Daily urinary calcium excretion in renal stone-forming subjects is shown to vary directly with moderate changes in dietary sodium intake. The changes produced are sufficient to alter the basic diagnostic classification from 'hypercalciuric' to 'normocalciuric' because dietary sodium is reduced from 200 to 80 mM/day. Similar changes were observed in fasting morning 'spot' urine samples, resulting in alteration of diagnostic subclassification between so-called 'absorptive' and 'renal' categories, in the absence of demonstrable change in parathyroid function. Diagnostic and therapeutic studies in stone-forming subjects require control of both dietary calcium and dietary sodium if misinterpretations are to be avoided. Habitual high sodium intake may be an etiological factor in the generation of excessive excretion of calcium, sodium, and phosphate--the hypercalciuria syndrome.

The pathogenesis of sodium retention in congestive heart failure has been a difficult problem to elucidate. The production in dogs of cardiac valvular lesions of increasing severity has enabled investigators to study the sequential alterations in salt and water balance in the same animal from the normal state through the progressive stages of cardiac impairment until frank failure is present. The findings in dogs suggest that: 1. Abnormalities in sodium metabolism are detectable in mild heart disease long before overt failure is present. 2. Total exchangeable sodium may be increased in animals with mild valvular damage. These animals have normal exercise tolerance and normal basal glomerular filtration rates. 3. Increased sympatho-adrenal (adrenergie) activity is responsible, in large measure, for the decreased sodium and water excretion in dogs with cardiac impairment. 4. Preliminary experiments suggest that the carotid sinus may be the receptor organ initiating the reflex increase in sympatho-adrenal tone, and may be the elusive "volume receptor" for which investigators have been searching. 5. Evidence is also available that the carotid sinus may play a major role in the regulation of the zona glomerulosa of the adrenal cortex, the site of aldosterone production.

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Potassium has long been known to be almost completely confined to the intracellular compartment, and the neutral fat present in muscle has been shown to have a low chloride content (1). It seemed probable, therefore, that the error associated with predictions of total exchangeable electrolyte from total body weight would diminish if the variable of depot fat was eliminated by the use of lean body mass as a reference standard. A close correlation of lean body mass with red cell mass (2) and urinary creatinine (3) has previously been shown. Accordingly, measurements of total exchangeable chloride and potassium have been correlated with lean body mass, red cell mass and creatinine excretion in a series of normal subjects. MATERIALS AND METHODSSixteen normal males and fourteen normal females were studied, their ages ranging from 18 to 81 years and their body weights from 44.5 to 100.2 Kg. They were selected to include both lean and obese subjects, the range of body fat being 5 to 50.8 per cent of total body weight.Total exchangeable potassium (K.) measurements were carried out according to the method of Corsa, Olney, Steenburg, Ball, and Moore (4), four spot urine specimes being collected between twenty-two and twenty-six hours after injection. The urinary potassium concentration was estimated by flume photometry. Siice the short half-life of C1 precluded its use, Br' wag

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