Overview of Disorders of Potassium Metabolism in Animals

Potassium homeostasis is determined mainly by the balance between the absorption of potassium from the GI tract and subsequent excretion of potassium by the kidneys (in all animals) and (in adult ruminants) in the saliva. Transport of potassium in the small intestine is passive; in the colon, transport is active, under the influence of aldosterone.

The most important hormone affecting renal and salivary potassium excretion is aldosterone, which is released from the zona glomerulosa of the adrenal gland in response to hyperkalemia and other factors. One of aldosterone’s primary actions is to enhance the secretion of potassium ions in the distal renal tubules and collecting ducts.

At least 95% of whole body potassium is intracellular, and skeletal muscle contains 60–75% of the intracellular potassium. Extracellular potassium concentrations are tightly regulated by renal excretion and shift of potassium between intracellular and extracellular locations.

Marked changes in serum or plasma potassium concentrations alter the resting membrane potential of cells, because the potassium gradient generated by Na⁺/K⁺-ATPase is the main reason for the negative electric potential across cell membranes. Therefore, both hypokalemia and hyperkalemia result in clinically important changes in cellular and organ function.

Hypokalemia can occur in any animal that has increased renal losses (via polyuria, tubular disease, or mineralocorticoid effect), increased GI losses (via vomiting or diarrhea), or decreased GI uptake (via GI stasis or sustained decrease in feed intake). It can also occur in animals receiving large volumes of IV fluid.

Hypokalemia usually indicates whole body depletion of potassium, unless it is identified in animals with hyperinsulinemia that is due to hyperglycemia, in which case potassium might have translocated intracellularly.

Clinical signs in most animals with mild to moderate hypokalemia are mild and nonspecific. Severe hypokalemia is associated with ventroflexion of the head or recumbencydue to generalized muscle weakness and cardiac arrhythmias, including both atrial and ventricular premature complexes that can lead to more complex cardiac arrhythmias.

Prolonged and profound hypokalemia can result in myopathy that is difficult to treat. Hyperaldosteronism in dogs and cats can cause severe hypokalemia. Cats in general can be affected by feline hypokalemic polymyopathy, and Burmese cats have an autosomal recessive disorder that leads to hypokalemic myopathy.

Hyperkalemia usually results from inadequate urinary excretion of ingested potassium and is common in animals with hypovolemia, urinary tract obstruction, or bladder rupture.

Hyperkalemia in horses and ruminants can also result from exertional rhabdomyolysis, because skeletal muscle contains a large percentage of whole body potassium. Hyperkalemia also occurs in heavily muscled Quarter Horses and related breeds as a genetic disorder (hyperkalemic periodic paralysis). Hyperkalemia frequently occurs in dogs with hypoadrenocorticism.

Whole body potassium status in hyperkalemia cannot be inferred, because many animals with hyperkalemia have concurrent acidemia and actually have whole body potassium depletion.

Severe hyperkalemia is associated with generalized muscle weakness, depression, and cardiac conduction disturbances that can lead to lethal cardiac arrhythmias.

Pseudohyperkalemia in serum and plasma occurs when extensive hemolysis is present because of the high potassium concentration in RBCs in most species. However, some species have genetic differences in their erythrocytic potassium concentration.