What commonly prescribed drugs cause hyperkalemia in patients with CKD and receiving dialysis?
Many drugs used as therapy for CKD and associated conditions, such as heart failure and hypertension, can cause or worse hyperkalemia. Often, it is combinations of these medications that lead to hyperkalemia.
Potassium (K+) supplements are used frequently in combination with diuretic therapy. K+-sparing diuretics (spironolactone, amiloride) inhibit kidney elimination of K+. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are common causes via alterations in the renin-angiotensin-aldosterone system (RAAS). Digoxin inhibits the basolateral Na-K ATPase in cardiac myocytes. Because of a narrow therapeutic window, overdose states are not uncommon and can result in elevated K+. Acute and/or chronic reductions in GFR in association with the previously mentioned medications can tip a patient into hyperkalemia by compromising K+ excretion by the kidneys. Nonsteroidal antiinflammatory drugs (NSAIDs) and beta blockers also impair kidney K+ excretion mainly through inhibition of RASS system leading to hyperkalemia. Digoxin inhibits the basolateral Na-K ATPase in cardiac myocytes. Penicillin infusion solutions contain a high amount of K+ for drug stability.
Calcineurin inhibitors (CNIs) such as tacrolimus or cyclosporine are the backbone of immunosuppression in kidney transplant and are additionally used in the treatment of some glomerulonephritis. Both of these are associated with various electrolyte abnormalities including hyperkalemia.
