| Amiloride (Midamor) and triamterene (Dyrenium) | Diminishes potassium secretion by reducing the electrical gradient between the intracellular space and the renal tubule, causing potassium to leave the cells |
| Amino acids* | Lysine, arginine, or epsilon-aminocaproic acid enters cells in exchange for potassium, causing hyperkalemia |
| ARBs and ACE inhibitors | Decreases aldosterone synthesis; hyperkalemia often can be reduced by concomitant diuretic use; ARBs less likely to cause hyperkalemia than ACE inhibitors |
| Azole antifungals | Inhibits adrenal steroid synthesis, which can lead to aldosterone deficiency |
| Beta blockers | Decreases sodium-potassium adenosine triphosphatase (ATPase) activity; beta2 agonists decrease potassium levels |
| Cyclosporine (Sandimmune) | Suppresses renin release, leading to decreased aldosterone synthesis, decreased potassium secretion in collecting duct |
| Digoxin at toxic levels | Decreases sodium-potassium ATPase activity |
| Fluoride toxicity | Decreases aldosterone synthesis; most common in patients on dialysis who drink water with high fluoride levels |
| Glucose infusions or insulin deficiency | Hypertonicity caused by hyperglycemia from glucose infusions can drive potassium out of the intracellular space, leading to hyperkalemia. Hyperkalemia may occur with continuous infusions or with boluses of hypertonic glucose. May be present with hypertonicity caused by other agents such as mannitol (Osmitrol) as well. |
| Heparins | Can cause hyperkalemia in patients with decreased renal function; inhibits adrenal aldosterone synthesis |
| Herbal remedies with digitalis-like effect | Specific agents include milkweed, lily of the valley, Siberian ginseng, Hawthorn berries, or preparations from dried toad skin (Bufo, Chan’su, Senso). All these agents act by decreasing sodium-potassium ATPase activity, leading to elevated extracellular potassium. |
| NSAIDs | Decreased prostaglandin production leads to decreased afferent arteriolar flow, suppressing renin and aldosterone secretion. Typical of NSAIDs as well as cyclooxygenase-2 selective inhibitor drugs. |
| Nutritional and herbal supplements | Herbs containing high potassium levels (e.g., Noni juice, alfalfa, dandelion, horsetail, nettle) |
| Packed red blood cells | Stored cells can partially hemolyze and release potassium when infused. |
| Penicillin G potassium | Can cause hyperkalemia in patients with impaired renal function caused by increased potassium load; can be administered orally or intravenously |
| Potassium supplements or salt substitutes | Ingestion of potassium can lead to hyperkalemia, particularly if renal function is impaired; dietary sources include bananas, melon, and orange juice. |
| Spironolactone (Aldactone) | Inhibits binding of aldosterone to receptors in the renal tubule |
| Succinylcholine (Anectine) | Increases nicotinic acetylcholine receptors in damaged skeletal muscle (e.g., trauma or burn patients) |
| Tacrolimus (Prograf) | Suppresses renin release, leading to decreased aldosterone synthesis and decreased potassium secretion in collecting duct |
| Trimethoprim (Proloprim) and pentamidine (Pentam 300) | Diminishes potassium secretion by reducing the electrical gradient between the intracellular space and the renal tubule, causing potassium to leave the cells. |