- aka K
- Principal intracellular cation
- Concentration within cells is maintained by the energy-dependent pumping of sodium out of the cells (ATPase)
- permeable to membranes and enters to replace the extruded sodium
- involved in neuromuscular irritability and effects on cardiac muscle
- Problems usually only when profound imbalances occur
- e.g., major shift in tissue water, diabetic acidosis
- Dietary sources: nuts, meat, fruit.
- Describe K+ balance, K+ distribution among the bodyâ€™s fluid compartments and factors that alter this distribution, and the relative importance of the routes of K+ excretion.
- Identify the tubular sites, transport mechanisms and regulatory factors (e.g., aldosterone, protons, luminal fluid flow rate) for K+ reabsorption and secretion in the kidney.
- Describe the nephron sites and molecular mechanisms of action of K+ wasting and K+ sparing diuretics.
On average, daily potassium intake is 100 mmoles per day. Daily excretion is also 100 mmoles per day, 10% of which is excreted in feces, and 90% in urine. Most of the bodyâ€™s potassium (~98%) is concentrated in cells. High plasma insulin after a meal stimulates muscle and liver cells to take up potassium from extracellular fluid more rapidly. This mitigates the rise in plasma potassium caused by ingestion. Alkalosis also causes potassium movement into cells.
High extracellular potassium (hyperkalemia) is a medical emergency because it may cause lethal cardiac arrhythmias. This is treated initially with an injection of sodium bicarbonate or else an insulin-glucose solution. In the longterm, hyperkalemia has to be treated with dialysis.
Normally, most of the potassium that is filtered is reabsorbed, with only 10-20% being excreted. If an individual experiences low potassium ingestion, hypokalemia results, and the kidney conserves potassium (only ~2% of filtered potassium is excreted). On the other hand, if an individual experiences high potassium ingestion, hyperkalemia results, and the kidney excretes potassium (almost 100% of filtered potassium is excreted).
Under normal or hypokalemic conditions, most filtered potassium is reabsorbed by:
- proximal tubules, mostly via paracellular leaks dependent on fluid movement and therefore on sodium transport
- the ascending limb of the loop of Henle
- early distal tubules
- intercalated cells of late distal tubules and collecting ducts
Under high potassium-intake conditions, adrenal glands increase their production of aldosterone. Potassium then couples with aldosterone to stimulate potassium secretion by principal cells, resulting in the excretion of more than 100% of filtered potassium.
Wasting vs. sparing
Drugs can be either potassium-wasting or potassium-sparing, a reference to whether or not they induce the rampant excretion of potassium. Furosemides and bumetanides are potassium-wasting diuretics because they inhibit the Na-K-2Cl cotransporter (NKCC2) in the thick ascending limb of Henle's loop, resulting in higher potassium excretion in urine.
Drugs are potassium-sparing when they impair renal potassium excretion by interfering with adrenal production of aldosterone, blocking the kaliuretic effect of aldosterone. Spironolactone is potassium-sparing for this reason.
Potassium sparing or wasting can also be contingent on how a drug affects sodium reabsorption. Inhibition of sodium reabsorption in the loop of Henle or early distal tubule results in diuresis, natriureis and potassium excretion. On the other hand, inhibition of sodium reabsorption in the late distal tubule and collecting duct cause diuresis, natriureis and potassium retention.