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Differential Diagnosis & Pitfalls

• Pseudohyperkalemia – This is a diagnosis of exclusion. It most often occurs with hemolysis during blood draws. The intracellular fluid containing a higher concentration of positively charged potassium ions (K⁺) is exposed to the collected sample, resulting in an artificially elevated K⁺ level on the laboratory results. This can be considered when the patient has no symptoms of hyperkalemia and no changes on ECG, or in cases of difficult blood draws with longer tourniquet times.
• Metabolic acidosis – K⁺ transcellularly shifts out of the cells to maintain electroneutrality as the increasing number of positively charged hydrogen ions (H⁺) accumulates in the cells.
• Diabetic ketoacidosis, hyperglycemia, and hyperosmolality
  • Insulin encourages K⁺ entry into cells. In diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS), insulin depletion (either compromised insulin secretion or insulin resistance) and concurrent hyperosmolality secondary to hyperglycemia lead to marked hyperkalemia.
  • As the plasma osmolality increases, the osmotic gradient favors water excretion out of the cell. Potassium exits the cells via 2 different mechanisms. As water exits the cell, the potassium gradient becomes more potent, favoring potassium excretion via K+ channels in the cell membrane. The other mechanism involves the concept of solvent drag, as K⁺ ions are carried out of the cell via water excretion.
  • Any mechanism that depletes insulin (octreotide or fasting) or that raises the serum osmolality (hypernatremia, mannitol, contrast) can cause hyperkalemia via these same mechanisms.
• Beta blockers – Beta-2 agonists promote K⁺ entry into cells. Beta blockers, primarily nonselective beta blockers, prevent this effect. The typical rise in K⁺ is approximately lower than 0.5 mEq/L, and true hyperkalemia is rare.
• Exercise – K⁺ is released during exercise, most likely to promote vasodilation. This mechanism is thought to contribute to pseudohyperkalemia via excessive hand clenching during blood draws. Hyperkalemia during exercise can be compounded by patients taking nonselective beta blockers and in patients who are in end-stage renal disease (ESRD).
• Hyperkalemic periodic paralysis – This autosomal dominant disorder involves a point mutation in the skeletal muscle cell sodium channel. It occurs when episodes of weakness or paralysis are precipitated by stress (eg, cold exposure, exercise, fasting, and ingestion of potassium).
• Other causes of increased excretion of K⁺:
  • Digitalis overdose
  • Red blood cell transfusion – K⁺ leaks out of cells while in storage

• Excess consumption of potassium-rich foods, such as bananas, potatoes, melons, citrus, and avocados
• Intake of salt substitutes (common in patients with chronic kidney disease)

• Acute or chronic kidney disease – Potassium excretion is mainly mediated by the kidneys. In both acute kidney injury and chronic kidney disease, potassium excretion is decreased and hyperkalemia may develop.
• Hyporeninemic hypoaldosteronism – Aldosterone promotes sodium ion (Na⁺) reabsorption and K⁺ excretion. In hyporeninemic hypoaldosteronism, there is decreased renin secretion and, therefore, decreased aldosterone secretion, allowing for K⁺ to accumulate in the blood.
• Type 4 renal tubular acidosis and cortical collecting duct defects – Type 4 renal tubular acidosis forms from decreased aldosterone responsiveness in the cortical collecting duct due to defects in the collecting duct or decreased aldosterone secretion.
• Drugs, including angiotensin inhibitors, NSAIDs, calcineurin inhibitors (cyclosporine, tacrolimus), heparin, and potassium-sparing diuretics.
  • Angiotensin inhibitors (ACE inhibitors, ARBs, aldosterone antagonists) – Decreased aldosterone decreases K⁺ excretion.
  • Calcineurin inhibitors (cyclosporine, tacrolimus) are nephrotoxic drugs that decrease the kidney's ability to excrete K⁺.
  • Heparin – Heparin-induced hypoaldosteronism can cause hyperkalemia.
  • K⁺-sparing diuretics – In the collecting duct, the blockage of epithelial sodium channels (ENaCs) (amiloride, triamterene) or the blockage of aldosterone receptors (spironolactone, eplerenone) cause a decrease in K⁺ excretion.

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