This case study elucidates the complex fluid and electrolyte shifts, including intracellular potassium transfer and plasma volume expansion, that occur during attacks of familial hypokalemic periodic paralysis.
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Hypothesis-generating for electrolyte shifts in hypokalemic periodic paralysis; larger studies needed before clinical adoption.
SUMMARY Metabolic studies have been made in a case of familial hypokalæmic periodic paralysis. The results suggest that during an attack of paralysis, sodium and water move out of muscle cells, associated with a reciprocal transfer of potassium. Plasma volume expansion was found during attacks without gain in overall body weight, consistent with a redistribution of water between cells and extra‐cellular fluid. Oliguria associated with sodium and potassium retention was found during attacks. During recovery, either spontaneous or produced by potassium chloride administration, a marked coincident diuresis of sodium, potassium and water occurred, with the excretion of an alkaline urine. Failure to demonstrate any reciprocity between sodium reabsorption and potassium and hydrogen ion excretion during oliguria or mannitol‐induced sodium diuresis, suggests that the site of sodium reabsorption is proximal to the distal convoluted tubule. The rate of excretion of aldosterone fell as paralysis increased, coinciding with the time of plasma volume expansion.
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Niall et al. (1966) studied this question.
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