Potassium

Introduction

Potassium is carefully regulated in the body - the consequences of altered Potassium levels are significant, including:

• reduced concentration of potassium in the ECF leads to plasma membranes hyperpolarization resulting in decreased firing of action potentials. This causes skeletal muscle weakness and cardiac abnormalities.
• increased concentration of potassium in the ECF leads to membrane depolarisation which is inappropriately triggered by action potentials. This can make the membrane insensitive to further stimulation causing cardiac abnormalities.

Potassium is largely an intracellular ion. Plasma potassium levels are not always a good indicator of intracellular levels; in acidosis the exchange of H+ and K+ ions leads to the depletion of intracellular potassium and elevated plasma potassium. The converse occurs in alkalosis. Aldosterone secretion promotes sodium retention and potassium excretion. Clinical features of potassium depletion include muscle weakness, ileus and cardiac arrhythmias, rhabdomyolysis and renal dysfunction. Hypokalaemia is of particular significance in the cat and is usually associated with CRF. In most cases, hyperkalaemia arises due to a diminished ability to excrete potassium. Potassium excess is therefore associated with hypoadrenocorticism and some forms of renal disease (especially post renal azotaemia). Marked hyperkalaemia is potentially life threatening causing bradycardia and cardiac arrest. Refrences: NationWide Laboratories

Sources of Potassium

Potassium is absorbed via passive diffusion from the small intestine and via active transport from the colon. It is regulated efficiently by aldosterone levels and recovery from cellular breakdown during haemolysis or tissue damage.

Methods of Control

The K⁺ in the ECF only represents a very small amount of the total K⁺ in the body; however its concentration is maintained within very strict parameters. The homeostasis of K⁺ is managed by three routes:

1. Cellular translocation - this is the main method of control; it is an acute response that triggers Potassium movement either into or out of the cells.
2. Renal excretion - this method makes up 90% of the chronic response (takes 4-6 hours to respond). It allows fine control and is regulated by aldosterone
3. GI excretion - this route makes up the other 10% of the chronic response and becomes significant in cases of renal failure. This response is also influenced by aldosterone

Cellular Translocation

• Vital for rapid control of potassium loads
• Helps control plasma concentration
• Moves potassium into the cell
• Stores potassium in skeletal muscle and liver
• Balances ECF and ICF
• Controlled by insulin and beta2 adrenoreceptors
  • Increases the activity of Na⁺ / K⁺ ATPases causing sodium efflux and potassium influx

Renal Control

• Potassium ions are reabsorbed and secreted at different points along the nephron
• Active reabsorption of potassium occurs along the proximal tubule (70%) and along the ascending limb of the Loop of Henle (10-20%)
• This results in there only being 10% of the original amount left in the distal tubule
• However net reabsorption / secretion of potassium occurs in the distal tubule and first part of collecting duct
  • Depends on bodies need
• Under the influence of aldosterone
• This is where the amount of potassium excreted is determined
• Reabsorption occurs in the final part of the collecting duct

Potassium and Aldosterone

• Aldosterone is the most important regulator of potassium
• It causes increased secretion of potassium
• Increased potassium directly stimulates Aldosterone secretion
• Increases the activity and number of Na⁺ / K⁺ ATPase in basolateral membranes of the principal cells in the collecting duct and distal tubule
• Potassium moves into the cells and is then excreted down an electro-chemical gradient

Factors Influencing Potassium Excretion

1.Sodium: High sodium = increased potassium excretion and:

• More sodium into cells
• Increased Na⁺ / K⁺ ATPase
• Pumps sodium into peritubular renal interstitium
• The resulting increased cellular uptake of potassium results in it moving down the electrochemical gradient into the nephron

2.Potassium: High potassium = increased potassium excretion which triggers the release of aldosterone.

Causes of Hyperkalaemia

Small Animals

• Acute renal failure
• Hypoadrenocorticism
• Post renal azotaemia (urethral obstruction, urinary tract trauma)
• Pseudohyperkalaemia:

EDTA contamination of serum

Thrombocytosis

Leucocytosis (leakage from cells)

Haemolysis (Akitas and Shibas)

• Massive tissue damage
• Metabolic acidosis (renal failure, certain types of diarrhoea)
• Peritoneal effusions

Equine

Potassium levels in the extracellular fluid are influenced most by renal function and do not always reflect potassium levels in the intracellular compartment. Potassium distribution depends on the acid-base status as it is exchanged for hydrogen ions across the cell membrane. Hyperkalaemia is a potential emergency due to induction of cardiac dysrhythmias.

• Reduced extracellular fluid volume, hypovolaemia with renal shut down
• Metabolic acidosis
• Polyuric renal disease
• Post renal obstruction in foals
• Pseudohyperkalaemia

In vitro haemolysis

Prolonged storage

• Muscle damage

Rare causes of hyperkalaemia in equine

• Anuric renal failure
• Urinary tract disruption
• Tissue necrosis
• Inherited hyperkalaemic periodic paralysis

Causes of Hypokalaemia

Small Animals

• Chronic renal failure (particularly cats)
• Diuretic therapy
• Vomiting and diarrhoea
• Hypokalaemic myopathy (hypokalaemic periodic paralysis) of Burmese kittens
• Insulin therapy
• Administration of potassium depleted fluids
• Excessive mineralocorticoid therapy
• Metabolic alkalosis for example gastric vomiting

Equine

• Prolonged anorexia
• Dietary deficiencies
• Gastrointestinal tract loss (lower bowel obstruction), diarrhoea
• Enterocolitis
• Profuse sweating
• Peritonitis

Rare causes of hypokalaemia in equines

• Metabolic alkalosis
• Renal tubular acidosis
• Iatrogenic (diuretics, bicarbonate or insulin administration)

Complementary tests

In small animals a Na:K ratio is an aid to the diagnosis of hypoadrenocorticism; a ratio <25:1 is supportive but an ACTH stimulation test is required for confirmation if the clinical signs are suggestive of Addison’s disease. The ratio can also be reduced by other factors increasing plasma potassium including renal disease.

In Equine urine clearance ratios will assist interpretation of serum electrolyte and mineral levels see fractional electrolyte excretion (FE) values (%).

Please visit www.nwlabs.co.uk or see our current price list for more information

References

Text referenced 'Nationwide Laboratories': NationWide Laboratories

Causes of Hyperkalaemia: NationWide Laboratories

Causes of Hypokalaemia: NationWide Laboratories

Complementary tests: NationWide Laboratories