Pathogenesis and management of hyperkalemia

Abstract

Hyperkalemia results from defects in both renal and extrarenal potassium metabolism. Acute potassium tolerance is largely determined by extrarenal potassium homeostasis, whereas chronic potassium homeostasis is primarily regulated by the kidney. When evaluating the patient with hyperkalemia, it is important to first exclude laboratory error, pseudohyperkalemia, acidemia, increased sources of potassium input, renal insufficiency, and drug-induced causes. These problems comprise approximately 75% of the cases of hyperkalemia. The remaining 25% result from defects in the renin-angiotensin-aldosterone axis, primary renal tubular secretory defects, and abnormal distribution of potassium between intracellular and extracellular compartments, treatment of chronic hyperkalemia requires definition of its etiology and removal of the specific cause. Treatment of acute hyperkalemia involves direct antagonism of the effects of potassium on the cell membrane (hypertonic sodium chloride and calcium), redistribution of potassium into cells (bicarbonate and insulin), and removal of potassium from the body (diuretics, cation-exchange resins, and dialysis).