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John Gennari M. Professor of Medicine, Director. You can also search for this author in PubMed Google Scholar. Reprints and permissions. Gennari, F. Disorders of Potassium Metabolism. In: Suki, W. Springer, Boston, MA. Publisher Name : Springer, Boston, MA. Print ISBN : Online ISBN : eBook Packages : Springer Book Archive.

Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Policies and ethics. Skip to main content. Abstract The concentration of potassium in our cells is some 37 times higher than in the extracellular compartment.

Keywords Renal Tubular Acidosis Metabolic Alkalosis Distal Nephron Aldosterone Secretion Periodic Paralysis These keywords were added by machine and not by the authors.

Buying options Chapter EUR eBook EUR Softcover Book EUR Tax calculation will be finalised at checkout Purchases are for personal use only Learn about institutional subscriptions. Preview Unable to display preview. References Holbrook JT, Patterson KY, Bodner JE, Douglas LW, Veillon C, Kelsay JL, Mertz W, Smith JC: Sodium and potassium intake and balance in adults consuming self-selected diets.

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Because many individuals in the population consume potassium in amounts that are well below the AI and because underconsumption of potassium is linked with adverse health effects, potassium has been recognized as a "nutrient of public health concern" in the Dietary Guidelines for Americans.

In , the US Food and Drug Administration FDA required manufacturers to display potassium content of foods on the Nutrition Facts food label Some relatively good dietary sources of potassium are listed in the Table 2 , along with their potassium content in milligrams mg.

For more information on the nutrient content of foods, search USDA's FoodData Central Multivitamin-mineral supplements in the US do not contain more than 99 mg of potassium per serving One milliequivalent mEq or one millimole mmol corresponds to about 39 mg of potassium.

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

Potassium is available in different supplemental forms, including potassium chloride, potassium citrate, potassium gluconate, potassium bicarbonate, potassium aspartate, and potassium orotate Because of the potential for serious side effects, one should seek medical advice before deciding to use a potassium supplement see Safety.

Finally, many salt substitutes contain potassium chloride, and acesulfame potassium Ace-K is an FDA-approved general purpose sweetener. Abnormally elevated serum potassium concentrations are referred to as hyperkalemia.

Hyperkalemia occurs when potassium intake exceeds the capacity of the kidneys to eliminate it. Acute or chronic kidney failure, the use of potassium-sparing diuretics , and insufficient aldosterone secretion hypoaldosteronism may result in the accumulation of potassium due to a decreased urinary potassium excretion.

Hyperkalemia may also result from a shift of intracellular potassium into the circulation, which may occur with the rupture of red blood cells hemolysis or tissue damage e. Symptoms of hyperkalemia may include tingling of the hands and feet, muscular weakness, and temporary paralysis.

The most serious complication of hyperkalemia is the development of an abnormal heart rhythm cardiac arrhythmia , which can lead to cardiac arrest See the section on Drug interactions for a discussion of the medications that increase the risk of hyperkalemia. Gastrointestinal symptoms are the most common side effects of potassium supplements , including nausea, vomiting, abdominal discomfort, and diarrhea.

Intestinal ulceration has been reported after the use of enteric-coated potassium chloride tablets. Taking potassium with meals or taking a microencapsulated form of potassium may reduce gastrointestinal side effects Rashes may occasionally occur.

The most serious adverse reaction to potassium supplementation is hyperkalemia, yet is rare in subjects with normal kidney function see Toxicity. Individuals with abnormal kidney function and those on potassium-sparing medications see Drug interactions should be monitored closely to prevent hyperkalemia 50, Table 3 lists the classes of medications known to increase the risk of hyperkalemia elevated serum potassium in patients who also use potassium supplements 50, 51 , Several classes of medications are known to induce hypokalemia low serum potassium; Table 4 ; In the absence of treatment, hypokalemia can have serious complications and even be fatal see Deficiency.

Various mechanisms explain how certain medications can lead to potassium depletion. For example, both loop and thiazide diuretics increase the urinary excretion of potassium.

Corticoids cause sodium retention that leads to a compensatory increase in urinary potassium excretion. Penicillins formulated as sodium salts also stimulate potassium excretion. Several medications, including aminoglycosides, anti-fungal agents amphotericin-B, fluconazole , and cisplatin, can damage the renal tubular epithelium and lead to severe potassium loss.

Outdated tetracycline antibiotics have been linked to electrolyte disturbances. Penicillins : penicillin G sodium Pfizerpen , mezlocillin Mezlin , carbenicillin Geocillin , ticarcillin Ticar. Loop diuretics : bumetanide Bumex , ethacrynic acid Edecrin , furosemide Lasix , torsemide Demadex.

Thiazide diuretics : Acetazolamide, thiazides, chlorthalidone Hygroton , indapamide Lozol , metolazone Zaroxolyn , chlorothiazide Diuril. fludrocortisone Florinef , hydrocortisone Cortef , cortisone Cortone , prednisone Deltasone.

There is substantial evidence suggesting that a diet high in potassium-rich food and beverages may be associated with lower risks of stroke , hypertension , kidney stones , and possibly osteoporosis.

However, currently there is insufficient evidence to establish a causal relationship between potassium intakes and the risk of these chronic conditions The revised AI values are 2.

Fruit and vegetables are among the richest sources of dietary potassium, and a large body of evidence supports the association of increased fruit and vegetable intakes with reduced risk of cardiovascular disease see the article on Fruit and Vegetables.

The Linus Pauling Institute recommends the consumption of a diet high in potassium-rich foods see Sources , especially fruit, vegetables, nuts , and dairy products to ensure adequate potassium intakes. A diet rich in fruit and vegetables that supplies 2.

This recommendation does not apply to individuals who have been advised to limit potassium consumption by a health care professional see Safety. Originally written in by: Jane Higdon, Ph. Linus Pauling Institute Oregon State University.

Updated in February by: Jane Higdon, Ph. Updated in December by: Victoria J. Drake, Ph. Updated in April by: Barbara Delage, Ph. Reviewed in April by Connie Weaver, Ph. Distinguished Professor and Department Head Department of Nutrition Science Purdue University.

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Metabolism of potassium and its clinical significance 1. Metabolism of Potassium and its clinical significance Dr. Rohini C Sane. Major intracellular cation 2. Transmission of nerve impulse 4. Acid base balance 5. Intracellular potassium concentration is necessary for protein biosynthesis by ribosomes.

preanalytical error. Homoeostasis of Potassium by Transcellular movement 2. Role of gastrointestinal tract in Homoeostasis of Potassium 3. Role of Kidney in Homoeostasis of Potassium. Potassium ions transport across the cell membrane. It action is by constricting arterioles and increasing heartbeats.

Angiotensin II later hydrolyzed by Angiotensinase. Since abnormalities in K metabolism can also cause lethal arrhythmia or sudden cardiac death, it is extremely important to monitor patients with a high risk of hyper- or hypokalemia and attempt to provide early and appropriate intervention.

Keywords: CKD; blood pressure; hypertension; potassium; potassium excretion; salt; sodium. Abstract Potassium K , the main cation inside cells, plays roles in maintaining cellular osmolarity and acid-base equilibrium, as well as nerve stimulation transmission, and regulation of cardiac and muscle functions.

Publication types Review. Substances Potassium.

Nature —, Corvol P, Pinet F, Galen FX, Plouin PF, Chatellier G, Pagny JY, Bruneval P, Camilleri JP, Ménard J: Primary reninism In: JH Laragh, BM Brenner, eds, Hypertension.

Simon N, Franklin SS, Bleifer KH, Maxwell MH: Clinical characteristics of renovascular hypertension. DAMA —, White RH, Schambelan M: Hypertension, hyperreninemia, and secondary hyperaldosteronism in systemic necrotizing vasculitis.

Ruby ST, Burch A, White WB: Unilateral renal artery stenosis seen initially as severe and symptomatic hypokalemia. Arch Surg —, Edwards CRW, Walker BR, Benediktsson R, Seckl JR: Congenital and acquired syndromes of apparent mineralocorticoid excess.

J Steroid Biochem Mol Biol 1—5, Biglieri EG, Kater CE: Mineralocorticoids in congenital adrenal hyperplasia. J Steroid Biochem Mol Biol —, Mantero F, Boscaro M: Glucocorticoid-dependent hypertension. Stewart PM, Come JET, Shackleton CHL, Edwards CRW: Syndrome of apparent mineralocorticoid excess.

Clore J, Schoolwerth A, Watlington CO: When is cortisol a mineralocorticoid? Stewart PM, Wallace AM, Valentine R, Burt D, Shackleton CHL, Edwards CRW: Mineralocorticoid activity of liquorice: beta-hydroxysteroid dehydrogenase deficiency comes of age. Farese RV, Biglieri EG, Shackleton CHL, Irony I, Gomez-Fontes R: Licorice-induced hypermineralocorticoidism.

Stewart PM, Wallace AM, Atherden SM, Shearing CH, Edwards CRW: Mineralocorticoid activity of carbenoxolone: contrasting effects of carbenoxolone and liquorice on - hydroxysteroid dehydrogenase activity in man.

Clin Sci Atchley DW, Loeb RF, Richards DW, Benedict EM, —54, Driscoll ME: On diabetic acidosis: a detailed study of electro-. Nielsen I, Pedersen RS: Life-threatening hypokalaemia lyte balances following the withdrawal and reestablishment caused by liquorice ingestion.

Lancet , of insulin therapy. Young WF, Klee GG: Primary aldosteronism. Diagnostic Brodsky WA, Rapoport S, West CD: The mechanism of evaluation. Endocrinol Metab Clin North Am —, glycosuric diuresis in diabetic man. J Clin Invest — Bravo EL: Primary aldosteronism. Urol Clin North Am Adrogué HJ, Lederer ED, Suki WN, Eknoyan G: Determi- —, nants of plasma potassium levels in diabetic ketoacidosis.

Biglieri EG: Spectrum of mineralocorticoid hypertension. Hypertension —, Fulop M: Hyperkalemia in diabetic ketoacidosis. Am J Med. Bartter FC, Pronove P, Gill JR Jr, MacCardle RC: Sci —, Hyperplasia of the juxtaglomerular complex with Semin Nephrol —, Shils ME: Experimental human magnesium depletion.

Ann Rev Med —, cine —85, Shils ME: Experimental production of magnesium deficiency. in man. Ann NY Acad Sci —, Kidney Int —93, Dunn MJ, Walser M: Magnesium depletion in normal man. Fichman MP, Telfor N, Zia P, Speckart P, Golub M, Rude R: Metabolism —, Evans RA, Carter JN, George CRP, Walls RS, Newland RC, drome.

Verbeckmoes R, van Damme B, Clement J, Amery A, losing kidney. renomedullary cells. Successful treatment with indo- Whang R, Flink EB, Dyckner T, Wester PO, Aikawa JK, methacin. Ryan MP: Magnesium depletion as a cause of refractory. Gill JR Jr, Frölich JC, Bowden RE, Taylor AA, Keiser HR, potassium repletion.

A Rodriguez M, Solanki DL, Whang R: Refractory potassium disorder characterized by high urinary prostaglandins and a repletion due to cisplatin-induced magnesium depletion. dependence of hyperreninemia on prostaglandin synthesis. Am J Med —51, Holmes AM, Hesling CM, Wilson TM: Drug-induced sec-.

Gitelman HJ: Hypokalemia, hypomagnesemia, and alkalosis: ondary hyperaldosteronism in patients with pulmonary tu- A rose is a rose—or is it?

J Pediatr —80, Q J Med —, Gill JR Jr, Bell NH, Bartter FC: Impaired conservation of Bar RS, Wilson HE, Mazzaferri EL: Hypomagnesemic sodium and potassium in renal tubular acidosis and its correc hypocalcemia secondary to renal magnesium wasting.

A pos- tion by buffer anions. sible consequence of high-dose gentamicin therapy. Ann In-. Gennari FJ, Cohen JJ: Renal tubular acidosis.

Annu Rev Med tern Med —, Gearhart MO, Sorg TB: Foscarnet-induced severe hypo-. Sebastian A, Hulter HN, Kurtz I, Maher T, Schambelan M: magnesemia and other electrolyte disorders. Ann Disorders of distal nephron function. Am J Med —, Pharmacother —, Barton CH, Pahl M, Vaziri ND, Cesario T: Renal magnesium.

Sebastian A, McSherry E, Morris RC Jr: Renal potassium wasting associated with amphotericin B therapy. Am J Med wasting in renal tubular acidosis RTA. Its occurrence in —, types 1 and 2 RTA despite sustained correction of systemic Burgess JL, Birchall R: Nephrotoxicity of amphotericin B, acidosis.

with emphasis on changes in tubular function. Wrong OM, Feest TG, Maclver AG: Immune-related —84, potassium-losing interstitial nephritis: a comparison with Mir MA, Brabin B, Tang OT, Leyland MJ, Delamore IW:.

distal renal tubular acidosis. Q J Med —, Hypokalaemia in acute myeloid leukaemia. Ann Intern Med. Caruana RJ, Buckalew VM: The syndrome of distal type I Fisher JR: Hypokalemia in leukemia. Ann Intern Med , renal tubular acidosis. Medicine 84—99, Lightwood R, Payne WW, Black JA: Infantile renal acidosis.

Lantz B, Carmark B, Reizenstein P: Electrolytes and whole. Pediatrics —, body potassium in acute leukemia. Acta Med Scand Brenes LG, Brenes JN, Hernandez MM: Familial proximal 50, renal tubular acidosis.

Perry MC, Bauer JH, Farhangi M: Hypokalemia in acute. Sebastian A, McSherry E, Morris RC Jr: On the mechanism myelogenous leukemia. of potassium wasting in renal tubular acidosis associated with Sterns RH, Cox M, Feig PU, Singer I: Internal potassium the Fanconi syndrome type 2 RTA.

J Clin Invest balance and the control of the plasma potassium concentra- , Harrington JT, Cohen JJ. Metabolic acidosis. In: JJ Cohen, Lawson DH: Adverse reactions to potassium chloride. Q J JP Kassirer with collaboration of FJ Gennari, JT Med —, Harrington, NE Madias , Acid—Base.

Little, Brown, Boston, Ponce SP, Jennings AE, Madias NE, Harrington JT: Drugpp —, indued hyperkalemia. Rimmer JM, Horn JF, Gennari FJ: Hyperkalemia as a complication of drug therapy.

Hultgren HN, Swenson R, Wettach G: Cardiac arrest due to oral potassium administration. McMahon FG, Ryan JR, Akdamar K, Ertan A: Effect of potassium chloride supplements on upper gastrointestinal mucosa. Clin Pharmacol Ther —, Alsop WR, Moore JG, Rollins DE, Tolman KE: The effects of five potassium chloride preparations on the upper gastrointestinal mucosa in healthy subjects receiving glycopyrrolate.

J Clin Pharmacol —, Strom BL, Carson JL, Schinnar R, Sim E, Maislin G, Soper K, Morse L: Upper gastrointestinal tract bleeding from oral potassium chloride. Schwartz AB, Swartz CD: Dosage of potassium chloride elixir to correct thiazide-induced hypokalemia.

Wan HH, Lye MDW. Moduretic-induced metabolic acidosis and hyperkalaemia. Cohen AB: Hyperkalemic effects of triamterene.

Paice B, Gray JMB, McBride D, Donnelly T, Lawson DH: Hyperkalaemia in patients in hospital. Br Med J , Mather A, Mackie NR: Effects of hemolysis on serum electrolyte values. Clin Chem 6: —, Bronson WR, DeVita VT, Carbone PP, Cotlove E: Pseudohyperkalemia due to release of potassium from white blood cells during clotting.

Bellevue R, Dosik H, Spergel G, Gussoff BD: Pseudohyperkalemia and extreme leukocytosis. J Lab Clin Med —, Stewart GW, Corrall RJM, Fyffe JA, Stockdill G, Strong JA: Familial pseudohyperkalaemia: a new syndrome.

Graber M, Subramani K, Corish D, Schwab A: Thrombocytosis elevates serum potassium. Am J Kidney Dis —, Lum G, Gambino SR: A comparison of serum versus heparinized plasma for routine chemistry tests. Am J Clin Pathol —, Ladenson JH, Tsai LB, Michael JM, Kessler G, Joist JH: Serum versus heparinized plasma for eighteen common chemistry tests.

Hartmann RC, Auditore JV, Jackson DP: Studies on thrombocytosis. Hyperkalemia due to release of potassium from platelets during coagulation. Kerr DJ, McAlpine LG, Dagg JH: Pseudohyperkalaemia. Don BR, Sebastian A, Cheitlin M, Christiansen M, Schambelan M: Pseudohyperkalemia caused by fist clenching during phlebotomy.

Finch CA, Sawyer CG, Flynn JM: Clinical syndrome of potassium intoxication. Am J Med 1: —, Davis JO, Urquhart J, Higgins JT Jr: The effects of alterations of plasma sodium and potassium concentration on aldosterone secretion.

Fredlund P, Saltman S, Kondo T, Douglas J, Catt KJ: Aldosterone production by isolated glomerulosa cells: modulation of sensitivity to angiotensin II and ACTH by extracellular potassium concentration. Miller PD, Waterhouse C, Owens R, Cohen E: The effect of potassium loading on sodium excretion and plasma renin activity in Addisonian man.

van Ypersele de Strihou C: Potassium homeostasis in renal failure. Gonick HC, Kleeman CR, Rubin ME, Maxwell MH: Functional impairment in chronic renal disease III. Studies of potassium excretion. Perez GO, Pelleya R, Oster JR, Kem DC, Vaamonde CA: Blunted kaliuresis after an acute potassium load in patients with chronic renal failure.

Kahn T, Kaji DM, Nicolis G, Krakoff LR, Stein RM: Factors related to potassium transport in chronic stable renal disease in man. Clin Sci Mol Med —, Bergström J, Alvestrand A, Fürst P, Hultman E, WidstamAttorps U: Muscle intracellular electrolytes in patients with chronic uremia.

Kidney Int 24 Suppl 16 : S — S, Boddy K, King PC, Lindsay RM, Briggs JD, Winchester JF, Kennedy AC: Total body potassium in non-dialyzed and dialyzed patients with chronic renal failure.

Br Med J 1: —, Widmer B, Gerhardt RE, Harrington JT, Cohen JJ: Serum electrolyte and acid—base composition. The influence of graded degrees of chronic renal failure. Restuccio A: Fatal hyperkalemia from a salt substitute. Sopko JA, Freeman RM: Salt substitutes as a source of potassium.

Luzi L, Barrett EJ, Groop LC, Ferrannini E, DeFronzo RA: Metabolic effects of low-dose insulin therapy on glucose metabolism in diabetic ketoacidosis. Diabetes —, DeFronzo RA: Obesity is associated with impaired insulin-mediated potassium uptake.

Cohen P, Barzilai N, Lerman A, Hard H, Szylman P, Karnieli E: Insulin effects on glucose and potassium metabolism in vivo: evidence for selective insulin resistance in humans.

DeFronzo RA: Hyperkalemia and hyporeninemic hypoaldosteronism. Sunderlin FS, Anderson GH, Streeten DHP, Blumenthal SA: The renin—angiotensin—aldosterone system in diabetic patients with hyperkalemia.

Conte G, Dal Canton A, Imperatore P, DeNicola L, Gigliotti G, Pisanti N, Memoli B, Furiano G, Esposito C, Andreucci VE: Acute increase in plasma osmolality as a cause of hyperkalemia in patients with renal failure.

Goldfarb S, Cox M, Singer I, Goldberg M: Acute hyperkalemia induced by hyperglycemia: hormonal mechanisms. Perez GO, Lespier L, Knowles R, Oster JR, Vaamonde CA: Potassium homeostasis in chronic diabetes mellitus.

Perez GO, Lespier L, Jacobi J, Oster JR, Katz FH, Vaamonde C, Fishman LM: Hyporeninemia and hypoaldosteronism in diabetes mellitus. Arrizabalaga P, Montoliu J, Martinez-Vea A, Andreu L, Lopez-Pedret J, Revert L: Increase in serum potassium caused by beta-2 adrenergic blockade in terminal renal failure: absence of mediation by insulin or aldosterone.

Proc Eur Dial Transplant Assoc —, Arthur S, Greenberg A: Hyperkalemia associated with intravenous labetabol therapy for acute hypertension in renal transplant recipients. Clin Nephrol —, Fletcher GF, Fletcher BJ, Sweeney ME: Effects of exercise testing, training and beta blockade on serum potassium in normal subjects.

Am J Cardiol —, Castellino P, Bia MJ, DeFronzo RA: Adrenergic modulation of potassium metabolism in uremia. Ericsson F, Carlmark B, Jogestrand T, Sundqvist K: Effect of digoxin upon intracellular potassium in man.

Scand J Clin Lab Invest —, Bismuth C,. Gaultier M, Conso F, Efthymiou ML: Hyperkalemia in acute digitalis poisoning: prognostic significance and therapeutic implications.

Clin Toxicol 6: —, Smith TW, Butler VP Jr, Haber E, Fozzard H, Marcus FI, Bremner WF, Schulman IC, Phillips A: Treatment of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments. Reza MJ, Kovick RB, Shine KI, Pearce ML: Massive intravenous digoxin overdosage.

Papadakis MA, Wexman MP, Fraser C, Sedlacek SM: Hyperkalemia complicating digoxin toxicity in a patient with renal failure. Am J Kidney Dis 5: 64—66, Evers W, Racz GB, Dobkin AB: A study of plasma potassium and electrocardiographic changes after a single dose of succinylcholine.

Can Anesth Soc J —, Weintraub HD, Heisterkamp DV, Cooperman LH: Changes in plasma potassium concentration after depolarizing blockers in anaesthetized man.

Br J Anaesth —, Cooperman L: Succinylcholine-induced hyperkalemia in neuromuscular disease. Brooke MM, Donovan WH, Stolov WC: Paraplegia: succinylcholine-induced hyperkalemia and cardiac arrest.

Arch Phys Med Rehab —, Greenawalt JW 3rd: Succinylcholine-induced hyperkalemia 8 weeks after a brief paraplegic episode.

Dickerman HW, Walker WG: Effect of cationic amino acid infusion on potassium metabolism in vivo. Levinsky NG, Tyson I, Miller RB, Reiman AS: The relation between amino acids and potassium in isolated rat muscle.

Hertz P, Richardson JA: Arginine-induced hyperkalemia in renal failure patients. Bushinsky DA, Gennari FJ: Life-threatening hyperkalemia induced by arginine.

McIvor M, Baltazar RF, Beltran J, Mower MM, Wenk R, Lustgarten J, Salomon J: Hyperkalemia and cardiac arrest from fluoride exposure during hemodialysis. Gabow PA, Kaehny WD, Kelleher SP: The spectrum of rhabdomyolysis.

Bluemle LW Jr, Webster GD, Elkinton JR: Acute tubular necrosis: analysis of one hundred cases with respect to mortality, complications and treatment with and without dialysis. Grossman RA, Hamilton RW, Morse BM, Penn AS, Goldberg M: Nontraumatic rhabdomyolysis and acute renal failure.

Gamstorp I, Hauge M, Helweg-Larsen HF, Mjönes H, Sagild U: Adynamica episodica hereditaria. Ptacek LJ, Johnson KJ, Griggs RC: Genetics and physiology of the myotonic muscle disorders. Ptacek LJ, George AL Jr, Griggs RC, Tawil R, Kallen RG, Barchi RL, Robertson M, Leppert MF: Identification of a mutation in the gene causing hyperkalemic periodic paralysis.

Cell —, Fontaine B, Khurana TS, Hoffman EP, Bruns GAP, Haines JL, Trofatter JA, Hanson MP, Rich J, McFarlane H, Yasek DM, Romano D, Gusella JF, Brown RH Jr: Hyperkalemic periodic paralysis and the adult muscle sodium channel a-subunit gene.

Cannon SC, Brown RH Jr, Corey DP: A sodium channel defect in hyperkalemic periodic paralysis: potassium-induced failure of inactivation.

Neuron 6: —, Streeten DHP, Dalakos TG, Fellerman H: Studies on hyperkalemic periodic paralysis. Evidence of changes in plasma Na and Cl and induction of paralysis by adrenal glucocorticoids.

Wang P, Clausen T: Treatment of attacks in hyperkalaemic familial periodic paralysis by inhalation of salbutamol. Lancet 1: —, Martin RS, Panese S.

Virginillo M, Gimenez M, Litardo M, Arrizurieta E, Hayslett JP: Increased secretion of potassium in the rectum of humans with chronic renal failure. Am J Kidney Dis 8: —, Hou S, McElroy PA, Nootens J, Beach M: Safety and efficacy of low-potassium dialysate.

Gennari FJ, Rimmer JM: Disturbances in fluid, electrolyte, and acid-base balance. Part 2. Dialysis patients. In: SG Massry, RJ Glassock, eds, Textbook of Nephrology , 3rd ed. Williams and Wilkins, Baltimore, pp —, Greenblatt DJ, Koch-Weser J: Adverse reactions to spironolactone.

DAMA 40—43, Walker BR, Capuzzi DM, Alexander F, Familiar RG, Hoppe RC: Hyperkalemia after triamterene in diabetic patients. Feinfeld DA, Carvounis CP: Fatal hyperkalemia and hyperchloremic acidosis.

DAMA , McNay JL, Oran E: Possible predisposition of diabetic patients to hyperkalemia following administration of potassium-retaining diuretic, amiloride MK Metabolism 58—70, Atlas SA, Case DB, Sealey JE, Laragh JH, McKinstry DN: Interruption of the renin-angiotensin system in hypertensive patients by captopril induces sustained reduction in aldosterone secretion, potassium retention and natriuresis.

Hypertension 1: —, Textor SC, Bravo EL, Fouad FM, Tarazi RC: Hyperkalemia in azotemic patients during angiotensin-converting enzyme inhibition and aldosterone reduction with captopril. Bauer JH: Role of angiotensin converting enzyme inhibitors in essential and renal hypertension.

Am J Med 77 Suppl 2A : 43—51, Zachariah PK, Bonnet G, Chysant SG, DeBackser G, Goldstein R, Herrera J, Lindner A, Materson BJ, Maxwell MH, McMahon FG, Merrill RH, Paton RR, Rapp AD, Roginsky MS, Seedat YK, Sime F, Vaicaitis JS, Weinberg MS, Zusman RM: Evaluation of antihypertensive efficacy of lisinopril compared to metaprolol in moderate to severe hypertension.

J Cardiovasc Pharmacol 9 Suppl 3 : S53 - S58, Donohoe JF, Laher M, Doyle GD, Cooper WD: Lisinopril in hypertension associated with renal impairment.

J Cardiovasc Pharmacol 9 Suppl 3 : S66 - S68, deJong PE, Apperloo AJ, Heeg JE, deZeeuw D: Lisinopril in hypertensive patients with renal function impairment.

Nephron 55 Suppl 1 : 43—48, Doman K, Perlmutter JA, Muhammedi M, Puschett JB: Life-threatening hyperkalemia associated with captopril administration. Lewis EJ, Hunsicker LG, Bain RP, Rohde RD: The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy.

Feig PU, Rutan GH: Angiotensin converting enzyme inhibitors: The end of end-stage renal disease? Praga M, Hernandez E, Montoyo C, Andrés A, Ruilope LM, Rodicio JL: Long-term beneficial effects of angiotensinconverting enzyme inhibition in patients with nephrotic proteinuria.

Captopril Multicenter Research Group. A placebo-controlled trial of captopril in refractory chronic congestive heart failure. J Am Coll Cardiol 2: —, Tan SY, Shapiro R, Franco R, Stockard H, Mulrow PJ: Indomethacin-induced prostaglandin inhibition with hyperkalemia.

Clive DM, Stoff JS: Renal syndromes associated with nonsteroidal anti-inflammatory drugs. Whelton A, Hamilton CW: Nonsteroidal anti-inflammatory drugs: effects on kidney function.

J Clin Pharmacol , Rotenberg FA, Giannini VS: Hyperkalemia associated with ketorolac. Ann Pharmacother —, Wilson ID, Goetz FC: Selective hypoaldosteronism after prolonged heparin administration.

Conn JW, Rovner DR, Cohen EL, Anderson JE Jr: Inhibition by heparinoid of aldosterone biosynthesis in man. Busch EH, Ventura HO, Lavie CJ: Heparin-induced hyperkalemia.

Aull L, Chao H, Coy K: Heparin-induced hyperkalemia. DICP Ann Pharmacother —, Edes TE, Sunderrajan EV: Heparin-induced hyperkalemia. Adu D, Turney J, Michael J, McMaster P: Hyperkalaemia in cyclosporin-treated renal allograft recipients.

Lancet 2: , Bantle JP, Nath KA, Sutherland DER, Najarian JS, Ferris TF: Effects of cyclosporine on the renin-angiotensinaldosterone system and potassium excretion in renal transplant recipients. Kamel KS, Ethier JH, Quaggin S, Levin A, Albert S, Carlisle EJF, Halperin ML: Studies to determine the basis for hyperkalemia in recipients of a renal transplant who are treated with cyclosporine.

J Am Soc Nephrol 2: —, Bantle JP, Boudreau RJ, Ferris TF: Suppression of plasma renin activity by cyclosporine.

Am J Med 59—64, Velazquez H, Perazella MA, Wright FS, Ellison DH: Renal mechanism of trimethoprim-induced hyperkalemia. Lachaal M, Venuto RC: Nephrotoxicity and hyperkalemia in patients with acquired immunodeficiency syndrome treated with pentamidine.

Briceland LL, Bailie GR: Pentamidine-associated nephrotoxicity and hyperkalemia in patients with AIDS. DICP —, A report of cases. Acta Endocrinol —, Lancet 1: 11—14, Yamamoto T, Fukuyama J, Hasegawa K, Sugiura M: Isolated corticotropin deficiency in adults.

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DeFronzo RA, Cooke R, Goldberg M, Cox M, Myers AR, Agus ZS: Impaired renal tubular potassium secretion in systemic lupus erythematosus.

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Alton M: Treatment and prevention of hyperkalemia in end-stage renal disease. Download references. Nephrology Unit, University of Vermont College of Medicine, , Burlington, VT, USA. John Gennari M. Professor of Medicine, Director. You can also search for this author in PubMed Google Scholar.

Reprints and permissions. Gennari, F. Disorders of Potassium Metabolism. In: Suki, W. Springer, Boston, MA. Publisher Name : Springer, Boston, MA. Print ISBN : Online ISBN : eBook Packages : Springer Book Archive. Anyone you share the following link with will be able to read this content:.

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Policies and ethics. Our bodies need far more potassium than sodium each day, but the typical U. But what may be even more important for health is the relationship of sodium to potassium in the diet.

Hypertension Observational studies of large groups of people show that sodium and potassium in the diet are associated with blood pressure. A review of randomized controlled trials found that the DASH diet Dietary Approaches to Stop Hypertension that is low sodium and high potassium was effective at lowering blood pressure in those with existing hypertension.

The Agency for Healthcare Research and Quality issued a report on the effects of sodium and potassium on chronic disease risk based on clinical trials and cohort studies. However there was not enough evidence or there was conflicting evidence of their effects on lowering overall risk of hypertension, kidney stones, cardiovascular diseases including stroke, and kidney disease.

Bone health Calcium is one of the most important nutrients required for bone health. Kidney stones A diet rich in potassium helps to prevent calcium from being excreted in the urine, and may also help to prevent calcium from being released from bone into the blood.

Is there any research behind Acid-Alkaline Diet claims? You may have heard of an acid-alkaline diet promoted for weight loss or cancer prevention. Most health experts rejected these claims because it is nearly impossible to dramatically change the pH of blood in healthy people through diet alone.

The body tightly regulates the pH level in blood to about 7. References National Academy of Medicine. Dietary Reference Intakes for Sodium and Potassium. Washington DC : National Academies Press US ; Mar. National Institutes of Health; Office of Dietary Supplements.

Potassium: Fact Sheet for Health Professionals. Brown IJ, Tzoulaki I, Candeias V, Elliott P. Salt intakes around the world: implications for public health.

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Yang Q, Liu T, Kuklina EV, Flanders WD, Hong Y, Gillespie C, Chang MH, Gwinn M, Dowling N, Khoury MJ, Hu FB.

Sodium and potassium intake and mortality among US adults: prospective data from the Third National Health and Nutrition Examination Survey. Archives of internal medicine. Aaron KJ, Sanders PW. Role of dietary salt and potassium intake in cardiovascular health and disease: a review of the evidence.

InMayo Clinic Proceedings Sep 1 Vol. Newberry SJ, Chung M, Anderson CA, Chen C, Fu Z, Tang A, Zhao N, Booth M, Marks J, Hollands S, Motala A. Sodium and Potassium Intake: Effects on Chronic Disease Outcomes and Risks.

Rockville MD : Agency for Healthcare Research and Quality US ; Jun. Report No. 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. Vinceti M, Filippini T, Crippa A, de Sesmaisons A, Wise LA, Orsini N.

Journal of the American Heart Association. Hanley DA, Whiting SJ. Does a high dietary acid content cause bone loss, and can bone loss be prevented with an alkaline diet?. Journal of Clinical Densitometry. How we vet brands and products Healthline only shows you brands and products that we stand behind.

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Read more about our vetting process. Was this helpful? Sources of potassium. Potassium deficiency. Potassium overdose. Treating imbalanced potassium levels. How we reviewed this article: Sources.

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Feb 28, Medically Reviewed By Deborah Weatherspoon, Ph. Share this article. Read this next. Understanding Hyperkalemia High Potassium. Medically reviewed by Angelica Balingit, MD. Potassium Blood Test. Medically reviewed by Sirisha Yellayi, DO. Symptoms of Low Potassium Hypokalemia.

By Katey Davidson, MScFN, RD, CPT and Ryan Raman, MS, RD. What Does Potassium Do for Your Body? A Detailed Review. Blood Tests for Hemochromatosis. Medically reviewed by Mia Armstrong, MD. What to Know About Gaucher Disease Type 3. Medically reviewed by Alana Biggers, M.

Biochemical and Physiological Aspects of Human Nutrition. Philadelphia: W. Saunders Company; Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate.

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Nutr Today. Binia A, Jaeger J, Hu Y, Singh A, Zimmermann D. It has also recently been shown that K has an antihypertensive effect by promoting sodium excretion, while it is also attracting attention as an important component that can suppress hypertension associated with excessive sodium intake.

Since most ingested K is excreted through the kidneys, decreased renal function is a major factor in increased serum levels, and target values for its intake according to the degree of renal dysfunction have been established.

In older individuals with impaired renal function, not only hyperkalemia but also hypokalemia due to anorexia, K loss by dialysis, and effects of various drugs are likely to develop. INTERNAL POTASSIUM BALANCE. Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells.

In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid figure 1. Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores.

The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [ 5,6 ]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected.

A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis or ketoacidosis [ 7,8 ]. The hyperkalemia that is commonly seen in diabetic ketoacidosis DKA , for example, is more closely related to the insulin deficiency and hyperosmolality than to the degree of acidemia.

See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis". Why this occurs is not well understood. Two factors that may contribute are the ability of the organic anion to accompany the hydrogen ion into the cell, perhaps as the lipid-soluble, intact acid [ 9 ], and differential effects on insulin and glucagon secretion [ 4,10 ].

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