the polarization state of both endothelial and vascular smooth muscle cells. 

Exists predominantly in the intracellular fluid at concentrations of 140 to 150 meq/liter and in the extracellular fluid at concentrations of 3.5 to 5 meq/liter.

Serum potassium concentration levels are maintained by the balance between intake, excretion, and distribution between intracellular and extracellular space.

Patients with hypokalemia or hyperkalemia have an increased risk of death from any cause.

Disturbance in potassium homeostasis is associated with progressive cardiac, and kidney disease and interstitial fibrosis.

Diets low in sodium are often rich in potassium, which may contribute to clinical benefits in as much as increase dietary potassium reduces blood pressure and lowers the risk of stroke and renal calculus disease.

Conversely, underconsumption of potassium, particularly when combined with high sodium intake, is associated with chronic disorders including: hypertension, diabetes, obesity, and renal calculi.

Renal  potassium loss is divided into two categories: those typically associated with low or normal blood pressure such as with renal tubular acidosis, the use of diuretics, magnesium deficiency, Bartter�s syndrome and those associated with hypertension including renal artery stenosis, hyperaldosteronism, and mineral corticoid excess.

The balance between intracellular and extracellular potassium is regulated by insulin and Beta2 adrenergic receptor activation.

After binding these receptors activate sodium/potassium adenosine triphosphatase, resulting in potassium moving from extra cellular to intracellular compartments.

Insulin can bind to a tyrosine kinase-coupled receptor signaling that allows for glucose and potassium to move intracellularly.

The kidney closely regulates potassium secretion, reabsorption, and excretion.

Ingested potassium is virtually completely absorbed from and minimally excreted via the intestine.

The sodium-potassium adenosine triphosphatase pump primarily regulates the homeostasis between sodium and potassium.


The sodium-potassium adenosine triphosphatase pump, pumps out sodium in exchange for potassium, which moves into the cells. 


In the kidneys, the filtration of potassium takes place at the glomerulus. 


The reabsorption of potassium takes place at the proximal convoluted tubule and thick ascending loop of Henle.


Potassium secretion occurs at the distal convoluted tubule. 

Western diet has 50 to 100 mmol per day of potassium, therefore protective mechanisms are needed to prevent increases in extracellular potassium.

Average adult has approximately 60-80 mmol of total extracellular potassium and levels of 20-25 mmol of total plasma potassium.

Meals may have more potassium than the total plasma potassium, but because of rapid clearance by the kidneys and extrarenal mechanisms variations in plasma potassium levels during the course of the day are no greater than 10%.

Serum potassium levels are heavily influenced by medications such as potassium wasting diuretics, renin-angiotensin-aldosterone system inhibitors, beta blockers, and potassium sparing diuretics.

Potassium ion concentrations are a major determinant in the magnitude of the electrochemical potential of cells.


The presence of hypokalemia makes it more likely that cells will depolarize spontaneously. 

Low potassium dietary intake is implicated in chronic diseases including hypertension, cardiovascular disease, osteoporosis, and nephrolithiasis.

Hypokalemia and hyperkalemia are associated with chronic kidney disease progression, end stage renal disease, and mortality in populations with chronic kidney disease and heart failure.

Higher values of serum potassium are associated with a higher risk of mortality in the general population, and lower levels of potassium are associated with adverse kidney outcomes and mortality among participants not taking potassium wasting diuretics.

The kidneys maintain long-term potassium balance, excreting almost 90% of ingested potassium, and the rest is secreted through the G.I. tract and skin.

Kidney potassium excretion as a circadian rhythm independent of food intake.

Potassium is freely filtered by the glomerulus and mostly reabsorbed in the proximal tubule and thick ascending limb such that only a small amount reaches the distal nephron.

The major K+ secretorty mechanism in the distal nephron in the electrogenic secretion through the ROMK (renal outer of medullary K+) channel.

The second channel also mediates K+ secretion under conditions of increased flow.

Potassium secretion begins and progressively increases in magnitude in the early convoluted tubule.

Reabsorption in the proximal tubule is primarily through the paracellular pathway in rough proportion to sodium and water.

Alldosterone and cortisol have endogenous circadian secretion patterns.

Because of circadian clock patterns there is substantial variation in urinary potassium excretion levels and random urine sampling to evaluate hypokalemia or hyperkalemia may underestimate or overestimate the 24 hour rate of potassium excretion.

The kidneys are able to reduce urinary potassium excretion to less than 20 mmol per day so that hypokalemia due to inadequate intake is uncommon.

Renal excretion is the major protective mechanism against abnormalities in potassium levels and depends on filtration, reabsorption, and a distal nephron secretory process.

Factors regulating potassium secretion include: potassium intake, intracellular potassium, delivery of sodium chloride and poorly reabsorbable anions to the distal nephron, urine flow rate, aldosterone and beta-catecholamines, and the integrity of the renal tubular cell.

Potassium is really filtered at the glomerulus.

Potassium undergoes reabsorption in the proximal tubules and the loop of Henle.

Urinary excretion of potassium relies on secretion in the distal nephron a process enhanced by aldosterone.

Aldosterone increases potassium secretion.


Potassium disorders are related to cardiac arrhythmias. 


Potassium ion concentrations are a major determinant in the magnitude of the electrochemical potential of cells.

Hypokalemia makes it more likely that cells will depolarize spontaneously, leading to PVCs.

Distribution of potassium inracellularly and extracelllarly depends on the integrity of the cell membrane and its pumps, serm osmolality, pH, and the hormones insulin, aldosterone, beta 2-catecholamines, alpha-catecholamines, and prostaglandins.

Regulation of potassium is essential for vital processes including resting cellular membrane potential and propagation of action potentials in nerves, muscles, and cardiac tissue, along with hormone secretion and action, vascular tone, systemic blood pressure control, G.I. motility, acid-base homeostasis, glucose metabolism, insulin metabolism, mineralocorticoid action, renal concentrating function, and fluid and electrolyte balance.

Requirements vary with age and growth.

Full-term infants requires 2 to 3 mEq/kg/d, whereas the adult uses 1.0 to 1.5 mEq/kg/d.

Potassium demands are related to metabolic rate, 2.0 mEq/100 kcal.

Requirements increase during cell growth.

Extremely high or low levels of potassium can be life threatening.

Potassium homeostasis is necessary to prevent adverse cardiovascular events.

There is a relationship between potassium levels less than 3.5 mEq per liter, and the risk and arrhythmias in patients with acute MI.

Historically it has been recommended that potassium levels should be maintained between 4.0-55 milliequivalents per liter in AMI patients.

In a retrospective study using the Cerner Health Facts database including 38,689 patients with biomarker confirmed AMI admitted to hospitals between January 2000 in December 2008: the lowest mortality was observed in patients with serum potassium levels between 3.5, and less than 4.5 mEq per liter compared with those who had a higher a lower potassium levels (Goyal A et al).

Epidemiologic studies have demonstrated an inverse correlation between K+ intake and the prevalence of hypertension.

The Intersalt Study found that higher urinary K+ excretion associated with lower blood pressures, even when adjusted for Na+ intake.

The US Professional Men Cohort and the Nurses’ Health Study found that increased K+ intake was associated with a decrease in risk for stroke.

K+ supplementation effective in lowering blood pressure in hypertensive individuals, and particularly among African Americans.

Potassium generally under consumed in the US and is associated with hypertension and cardiovascular diseases.

Recommended intake levels 4700 mg/day.

Estimated mean potassium intake in US 2290 mg/day for women and 3026 mg/day for men.

Daily intake of salt is about 3 times higher than the daily intake of K on a molar basis.

Changes in potassium and sodium intake a shift from traditional plant based diets high in K and low in Na such as fruits, leafy greens, roots and tubers, to processed foods high in Na and low in K.

Inadequate consumption of K combined with excessive NA intake contributes to obesity, hypertension, kidney stones, and bone disease.

Sodium retention occurs in response to K+ depletion and vice versa.

K+ can stimulate endothelium-dependent vasodilatation, may increase nitric oxide synthesis and may lower sympathetic activity and reduce the negative actions of aldosterone.

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