Studies on the Renal Excretion of Water and Electrolytes in Cases of Addison's Disease

IN 1938 Cutler, Power and Wilder (1), while working on a quantitative diagnostic procedure for adrenal cortical insufficiency noticed that patients who had Addison's disease voided only small amounts of urine after drinking a large volume of water. These patients were studied under unusual circumstances (1, 2). Their intake of sodium salts previously had been restricted and the dietary content of potassium had been increased to a high level by the administration of potassium citrate. Subsequently it became apparent that the small urinary volumes were not the result of the regimen which the patients were undergoing but that, even under more normal conditions, water did not act as a diuretic agent. This phenomenon was explored further by Robinson, Power and Kepler (3) and eventually became the basis of another diagnostic procedure for Addison's disease which became known as the water test. Because of its simplicity the practicality of the water test soon became evident and, as our experience with it increased, we began placing more and more reliance on it, particularly as a means of quickly excluding adrenal cortical insufficiency as a cause of illness. Furthermore, from the strictly scientific point of view the test aroused our interest. Why did Foundait work? What became of the water? Was the water absorbed with normal rapidity? Was an abnormal response dependent on a depleted supply of electrolytes and water? Would the test still give a positive result if the patient were previously “saturated” with salt and water? These were some of the questions we asked ourselves. The present study was undertaken with only the last of these questions in mind. We reasoned that if a normal subject were given a large amount of sodium salts and water the volume of his extracellular fluid would be increased. Then when additional water was administered, a large amount of both salt and water would be available for excretion. It was questionable whether or not the Addisonian patient would respond in the same manner. If we could demonstrate that he did not, the difference in his response might be utilized to diagnostic advantage. To anyone who has seen a patient go into an Addisonian crisis when deprived of salt, the value of a test procedure based on the administration rather than on the restriction of salt is obvious and needs no further comment.