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. The normal subjects were 24 medical students of the freshman class of Boston University School of Medicine. Patients in various states of electrolyte imbalance and dehydration were studied from the wards of Boston City Hospital. Normal subjects came to the laboratory following an overnight fast. Blood was withdrawn, using minimal stasis, under mineral oil, and serum was separated anaerobically within one hour of clot format A portion of serum from the centrifuged blood was aspirated from beneath its thin protective coat of oil into Lavietes' ultrafiltration chambers (11). Anaerobic ultrafiltration transpired through cellophane membranes at room temperature for about 48 hours. Technical details and equipment were identical with those described by Lavietes (11). Both original serum and ultrafiltrate were analyzed simultaneously. Serum residue was not analyzed.Sodium and potassium were determined on the Barclay flame photometer using lithium as the internal standard (12). All fluids were analyzed in duplicate-ie., two separate dilutions of 1 to 50 and 1 to 100 for potassium and 1 to 200 and 1 to 400 for sodium. Each unknown solution was "bracketed" by two knowns, and serum and corresponding ultrafiltrate were read together. Final values were averages of the results of two or more readings of each unknown solution. Average readings of duplicate dilutions were within 2% of one another. Before each group of determinations, the accuracy and precision o...