Ineffective elimination Decreased kidney function is a major cause of<unk> . This is especially pronounced in acute kidney injury where the glomerular filtration rate and tubular flow are markedly decreased, characterized by reduced urine output. This can lead to a dramatically elevated potassium in conditions of increased cell breakdown as the potassium is released from the cells and cannot be eliminated in the kidney. In chronic kidney disease,<unk>  occurs as a result of reduced aldosterone responsiveness and reduced sodium and water delivery in distal tubules. Medications that interfere with urinary excretion by inhibiting the renin–angiotensin system is one of the most common causes of<unk> . Examples of medications that can cause<unk>  include ACE inhibitors, angiotensin receptor blockers, beta blockers, and calcineurin inhibitor immunosuppressants such as ciclosporin and tacrolimus. 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. Spironolactone acts by competitively inhibiting the action of aldosterone. NSAIDs such as ibuprofen, naproxen, or celecoxib inhibit prostaglandin synthesis, leading to reduced production of renin and aldosterone, causing potassium retention. The antibiotic trimethoprim and the antiparasitic medication pentamidine inhibits potassium excretion, which is similar to mechanism of action by amiloride and triamterene. Mineralocorticoid (aldosterone) deficiency or resistance can also cause<unk> . Primary adrenal insufficiency are: Addison's disease and congenital adrenal hyperplasia (CAH) (including enzyme deficiencies such as 21α hydroxylase, 17α hydroxylase, 11β hydroxylase, or 3β dehydrogenase). * Type IV renal tubular acidosis (aldosterone resistance of the kidney's tubules) * Gordon's syndrome (pseudohypoaldosteronism type II) ("familial hypertension with<unk> "), a rare genetic disorder caused by defective modulators of salt transporters, including the thiazide-sensitive Na-Cl cotransporter. Excessive release from cells Metabolic acidosis can cause<unk>  as the elevated hydrogen ions in the cells can displace potassium, causing the potassium ions to leave the cell and enter the bloodstream. However, in respiratory acidosis or organic acidosis such as lactic acidosis, the effect on serum potassium are much less significant although the mechanisms are not completely understood. Insulin deficiency can cause<unk>  as the hormone insulin increases the uptake of potassium into the cells. Hyperglycemia can also contribute to<unk>  by causing hyperosmolality in extracellular fluid, increasing water diffusion out of the cells and causes potassium to move alongside water out of the cells also. The co-existence of insulin deficiency, hyperglycemia, and hyperosmolality is often seen in those affected by diabetic ketoacidosis. Apart from diabetic ketoacidosis, there are other causes that reduce insulin levels such as the use of the medication octreotide, and fasting which can also cause<unk> . Increased tissue breakdown such as rhabdomyolysis, burns, or any cause of rapid tissue necrosis, including tumor lysis syndrome can cause the release of intracellular potassium into blood, causing<unk> . Beta2-adrenergic agonists act on beta-2 receptors to drive potassium into the cells. Therefore, beta blockers can raise potassium levels by blocking beta-2 receptors. However, the rise in potassium levels is not marked unless there are other co-morbidities present. Examples of drugs that can raise the serum potassium are non-selective beta-blockers such as propranolol and labetalol. Beta-1 selective blockers such as metoprolol do not increase serum potassium levels. Exercise can cause a release of potassium into bloodstream by increasing the number of potassium channels in the cell membrane. The degree of potassium elevation varies with the degree of exercise, which range from 0.3 meq/L in light exercise to 2 meq/L in heavy exercise, with or without accompanying ECG changes or lactic acidosis. However, peak potassium levels can be reduced by prior physical conditioning and potassium levels are usually reversed several minutes after exercise. 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.<unk>  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. SCN4A is an important component of sodium channels in skeletal muscles. During exercise, sodium channels would open to allow influx of sodium into the muscle cells for depolarization to occur. But in<unk>  periodic paralysis, sodium channels are slow to close after exercise, causing excessive influx of sodium and displacement of potassium out of the cells. Rare causes of<unk>  are discussed as follows. Acute digitalis overdose such as digoxin toxicity may cause<unk>  through the inhibition of sodium-potassium-ATPase pump. Massive blood transfusion can cause<unk>  in infants due to leakage of potassium out of the red blood cells during storage. Giving succinylcholine to people with conditions such as burns, trauma, infection, prolonged immobilisation can cause<unk>  due to widespread activation of acetylcholine receptors rather than a specific group of muscles. Arginine hydrochloride is used to treat refractory metabolic alkalosis. The arginine ions can enter cells and displace potassium out of the cells, causing<unk> . Calcineurin inhibitors such as cyclosporine, tacrolimus, diazoxide, and minoxidil can cause<unk> . Box jellyfish venom can also cause<unk> . Excessive intake Excessive intake of potassium is not a primary cause of<unk>  because the human body usually can adapt to the rise in the potassium levels by increasing the excretion of potassium into urine through aldosterone hormone secretion and increasing the number of potassium secreting channels in kidney tubules. Acute<unk>  in infants is also rare even though their body volume is small, with accidental ingestion of potassium salts or potassium medications.<unk>  usually develops when there are other co-morbidities such as hypoaldosteronism and chronic kidney disease. Pseudohyperkalemia Pseudohyperkalemia occurs when the measured potassium level is falsely elevated. This condition is usually suspected when the patient is clinically well without any ECG changes. Mechanical trauma during blood drawing can cause potassium leakage out of the red blood cells due to haemolysis of the blood sample. Repeated fist clenching during the blood draw can cause a transient rise in potassium levels. Prolonged length of blood storage can also increase serum potassium levels.<unk>  may become apparent when a person's platelet concentration is more than 500,000/microL in a clotted blood sample (serum blood sample). Potassium leaks out of platelets after clotting has occurred. A high white cell count (greater than 120,000/microL) in people with chronic lymphocytic leukemia increases the fragility of red blood cells, thus causing pseudohyperkalemia during blood processing. This problem can be avoided by processing serum samples, because clot formation protects the cells from haemolysis during processing. A familial form of pseudohyperkalemia, a benign condition characterised by increased serum potassium in whole blood stored at cold temperatures, also exists. This is due to increased potassium permeability in red blood cells.
Hyperkalemia
Alkalosis
Hyponatremia
Hypermagnesemia
Hypernatremia
Digoxin toxicity
Hypokalemia
Ketosis