Acidosis and Potassium Balance

Acidosis typically causes hyperkalemia, but the specific effect depends on whether it is a mineral acidosis or an organic acidosis.

Types of Acidosis and Their Effects on Potassium

Mineral acidosis (respiratory acidosis, end-stage uremic acidosis, or acidosis induced by mineral acids like NH₄Cl or CaCl₂) predictably causes hyperkalemia due to shifts of potassium from the intracellular to extracellular compartment 1
This occurs because hydrogen ions enter cells in exchange for potassium ions, which move into the extracellular fluid 1
In primary adrenal insufficiency, hyperkalaemia is present in approximately half of patients at diagnosis due to aldosterone deficiency, impaired glomerular filtration, and acidosis 2

Uncomplicated organic acidosis (diabetic ketoacidosis, alcoholic acidosis, lactic acidosis) typically does not cause hyperkalemia 1
In these conditions, serum potassium concentration usually remains within the normal range in uncomplicated cases 1
The organic anion can freely penetrate cells without creating a gradient for hydrogen ions, thus not triggering potassium efflux from cells 1

In mineral acidosis, hydrogen ions enter cells in exchange for potassium, leading to hyperkalemia 1, 3
Cell studies show that acidification with HCl (mineral acid) decreases cellular potassium content, while acidification with organic acids (butyric or lactic acid) actually increases cellular potassium 3
The rate of cell pH acidification is significantly slower with HCl compared to organic acids, which may explain the different effects on potassium movement 3

In diabetic ketoacidosis, hyperkalemia can occur despite total body potassium depletion due to:
- Reduced renal function
- Acidosis
- Release of potassium from cells due to glycogenolysis
- Lack of insulin 4
During treatment of diabetic ketoacidosis, correction of acidosis and volume expansion decrease serum potassium concentration 2
To prevent hypokalemia during treatment, potassium replacement should be initiated after serum levels fall below 5.5 mEq/l, assuming adequate urine output 2

Hyperkalemic renal tubular acidosis is usually attributable to real or apparent hypoaldosteronism 5
Hyperkalemia itself can lead to acidosis by suppressing renal ammonium excretion 6, 5
Correction of hyperkalemia alone (without mineralocorticoid therapy) can resolve acidosis and restore urinary ammonium excretion 6

In preterm infants, non-oliguric hyperkalemia can develop after birth even without potassium intake 2
Risk factors include lack of antenatal corticosteroids, systemic acidosis, birth asphyxia, and catabolic states 2
Severe hyperkalemia (K > 7 mmol/L) requires prompt intervention 2

Rhabdomyolysis can cause hyperkalemia due to release of intracellular potassium from damaged muscle cells 7
Risk is further increased when rhabdomyolysis leads to acute kidney injury 7
Close monitoring of serum potassium is essential to prevent cardiac complications 7

Treatment of hyperkalemia should be based on the underlying cause 2
In patients with cardiovascular disease and chronic kidney disease, up to 50% of hyperkalemia cases recur within one year 2
Life-threatening hyperkalemia requires immediate treatment with calcium carbonate to stabilize myocardial cell membrane, insulin with or without glucose, and/or beta-adrenergic agonists to shift potassium into cells 2
These treatments provide only temporary benefit (1-4 hours), so definitive treatment to increase potassium excretion should be initiated early 2