Potassium

Potassium is an abundant electrolyte in the body, and potassium ion (K+) is the dominant cation in the intracellularcellular space. 98% of all potassium in the body is intracellular. In the intracellular space the concentration is approx 150 mM, while in the extracellular space it is just 3.5 – 5.5 mM.

The serum potassium level depends in two things:

• The internal potassium balance, the balance between the intracellular and extracellular compartments
• The external potassium balance, the balance between potassium intake and potassium loss

Abnormally low or high potassium (hypokalaemia and hyperkalaemia, respectively), are common but potentially lethal disorders in the worst case.

Reference range

Parameter	Sample	Reference range
Potassium	Serum	3.5 - 5.5 mmol/L

Function of potassium

The main function of potassium is to maintain fluid and electrolyte balance. Potassium is involved in nerve impulse transmission and muscle contraction by maintaining the resting membrane potantial.

Because there is much more potassium in the intracellular space than the extracellular, there is a large concentration gradient from the intracellular space to the extracellular. To maintain this gradient, potassium is constantly pumped into cells by the Na+/K+-ATPase.

Regulation of potassium level

The potassium level is mainly regulated by the renin-angiotensin-aldosterone system in the kidneys. Increasing levels of potassium stimulates RAAS and therefore aldosterone production, which in turn stimulates the Na+/K+-ATPase in the distal tubules and collecting duct. This causes K+ and H+ loss. This system is very effective and therefore prevents hyperkalaemia from developing, as long as the kidneys are functioning.

The daily intake of potassium in the diet is approximately 40 – 120 mmol K+. This extra potassium reaches the extracellular space and not the cells in normal cases. 90% of excreted potassium is excreted by the kidneys, the remaining through the GI tract.

Factors influencing potassium levels

Internal influencers

The internal balance of depends on 6 things:

• pH
• Tonicity of the extracellular space
• Insulin
• Catecholamines
• Mineralocorticoids
• Physical activity

pH

When acidosis occurs, the body attempts to buffer the increasing plasma H+. One of these is the intracellular buffer, where H+ in the plasma is moved inside cells. To maintain electroneutrality, the cells exchange K+ to the plasma. The total amount og potassium ion in the body doesn’t change, but a larger fraction of it is moved to the plasma, potentially causing hyperkalaemia. Hyperkalaemia reduces the kidney’s ability to excrete ammonia, which may further worsen the acidosis. For every 0.1 unit reduction in blood pH the plasma potassium concentration increases by approximately 0.2 – 2 mM.

The opposite can occur in case of alkalosis. Hydrogen ions are buffered out of the cells, requiring cells to move K+ ions into the cells, potentially causing hypokalaemia.

Reciprocally, an increase in plasma K+ concentration (hyperkalaemia) causes cells to buffer this change by moving K+ ions into the cells. To maintain electroneutrality, the cells exchange H+ to the plasma, potentially causing acidosis. The opposite can occur in case of hypokalaemia.

Tonicity

When the extracellular space is hypertonic (due to increased sodium or glucose concentration for example) will water flow out of cells and into the EC space. Because the K+ level inside the cell doesn’t change will the K+ concentration increase, as the cells have lost water. This concentration increase causes K+ to flow out of the cell, potentially causing hyperkalaemia.

Insulin

Insulin enhances Na+/K+ ATPase activity, causing K+ to enter the cells. We use the fact that insulin causes intracellular movement of H+ in the management of hyperkalaemia.

Beta-2-receptor

Catecholamines enhance Na+/K+ ATPase activity, via β2-receptors, causing potassium to enter cells. α-receptors decrease the activity.

Others

Mineralocorticoids contribute to the balance. I don’t know how it contributes to the internal balance (book doesn’t explain). Their effect on the external balance is much more important.

Physical activity causes K+ outflow from muscle cells.

External influencers

The external balance depends on 5 things:

• K+ intake
• Mineralocorticoids
• Filtration
• pH
• GI excretion

Potassium intake

K+ intake is counter-regulated by kidney and GI excretion, so even a high potassium intake isn’t dangerous (unless it’s intravenous), unless there is severe kidney failure. In end-stage renal failure, when the GFR < 5 mL/min even a few bananas can cause severe hyperkalaemia.

Mineralocorticoids

Mineralocorticoids play a much larger role in the external balance than the internal. Aldosterone and some of its weaker precursors enhance Na+/K+ and Na+/H+ exchange in the distal tubules and collecting duct. This causes K+ and H+ loss.

GFR

The GFR determines how much K+ is filtered. When it’s increased will more water and sodium reach the distal tubules, which increases Na+/K+ exchange, causing sodium to be reabsorbed and more potassium to be excreted. Increased flow rate, such as in osmotic diuresis, inhibits K+ reabsorption. Increased level of anions in the filtrate, like bicarbonate, increases K+ excretion because of electroneutrality.

pH

pH also influences the potassium excretion. Renal K+ excretion decreases in acidosis and increases in alkalosis.

GI excretion

GI excretion only accounts for 10% of potassium loss in healthy people, but in severe renal failure may this number go up to 50% to compensate for the failing kidneys.