Abstract
Selective calcification in the zona intermedia of the kidney can be obtained by the oral administration of 1% NaH2PO4 solution instead of drinking water, even in adrenalectomized rats, within 12 days. This lesion is minimal in adrenalectomized, otherwise untreated rats, and maximal in animals given large doses of desoxycorticosterone acetate (DOCA). It is virtually absent in rats maintained exclusively with cortisol acetate (COLA). COLA not only fails to promote, but actually inhibits this type of nephrocalcinosis, since the sensitizing effect of DOCA is counteracted by concurrent administration of COLA. It appears that the corticoids exert an important regulating influence upon the ability of the kidney to handle an excess of phosphate. Through its influence upon the factors governing the precipitation of pathologic Ca deposits in the urinary passages, the adrenal cortex may be involved in the pathogenesis of calcified renal concrements.

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