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.