Potassium balance

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Glomerulus:
Distal tubule & collecting duct

Potassium (K⁺ is the major intracellular cation. The normal distribution of potassium is shown in the table below:

Ion	Intracellular concentration	Extracellular concentration
K⁺	140 mmol/L	4 mmol/L

Hypokalaemia and hyperkalaemia
Disturbances of potassium concentration can have significant adverse effects. Most UK trusts quote the normal range for plasma potassium as 3.5 -5.3 mmol/l however the RCEM considers normal potassium as 3 - 4.5 mmol/l according to their 2021 glossary of terms for RCEM examinations.

	Hypokalaemia	Hyperkalaemia
Clinical features	Mild: Lassitude Generalised weakness Muscle pain. Constipation Severe (potassium <2.5 mmol/l): Severe muscle weakness or paralysis (typically starts in lower limbs & progresses to upper limbs & torso). Respiratory failure (due to respiratory muscle weakness). Ileus (due to involvement of GI muscles). Paraesthesia. Tetany (rare)	Weakness Paraesthesia Fatigue Bradycardia due to heart block Respiratory muscle weakness Muscle weakness and flaccid paralysis. Depressed or absent tendon reflexes
ECG changes	U waves Small, absent or inverted T waves Prolonged PR interval ST depression long QT	Flattened P waves Prolonged PR interval Widened QRS Tall tented T waves AV dissociation Sine wave or asystole (severe hyperkalaemia)

Key factors influencing potassium handling in the renal tract
The main factors that influence potassium handling by the kidney are:

Aldosterone
pH
Sodium excretion
Flow rates

Aldosterone's overall effect is to increase sodium reabsorption and potassium secretion.

Aldosterone
Aldosterone is released by the zona glomerulosa of the adrenal cortex in response to raised angiotensin II, raised potassium, and raised ACTH levels.

Aldosterone causes retention of Na⁺ in exchange for K⁺ and H⁺ ions in the distal tubule

Aldosterone acts by increasing synthesis of transport proteins (including the Na⁺-K⁺-ATPase pump, Na⁺-H⁺ symporter, Na⁺ channels, K⁺ channels and H⁺-ATPase ) so its effects take hours to work

pH changes have predictable effects on potassium secretion. Acidosis causes decreased K⁺ secretion and increased reabsorption in the collecting duct which may lead to hyperkalaemia. Alkalosis has the opposite effects and may lead to hypokalaemia.

Hypokalaemia is associated with metabolic alkalosis. In alkalosis a number of mechanisms are triggered that enhance H⁺ ion secretion, including stimulation of ammonia production, increased Na⁺-H⁺ exchange and increased H⁺-K⁺-ATPase activity.

Hyperkalaemia inhibits NH4₄⁺ reabsorption by competing with Na⁺-K⁺-2Cl^- binding sites.

The concentration of sodium in the tubular fluid which enters the collecting duct has an effect on potassium levels. In the distal tubule K⁺ may be passively excreted via ROMK channels and through K⁺-Cl^- symporters. This passive movement is driven by the electrical gradient generated by sodium ion reabsorption (reabsorbing sodium into the principle cells leaves a relative negative charge in the lumen which attracts positively charged K⁺ ions). Decreased Na⁺ ion delivery to the collecting duct results in reduced Na⁺ ion reabsorption and hence a reduced gradient for K+ secretion.

Increased tubular flow washes away secreted K⁺ ions and enhances K⁺ secretion.

Potassium handling through the renal tract

Glomerulus:

K⁺ ions are freely filtered at the glomerulus.

Proximal convoluted tubule (PCT):

Approximately 65 - 70% of filtered K+ is reabsorbed in the PCT
Reabsorption is primarily via paracellular pathways and is driven by the concentration gradient created by the reabsorption of water.

Loop of Henle:

There is insignificant net movement of K⁺ in the descending limb.
In the thick ascending limb K⁺ is pumped from the lumen into tubular cells by the Na⁺-K⁺-2Cl co-transporter. Some K⁺ leaks back into the lumen via ROMK channels which helps maintain an electrical gradient. Approximately 20% of filtered K⁺ is reabsorbed here.

Distal tubule & collecting duct

K⁺ is typically secreted for excretion in the distal tubule and collecting duct.
K⁺ is actively pumped from the interstitial fluid into principle cells by the Na⁺-K⁺ -ATPase and then secreted into the lumen passively via ROMK channels and K⁺-Cl^- cotransporters.