It has been demonstrated that the renal tubules of dog and man are capable of reabsorbing a fixed and limited quantity of phosphate per unit of time when presented with an excess in the glomerular filtrate (Pitts et al., 1944; Schiess et al., 1948). Since absorptive capacity is independent of glomerular filtration rate over a fairly wide range (Ayer et al., 1947) the renal mechanism which handles phosphate, like that which handles glucose, exhibits a true Tm relationship. More recently, it has been observed, in man, that an increased renal excretion of phosphate follows the administration of cortisone and ACTH. Moreover, negative phosphate balance, depletion of intracellular stores of phosphate and demineralization of bone have been observed in conditions of hyper-adrenocorticism (Albright 1942, Eliel et al., 1951; Ingbar et al., 1951; Pearson el al., 1950; Freeman et al., 1950; Soffer et al., 1950). Although logically inferred, it has not been clearly defined that this increment in phosphate excretion
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Roberts et al. (1953) studied this question.
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