Potassium

Serum K⁺ is not a good indicator of total body K⁺ because 90% is intracellular (see Table 6.1). The source of K⁺ is the diet and regulation is through the action of aldosterone which promotes renal K⁺ excretion. Some K⁺ losses occur through feces and sweat. Under certain circumstances, abnormalities in K⁺ may relate to acid-base disturbances.

Hyperkalemia

Total body K⁺ is usually increased, due to decreased renal excretion, with oliguric or anuric renal disease, as well as with postrenal obstruction. With uroabdomen, hyperkalemia results from movement of high K⁺ fluid in the abdomen into the intravascular space, however hyperkalemia is variable in these cases (see Chapter 7:Renal System, Fig. 7.1). As indicated earlier, hypoadrenocorticism usually involves both glucocorticoid and mineralocorticoid (aldosterone) lack. Therefore, hyperkalemia and hyponatremia are typically expected with this disease. Occasionally, hyperkalemia is iatrogenic due to oversupplementation of K⁺-rich intravenous fluids or increased ingestion of K⁺, especially if there is compromised renal function.

Hyperkalemia can also develop secondary to acid-base imbalances. When metabolic acidosis is due to bicarbonate loss rather than titration of acids, H⁺ moves into cells and K⁺ moves out of cells, resulting in hyperkalemia (see Acid-Base section below). Although serum K⁺ is increased under these circumstances, total body K⁺ is not increased, emphasizing the fact that serum K⁺ is not a good indicator of total body K⁺.

Muscle necrosis is a potential cause of hyperkalemia. The release of massive amounts of K⁺ from tissues probably requires extreme circumstances, such as capture myopathy in large wildlife species. Ion channel abnormalities in skeletal muscle can result in transient hyperkalemia and muscle paresis or paralysis, called hyperkalemic periodic paralysis/paresis (HYPP). The hyperkalemia is inconsistent and may only be detected if evaluated during a severe attack. HYPP is caused by a point mutation in the Na⁺ channel gene and has been described in the Quarter Horse and some Quarter Horse cross breeds (see Chapter 11: Muscle).

Pseudohyperkalemia will occur due to sample aging and lack of serum separation from cells. K⁺ leaches from leukocytes and platelets, particularly when numbers are high. Erythrocyte [K⁺] is higher than serum concentrations in most species, therefore leaching of K⁺ from RBCs can also occur with hemolysis or delayed separation of RBCs from serum. However, cats and most dogs do not have higher RBC K⁺ concentrations. Exceptions are Akita, Japanese Shiba Inu, several Korean breeds, and certain crossbred dogs, where pseudohyperkalemia from erythrocyte leaching may occur. Reticulocytosis, even in dogs and cats, can erroneously increase serum K⁺ due to high concentrations of K⁺ within immature erythrocytes.

Hypokalemia

Following are many potential reasons for a finding of hypokalemia on serum analysis. Decreased body K⁺ frequently occurs due to decreased intake. Vomiting and diarrhea are associated with hypokalemia, from both intestinal losses and increased aldosterone activity caused by ECF volume depletion. The polyuric stage of renal failure is often associated with K⁺ wasting by the kidneys, as is the use of non-K⁺-sparing diuretics. Excessive salivation and sweating may be responsible for hypokalemia in horses, particularly with endurance activities. Primary hyperaldosteronism, though rare, results in hypokalemia and hypernatremia. With metabolic alkalosis, hypokalemia develops because K⁺ is redistributed from the extracellular to the intracellular space, concurrent with H⁺ leaving the cells. Since insulin promotes the cellular uptake of K⁺, the institution of insulin therapy can lead to the rapid development of hypokalemia as K⁺ moves into cells.