[1] A number of medications can also cause high blood potassium including spironolactone, NSAIDs, and angiotensin converting enzyme inhibitors.

[1][3] Other medications used to rapidly reduce blood potassium levels include insulin with dextrose, salbutamol, and sodium bicarbonate.

[1] Measures to remove potassium from the body include diuretics such as furosemide, potassium-binders such as polystyrene sulfonate (Kayexalate) and sodium zirconium cyclosilicate, and hemodialysis.

[2] It is associated with an increased mortality, whether due to hyperkalaemia itself or as a marker of severe illness, especially in those without chronic kidney disease.

This is especially pronounced in acute kidney injury where the glomerular filtration rate and tubular flow are markedly decreased, characterized by reduced urine output.

[15] For potassium-sparing diuretics, such as amiloride and triamterene; both the drugs block epithelial sodium channels in the collecting tubules, thereby preventing potassium excretion into urine.

[13] NSAIDs such as ibuprofen, naproxen, or celecoxib inhibit prostaglandin synthesis, leading to reduced production of renin and aldosterone, causing potassium retention.

[16] The antibiotic trimethoprim and the antiparasitic medication pentamidine inhibits potassium excretion, which is similar to mechanism of action by amiloride and triamterene.

Examples of drugs that can raise the serum potassium are non-selective beta-blockers such as propranolol and labetalol.

[14] High levels of adrenaline and noradrenaline have a protective effect on the cardiac electrophysiology because they bind to beta 2 adrenergic receptors, which, when activated, extracellularly decrease potassium concentration.

[20] Hyperkalemic periodic paralysis is an autosomal dominant clinical condition where there is a mutation in gene located at 17q23 that regulates the production of protein SCN4A.

Acute digitalis overdose such as digoxin toxicity may cause hyperkalemia[22] through the inhibition of sodium-potassium-ATPase pump.

[14] Giving succinylcholine to people with conditions such as burns, trauma, infection, prolonged immobilisation can cause hyperkalemia due to widespread activation of acetylcholine receptors rather than a specific group of muscles.

[24] Repeated fist clenching during the blood draw can cause a transient rise in potassium levels.

A familial form of pseudohyperkalemia, a benign condition characterised by increased serum potassium in whole blood stored at cold temperatures, also exists.

In the kidneys, elimination of potassium is passive (through the glomeruli), and reabsorption is active in the proximal tubule and the ascending limb of the loop of Henle.

[medical citation needed] Regulation of serum potassium is a function of intake, appropriate distribution between intracellular and extracellular compartments, and effective bodily excretion.

In healthy individuals, homeostasis is maintained when cellular uptake and kidney excretion naturally counterbalance a patient's dietary intake of potassium.

To compensate for this deficit in function, the colon increases its potassium secretion as part of an adaptive response.

However, serum potassium remains elevated as the colonic compensating mechanism reaches its limits.

[28][29] Hyperkalemia develops when there is excess production (oral intake, tissue breakdown) or ineffective elimination of potassium.

Ineffective elimination can be hormonal (in aldosterone deficiency) or due to causes in the kidney that impair excretion.

Since depolarization due to concentration change is slow, it never generates an action potential by itself; instead, it results in accommodation.

Of most concern is the impairment of cardiac conduction, which can cause ventricular fibrillation and/or abnormally slow heart rhythms.

[13] To gather enough information for diagnosis, the measurement of potassium must be repeated, as the elevation can be due to hemolysis in the first sample.

[medical citation needed] Also, electrocardiography (ECG) may be performed to determine if there is a significant risk of abnormal heart rhythms.

Bradycardia, junctional rhythms and QRS widening are particularly associated with increased risk of adverse outcomes[33] The serum potassium concentration at which electrocardiographic changes develop is somewhat variable.

[13] High dietary sources include vegetables such as avocados,[34][35] tomatoes and potatoes, fruits such as bananas, oranges and nuts.

Clinical practice guidelines recommend giving 6.8 mmol for typical EKG findings of hyperkalemia.

[45] Patiromer is taken by mouth and works by binding free potassium ions in the gastrointestinal tract and releasing calcium ions for exchange, thus lowering the amount of potassium available for absorption into the bloodstream and increasing the amount lost via the feces.