Basic Science and Pathophysiology

Potassium is the most abundant cation in the body. Ninety-eight percent of body potassium is intracellular and only 2% is present in the extracellular space.

Potassium balance can be affected by:


Potassium intake in normal diets varies between 40 and 100 mmol/day.

Ingested potassium is quickly moved to the intracellular space via the Na-K-ATPase pump in the cell membrane in exchange for sodium. This transfer is regulated by insulin, acid base status, β2 adrenoceptors and serum tonicity.

Abnormal Intake

The kidney is unable to stop all urinary loss of potassium ions (K+). Therefore inadequate intake over time can lead to hypokalaemia.


Potassium balance in the extracellular space is maintained by the kidneys and to a lesser extent by the GI tract.

In the kidneys, the filtered potassium is almost totally resorbed in the proximal tubules with the majority of potassium excretion in urine being passive. This excretion is in response to the membrane potential created by active sodium reabsorption in exchange for potassium and hydrogen ions (H+). This membrane potential can be neutralised by hydrogen or potassium so there is a close relationship between potassium and hydrogen ion homoeostasis. Some active secretion of K+ occurs in the distal tubules.

Cirrhotic patients commonly suffer from secondary hyperaldosteronism and thus have low body potassium and increased body sodium (although serum sodium may be low due to altered distribution).

Abnormal Distribution

In acidosis, when K(s) moves into the extracellular space in exchange for H+ ions to be buffered intracellularly, H+ ions will be preferentially secreted. This leads to the development of hyperkalaemia.

Small changes in the extracellular potassium have large effects on the transmembrane electrical gradient and thus the function of neuromuscular and cardiac tissues. K(s) is tightly regulated under normal conditions between 3.5 and 5 mmol/L.


The excretion of potassium is controlled by the kidney and GI tract. This excretion can be altered in several situations.

Problems with Excretion

In alkalosis there will be increased potassium excretion and hypokalaemia as H+ is reabsorbed in exchange for K+. Likewise, chloride loss from the body leads to secretion of potassium in the kidney.

Types 1 and 2 renal tubular acidosis lead to the rare scenario of hypokalaemia with acidosis.

GI tract elimination of K+ is minimal in healthy individuals but this can increase from 5% of total excretion to 25% in patients with end-stage renal failure (ESRF).

Aldosterone stimulates potassium excretion and sodium reabsorption in the kidney. Hyperkalaemia and hypovolaemia stimulate aldosterone secretion from the adrenal cortex.

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