Epidemiology
Etiology
Potassium excess: due to altered K+ metabolism or intake
Reduced excretion: acute and chronic kidney disease
Endocrine causes: hypocortisolism, hypoaldosteronism
Drugs: potassium-sparing diuretics , ACE inhibitors, angiotensin receptor blockers, NSAIDs , and trimethoprim-sulfamethoxazole
Especially in HIV patients who are taking high-dose TMP-SMX Similar to the actions of amiloride, trimethoprim blocks the epithelial sodium channel in the distal tubule and collecting duct. This reduces transepithelial voltage and impairs sodium-potassium exchange, leading to reduced potassium excretion and hyperkalemia.
Type IV renal tubular acidosis
Increased intake
High potassium diet, e.g., fresh fruits, dried fruits and legumes, vegetables, nuts, seeds, bran products, milk, and dairy products
K+ containing IV fluids
Extracellular shift
Extracellular release
Pathophysiology
Clinical features
Diagnostics
Treatment
Enhanced potassium elimination
Cation-exchange medications
Mechanism of action: These drugs release Na+ or Ca2+ ions in the gut, which are exchanged for K+ , thereby enhancing enteral K+ elimination. Clinical applications: nonurgent lowering of K+
Options
Cation-exchange resins
Sodium polystyrene sulfonate: falling out of favor due to adverse effects
Sodium zirconium cyclosilicate
Cation-exchange polymers, e.g., patiromer
Adverse effects