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Drug-induced abnormalities of potassium metabolism.

Abstract
Pharmacotherapy has progressed rapidly over the last 20 years with the result that general practioners more and more often use drugs which may influence potassium metabolism at the kidney or gastrointestinal level, or the transmembrane transport of potassium at the cellular level. Potassium abnormalities may result in life-theatening clinical conditions. Hypokalemia is most frequently caused by renal loss of this electrolyte (thiazide, thiazide-like and loop diuretics, glucocorticoids) and the gastrointestinal tract (laxatives, diarrhea, vomiting, external fistula), and may be the result of an increased intracellular potassium influx induced by sympathicomimetics used mostly by patients with asthma, or by insulin overdosage in diabetic subjects. The leading symptoms of hypokalemia are skeletal and smooth muscle weakness and cardiac arrhythmias. Hyperkalemia may be caused by acute or end-stage renal failure, impaired tubular excretion of potassium (blockers of the renin-angiotensin-aldosterone system, nonsteroidal anti-inflammatory drugs, cyclosporine, antifungal drugs, potassium sparing diuretics), acidemia, and severe cellular injury (tumor lysis syndrome). Hyperkalemia may be the cause of severe injury of both skeletal and smooth muscle cells. The specific treatment counteracting hyperkalemia is a bolus injection of calcium salts and, when necessary, hemodialysis.
AuthorsFranciszek Kokot, Lidia Hyla-Klekot
JournalPolskie Archiwum Medycyny Wewnetrznej (Pol Arch Med Wewn) 2008 Jul-Aug Vol. 118 Issue 7-8 Pg. 431-4 Poland
PMID18714739 (Publication Type: Journal Article, Review)
Chemical References
  • Antihypertensive Agents
  • Diuretics
  • Potassium
Topics
  • Acid-Base Equilibrium (drug effects)
  • Antihypertensive Agents (adverse effects)
  • Cardiovascular Diseases (etiology)
  • Diuretics (adverse effects)
  • Humans
  • Hyperkalemia (chemically induced, prevention & control)
  • Hypokalemia (chemically induced, prevention & control)
  • Potassium (metabolism)

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