Hypokalemia Differential Diagnoses
Normal Reference Range for Serum Potassium: 3.5 to 5.5 mEq/L
- Associations: pH > 7.45 +/- elevated bicarbonate (HCO3-)
- Pathophysiology: The body responds to shifts in acid-base balance by moving H+ ions out of the cell, resulting in K+ ions moving into the cell.
- Associations: Low serum Mg++ +/- evidence of nephrotoxicity (elevated serum creatinine)
- Pathophysiology: Damages the cell membranes by creating pores in the luminal cells of the nephron decreasing their ability to regulate Mg++ and K+ reabsorption.
- Associations: Hypochloremic metabolic alkalosis
- Pathophysiology: A defect in chloride transport at the thick ascending loop of Henle resulting in Cl- and K+ loss and metabolic alkalosis.
- Associations: Continuous nebulized albuterol for asthma or COPD exacerbation or as a therapy for hyperkalemia
- Pathophysiology: Beta-receptor agonists (e.g., albuterol) causes a shift of K+ into the cells by increasing the activity of Na+/K+ ATPase pump.
- Associations: Patients being given bicarbonate for treatment of hyperkalemia or tricyclic antidepressant overdose or severe rhabdomyolysis
- Pathophysiology: Increased blood pH causes cells to shift H+ ions out of the cells, resulting in the movement of K+ ions into the cell.
- Association: Presence of severe fungal infection +/- hypocalcemia
- Pathophysiology: Chelates with cations, especially Ca++ and Mg++ which can cause seizures and cardiac dysrhythmias.
- Associations: Low urine Ca++ levels + hypochloremic metabolic alkalosis.
- Pathophysiology: Renal salt wasting due to a defect in thiazide Na+/Cl- co-transporter in the distal convoluted tubule.
- Associations: Intermittent episodes of paralysis + positive family history of this condition
- Pathophysiology: Autosomal dominant problem with excessive renal and GI losses of K+ decreasing the ability of the nerve to depolarize.
- Associations: Elevated blood pressure +/- moon facies or edema +/- hypernatremia
- Pathophysiology: Excess mineralocorticoid activity of aldosterone results in the unbalanced reabsorption of Na+ and water and release of K+ in the distal collecting tubule of the nephron.
- Associations: Dietary or nutritional deficiency +/- alcoholic
- Pathophysiology: Prevents K+ repletion and maintenance of K+ because the Na+/K+ ATPase pump uses Mg++ as a co-factor for function.
- Associations: Iatrogenic due to treatment of diabetes or hyperkalemia or Munchausen syndrome
- Pathophysiology: Insulin causes K+ to shift into the cell via activation of the Na+/K+ ATPase pump which causes 2 K+ ions to move into the cell and 2 Na+ cations to move out of the cell.
- Associations: High blood pressure +/- resistant to typical treatment
- Pathophysiology: Mutation in SCNN1B and SCNN1G genes resulting in epithelial Na+ channels that do not get degraded and cause excessive Na+ reabsorption & loss of K+.
- Associations: Past medical history of heart failure or fluid overload or cirrhosis on high dose spironolactone
- Pathophysiology: Inhibits the Na+/K+/Cl- cotransporter in the thick ascending loop of Henle which results in the reduction of paracellular reabsorption of magnesium and calcium. The net effect is a loss of both K+ and Mg++ from the body.
- Associations: Nausea and vomiting +/- bowel obstruction where a nasogastric tube is being used for management
- Pathophysiology: The parietal cells within the gastric mucosa utilize the K+/H+ ATPase pump to regulate the gastric contents of K+ and H+ ions. When nasogastric (NG) tubes are being used at low intermittent or continuous suction, there is a loss of both due to removal through the NGT tube.
- Associations: Hypokalemia + metabolic acidosis
- Pathophysiology: Damage to the renal tubule results in impairment in ability to regulate the reabsorption of electrolytes from the urine filtrate.
Amphotericin B Toxicity
Beta Agonist Excess
Hypokalemia Periodic Paralysis
Loop Diuretics (Bumetanide, Furosemide, Torsemide)
Renal Tubular Acidosis - Types 1 & 2