The Ultrafiltrability of Potassium and Sodium in Human Serum

One of the puzzling clinical aspects of the metabolism of electrolytes is the genesis of symptoms and signs of potassium depletion and potassium intoxication (1-3). Precipitous flaccid paralysis, sensory disturbances and respiratory failure, altogether analogous to the sequence of events in familial periodic paralysis, may occur in these disturbances of potassium metabolism characterized by either deficit or plethora of the ion. The preponderance of evidence indicates that such gross clinical derangements are observed in but a minority of instances of abnormality in the metabolism of potassium (1-9). Review of existing data, furthermore, fails to disclose a clinical, chemical, or physiologic difference which could account for the capricious incidence of serious manifestations in this minority of patients. The extensive metabolic studies of Jantz (10) in nine cases of familial periodic paralysis seem to afford a clue to the solution of this problem. He found that episodes of paralysis could be consistently related to a profound reduction in the ultrafiltrable fraction of plasma potassium. Although this finding has not been confirmed or negated, such an explanation might in part account for paralytic phenomena which occasionally supervene in patients without familial periodic paralysis, who develop disturbances of potassium metabolism. The present investigation comprises an analysis of the diffusibility in vitro of potassium and sodium of sera obtained from a group of normal subjects and an analogous preliminary survey of patients with derangements of electrolyte metabolism.