Potassium - Metabolism
Intake - Absorption
A normal diet supplies from 2 to 4 g corresponding to 50 to 100 mmol of potassium daily. The digestive absorption is fast and almost complete. It is achieved by active transport. The foods rich in potassium are dairy products, plants, fruits and meats.
Several studies showed that a diet rich in potassium tends to lower arterial pressure and to reduce the frequency of the cardiovascular accidents.
Tissue distribution
Blood
- Plasma: the normal plasma concentration of potassium or kalemia is 4.2 mmol/L. It is maintained constant by the equilibrium between intake, elimination and exchanges between tissues.
- Red cells: the erythrocytes are very rich in potassium, they contain approximately 90 mmol/L.
Tissues
All the cells are rich in potassium. Its entry into the cell is achieved primarily by the membrane Na+/K+-ATPASE.
Because of the importance of their mass in the body, liver, erythrocytes, muscles and bone contain most of the potassium. The muscles alone contain 40% of the total. A variation of 1% of the muscular potassium concentration can induce a variation of 50% of its plasma concentration. The measurement of potassium concentration in muscular biopsies is a means for appreciating potassium balance.
Elimination
About 90% of the potassium taken is eliminated to by the kidney, that is to say approximately 90 mmol/day, and 5 to 10% are eliminated in stools.
At the renal level, potassium passes freely through the glomerulus. Approximately 65% of filtered potassium is actively reabsorbed by the proximal tubule, 25 to 30% by the ascending limb of Henle loop, so that in the tubular fluid of the final part of the nephron there is very little potassium.
Potassium present in the urine comes from its renal secretion which is regulated by aldosterone.
Kalemia disorders
Hypokalemia
Hypokalemia can result from an urinary or digestive excessive loss but also from an alkalosis because the decrease of H+ ions in the extracellular fluid induces the influx of potassium ions into the cells; because of the competition between H+ and K+, the decrease of the concentration of one of them increases the penetration of the other.
It can also result from the intake of drugs:
- increasing tissue potassium uptake: thyroid hormones, insulin, beta-2-mimetics, theophylline.
- increasing its urinary elimination: aldosterone, glycirrhizine which has an aldosterone-like effect, corticosteroids, thiazide and loop diuretics , antibiotics such as aminoglycosides.
Hypokalemia can moreover be observed during poisoning by soluble barium salts and toluene, but the mechanisms responsible are not well known.
The manifestations of hypokalemia are neuromuscular disorders going from a muscular weakness to paralysis, muscular damage even rhabdomyolysis, electrocardiographic disorders and digestive disorders, sometimes a paralytic ileus.
Periodic paralysis can occur in patients with hyperkalemia or hypokalemia.
Hyperkalemia
Hyperkalemia can result from an excessive potassium intake by oral or parenteral route, a disorder of renal elimination, a defect of hormonal regulation, an acidosis.
It can also result from the intake of drugs:
- which decrease the uptake of potassium by tissues :adrenergic alpha-mimetics , beta-blockers, suxamethonium
- which decrease its renal elimination: anti-aldosterone diuretics (spironolactones), diuretics such as modamide and triamterene, heparin by its anti-aldosterone effect , ACE inhibitors, NSAIDs.
Hyperkalemia induces specific disturbances of the electrocardiogram.
Correction of kalemia disorders
Hypokalemia
Hypokalemia can be prevented or corrected by oral administration of potassium salts, in particular chloride. Potassium chloride has a displeasing taste and is irritating, disadvantage reduced by coating solid formulations or addition of excipients to liquid formulations.
If an intravenous potassium administration is necessary, one must use a diluted solution, in slow perfusion and under strict electrocardiographic control because a cardiac arrest is possible.
Hyperkalemia
It is very often sufficient to stop the intake of potassium or drugs which increase its retention to correct hyperkalemia. It is moreover possible to give calcium, which reduces the effects of potassium, or insulin and bicarbonate which facilitate its penetration into cells.
The intake by oral route of a cation-exchanger resin having a great affinity for potassium increases its elimination in stools. The resin is administered in sodium form, sodium polystyrene sulfonate, or in calcium form, calcium polystyrene sulfonate. The resin exchanges in the digestive tract its sodium or calcium for potassium for which it has a very high affinity. Potassium thus is eliminated in stools, bound to the resin which is not absorbed by the digestive tract. Sodium polystyrene sulfonate is marketed as Kayexalate* and Resonium*.
The most frequent adverse effect of these cation-exchangers is constipation.
These resins should be reserved for the treatment of hyperkalemias unresponsive to simpler approaches.
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