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For further information, see CMDT Part 21-04: Hypokalemia
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Essentials of Diagnosis
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Serum K+ < 3.5 mEq/L (< 3.5 mmol/L)
Severe hypokalemia may induce arrhythmias and rhabdomyolysis
Transtubular potassium concentration gradient (TTKG) can distinguish renal from nonrenal loss of potassium
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General Considerations
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Gastrointestinal loss due to infectious diarrhea is most common cause
Potassium shift into the cell is transiently stimulated by insulin and glucose and facilitated by β-adrenergic stimulation
α-Adrenergic stimulation blocks potassium shift into the cell
Aldosterone is an important regulator of body potassium, increasing potassium secretion in the distal renal tubule
Magnesium is an important cofactor for potassium uptake and for maintenance of intracellular potassium levels
Magnesium depletion should be suspected in persistent hypokalemia refractory to potassium repletion
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Potassium shift into cell (Table 21–3)
Insulin excess, eg, postprandial
Alkalosis
β-Adrenergic agonists
Trauma (via epinephrine release)
Hypokalemic periodic paralysis
Barium or cesium intoxication
Renal potassium loss (urine K+ > 40 mEq/L)
Increased aldosterone (mineralocorticoid) effects
Primary hyperaldosteronism
Secondary hyperaldosteronism (dehydration, heart failure)
Renovascular or malignant hypertension
Cushing syndrome
European licorice (inhibits cortisol)
Renin-producing tumor
Congenital abnormality of steroid metabolism (eg, adrenogenital syndrome, 17α-hydroxylase defect)
Increased flow of distal nephron
Hypomagnesemia
Renal tubular acidosis (type I or II)
Genetic disorder of the nephron
Bartter syndrome
Liddle syndrome
Extrarenal potassium loss (urine K+ < 20 mEq/L)
Vomiting, diarrhea, laxative abuse
Villous adenoma, Zollinger-Ellison syndrome
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Muscular weakness, fatigue, and muscle cramps are common in mild to moderate hypokalemia
Constipation or ileus may result from smooth muscle involvement
Flaccid paralysis, hyporeflexia, hypercapnia, tetany, and rhabdomyolysis may be seen in severe hypokalemia (serum K+ < 2.5 mEq/L)
Hypertension may result from aldosterone or mineralocorticoid excess
Renal manifestations include nephrogenic diabetes insipidus and interstitial nephritis
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