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
  • Gastrointestinal upset
  • Hypokalemia