ESSENTIALS OF DIAGNOSIS
Serum potassium < 3.5 mEq/L (3.5 mmol/L).
Severe hypokalemia may induce arrhythmias and rhabdomyolysis.
Assessment of urine potassium excretion (urine potassium to creatinine ratio) can distinguish renal from nonrenal loss of potassium.
Hypokalemia can result from insufficient dietary potassium intake, intracellular shifting of potassium from the extracellular space, or potassium loss (renal or extra-renal) (Table 21–3). Genetic disorders can be associated with some electrolyte disturbances (eTable 21–1). A low dietary potassium intake is usually not sufficient as the kidneys can lower urine potassium excretion to very low levels (less than 15 mEq/L). Shift of potassium into cells is increased by insulin and beta-adrenergic stimulation. Excess potassium excretion by the kidneys is usually due to increased aldosterone action in the setting of preserved delivery of sodium to the distal nephron. Magnesium is an important regulator of potassium handling and low levels lead to persistent renal excretion of potassium; hypokalemia is often refractory to treatment until the magnesium deficiency is corrected. Loop diuretics (eg, furosemide) cause substantial renal potassium and magnesium losses.
Table 21–3.Causes of hypokalemia. ||Download (.pdf) Table 21–3. Causes of hypokalemia.
Decreased potassium intake
Potassium shift into the cell
Insulin release (postprandial, exogenous, insulinoma)
Hypokalemic periodic paralysis
Renal potassium loss with metabolic acidosis
Proximal and distal RTAs
Toluene inhalation (glue sniffing)
Renal potassium loss with metabolic alkalosis
Normal/low blood pressure
High blood pressure
Elevated renin and aldosterone
Renal artery stenosis
Depressed renin and elevated aldosterone
Glucocorticoid remediable aldosteronism
Depressed renin and aldosterone
Apparent mineralocorticoid excess
Increased GI losses
eTable 21–1.Genetic disorders associated with electrolyte metabolism disturbances. ||Download (.pdf) eTable 21–1. Genetic disorders associated with electrolyte metabolism disturbances.
|Disease ||Site of Mutation |
| Hypokalemia || |
| Hypokalemic periodic paralysis ||Dihydropyridine-sensitive skeletal muscle voltage-gated calcium channel |
| Bartter syndrome ||Na+-K+-2Cl– cotransporter, K+ channel (ROMK), or Cl– channel of thick ascending limb of Henle (hypofunction), barttin |
| Gitelman syndrome ||Thiazide-sensitive Na+-Cl– cotransporter |
| Liddle syndrome ||Beta or gamma subunit of amiloride-sensitive Na+ channel (hyperfunction) |
| Apparent mineralocorticoid excess ||11-beta-hydroxysteroid dehydrogenase (failure to inactivate cortisol) |
| Glucocorticoid-remediable hyperaldosteronism ||Regulatory sequence of 11-beta-hydroxysteroid controls aldosterone synthase inappropriately |
| Hyperkalemia || |
| Hyperkalemic periodic paralysis ||Alpha subunit of calcium channel |
| Pseudohypoaldosteronism type I ||Beta or gamma subunit of amiloride-sensitive Na+ channel (hypofunction) |
| Pseudohypoaldosteronism type II (Gordon syndrome) ||WNK2, WNK4 |
| Familial hypocalciuric hypercalcemia ||Ca2+-sensing protein (hypofunction) |
| Familial hypocalcemia ||Ca2+-sensing protein (hyperfunction) |
| Hypophosphatemic rickets ||PEX gene, FGF23 |
| Hypomagnesemia-hypercalciuria syndrome ||Paracellin-1 |
| Nephrogenic diabetes insipidus ||V2 receptor (Type 1), aquaporin-2 |
| Proximal RTA ||Na...|