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Hyperkalemia may be caused by medications, including medications that affect kidney function (potassium sparing diuretics, such as [[spironolactone]], [[amiloride]], or[[triamterene]]) and potassium supplements (especially intravenous potassium).
Hyperkalemia may be caused by medications, including medications that affect kidney function (potassium sparing diuretics, such as [[spironolactone]], [[amiloride]], or[[triamterene]]) and potassium supplements (especially intravenous potassium).
==[[causes|Causes]]==
==[[causes|Causes]]==
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{{Hyperkalemia}}
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com]; {{RT}}
==Causes==
===Common Causes===
===Common Causes===
* [[ACE inhibitors]]
* [[ACE inhibitors]]

Revision as of 18:01, 25 July 2013



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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Raviteja Guddeti, M.B.B.S. [3]

Synonyms and keywords: Hyperkalaemia.

Overview

Hyperkalemia (AE) or Hyperkalaemia (BE) is an elevated blood level (above 5.0 mmol/L) of the electrolyte potassium. The prefix hyper- means high (contrast with hypo-, meaning low). The middle kal refers to kalium, which is Latin for potassium. The end portion of the word, -emia, means "in the blood". Extreme degrees of hyperkalemia are considered a medical emergency due to the risk of potentially fatal arrhythmias

Pathophysiology

Potassium is the most abundant intracellular cation. It is critically important for many physiologic processes, including maintenance of cellular membrane potential, homeostasis of cell volume, and transmission of action potentials in nerve cells. Its main dietary sources are vegetables (tomato and potato), fruits (orange and banana) and meat. Elimination is through the gastrointestinal tract and the kidney.

The renal elimination of potassium is passive (through the glomeruli), and resorption is active in the proximal tubule and the ascending limb of the loop of Henle. There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone.

Hyperkalemia develops when there is excessive production (oral intake, tissue breakdown) or ineffective elimination of potassium. Ineffective elimination can be hormonal (inaldosterone deficiency) or due to causes in the renal parenchyma that impair excretion.

Increased extracellular potassium levels result in depolarization of the membrane potentials of cells. This depolarization opens some voltage-gated sodium channels, but not enough to generate an action potential. After a short while, the open sodium channels inactivate and become refractory, increasing the threshold to generate an action potential. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.

Patients with the rare hereditary condition of hyperkalemic periodic paralysis appear to have a heightened sensitivity of muscular symptoms that are associated with transient elevation of potassium levels. Episodes of muscle weakness and spasms can be precipitated by exercise or fasting in these subjects.==[[Hyperkalemia ==Risk factors

Risk Factors

The kidneys normally remove excess potassium from the body. Most cases of hyperkalemia are caused by disorders that reduce the kidneys' ability to get rid of potassium. This may result from disorders such as:

The hormone aldosterone regulates kidney removal of sodium and potassium. Lack of aldosterone can result in hyperkalemia with an increase in total body potassium.Addison's disease is one disorder that causes reduced aldosterone production.

Any time potassium is released from the cells, it may build up in the fluid outside the cells and in the bloodstream. Acidosis leads to the movement of potassium from inside the cells to the fluid outside the cells. Tissue injury can cause the cells to release potassium. Such injury includes:

If the kidney is working properly, and there is enough aldosterone, tissue trauma alone rarely leads to hyperkalemia. A normally functioning kidney will remove the excess potassium that has been released from the cells.

Increased intake of potassium can cause hyperkalemia if kidney function is poor. Salt substitutes often contain potassium, as do many "low-salt" packaged foods.

Hyperkalemia may be caused by medications, including medications that affect kidney function (potassium sparing diuretics, such as spironolactone, amiloride, ortriamterene) and potassium supplements (especially intravenous potassium).

Causes

Common Causes

Causes by Organ System

Cardiovascular Heart failure, Volume depletion
Chemical / poisoning Ammonium Bifluoride, Arsenicals, Fluoride toxicity, Foxglove Poisoning, Oleander Poisoning, Tungsten, White ChameleonPoisoning
Dermatologic No underlying causes
Drug Side Effect ACE inhibitors, Acetylsalicylic Acid, Aldosterone antagonists, Amiloride, Angiotensin receptor blockers, Beta blockers,Celecoxib, Cyclosporine, Diazoxide, Digoxin, Eplerenone, Epsilon amino caproic acid (EACA), Erythropoietin, Heparin, Ibuprofen,Indomethacin, Isoflurane, Ketoprofen, Low-molecular weight heparin, Mannitol, Melarsoprol, Methotrexate, Minoxidil, Naproxen,Pancuronium bromide, Pimecrolimus, Potassium chloride, Potassium citrate, Propofol infusion syndrome, Sodium thiopental, Somatostatin therapy,Spironolactone, Succinylcholine, Suxamethonium, Tacrolimus, Triamterene, Trimethoprim
Ear Nose Throat No underlying causes
Endocrine ACTH Deficiency, Addisonian crisis, Addison's disease, Adrenal gland disorders, Adrenal hyperplasia, congenital type 3, Autoimmune adrenalitis, Congenital adrenal hyperplasia -- sodium-wasting form, Diabetes, Diabetic ketoacidosis, Hyperglycemia, Hypoadrenocorticism --hypoparathyroidism -- moniliasis, Hyporeninemic hypoaldosteronism, Isolated aldosterone synthase deficiency, Lipoid congenital adrenal hyperplasia,Pseudohypoaldosteronism type 1, Pseudohypoaldosteronism type 2
Environmental No underlying causes
Gastroenterologic Cirrhosis, Gastrointestinal bleeding
Genetic 18-Hydroxylase deficiency, Congenital adrenal hyperplasia type 3, Congenital adrenal hyperplasia -- sodium-wasting form, Isolated aldosterone synthase deficiency, Lipoid congenital adrenal hyperplasia, Pseudohypoaldosteronism type 1, Pseudohypoaldosteronism type 2
Hematologic Hemolytic anemia, Leukaemia, Leukocytosis, Sickle cell disease, Thrombotic thrombocytopenic purpura, congenital
Iatrogenic Oxalate blood sample, Blood transfusion and complications, Cuffed blood sample, Delayed separation blood sample, Drip arm sample,EDTA blood sample, Hemolysed blood sample, IV fluids containing potassium, Using clenched fist while collection of blood
Infectious Disease HIV infection
Musculoskeletal / Ortho Muscle damage, Muscle wasting
Neurologic Amelo-cerebro-hypohidrotic syndrome, Kohlschutter-Tonz syndrome
Nutritional / Metabolic Arginine hydrochloride, Increased ingestion of high Potassium foods, Increased ingestion of Potassium containing drugs, Malnutrition
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Opthalmologic No underlying causes
Overdose / Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal / Electrolyte Acidosis, Acute glomerulonephritis, Acute renal failure, Chronic Interstitial nephritis, Chronic renal failure, Diabetic nephropathy, Distal chloride shunt, Distal renal tubular acidosis type IV, Gordon's syndrome, Hemolytic uremic syndrome, Hyperkalemic periodic paralysis, Hyperkalemic Renal tubular acidosis, Hypernatremia, Hyperosmolality, Hyperphosphataemia, Lupus nephritis, Obstructive uropathy,Polycystic kidney disease, Familial Pseudohyperkalemia-due to red cell leak, Distal Renal tubular acidosis type 1, Transplanted kidneys, Tubulointerstitial disease, Urinary tract obstruction, Urolithiasis, Hyporeninemic hypoaldosteronism, Amyloidosis - Renal
Rheum / Immune / Allergy Systemic lupus erythematosus, Autoimmune adrenalitis
Sexual No underlying causes
Trauma Crush syndrome
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Amyloidosis - Renal, Burns, Dehydration, Fasting, Hypothermia, Internal bleeding, Intravenous infusion, hyperpyrexia, Phlebotomy complication, Rhabdomyolysis, Sea snake poisoning, Selective impairment of potassium excretion, exercise,Transplant rejection, Tumor lysis syndrome, Ureterojejunostomy|}

Causes in Alphabetical Order

  1. Sevastos N et al. (2006) Pseudohyperkalemia in serum: the phenomenon and its clinical magnitude. J Lab Clin Med, 147(3):139-44; PMID 16503244.
  2. Don BR et al. (1990) Pseudohyperkalemia caused by fist clenching during phlebotomy. N Engl J Med, 322(18):1290-2; PMID 2325722.
  3. Iolascon A et al. (1999) Familial pseudohyperkalemia maps to the same locus as dehydrated hereditary stomatocytosis. Blood, 93(9):3120-3; PMID 10216110.