The formation of renal calculi of calcium phosphate origin probably requires a state of supersaturation of urine with respect to brushite (CaHPO4 · 2H2O). The reduction in the degree of saturation of urine with respect to this phase should therefore be one of the basic aims of medical therapy for the patient in whom kidney stones form. This hypothesis was tested in eleven patients who had a history of passage of recurrent calcium-containing renal calculi by repeated estimation of the degree of saturation of urine from the urinary activity product of divalent calcium ions (Ca++) and divalent phosphate ions (HPO4-). In ten of the eleven patients urine specimens were supersaturated, largely attributable to a high urine pH or an abnormally high urinary calcium content. The administration of ammonium chloride lowered the activity product of Ca++ and HPO4- in the urine of two patients who responded with a satisfactory degree of urinary acidification. In a patient with renal tubular acidosis, this therapy resulted in a marked increase in the activity product. Orally administered sodium phosphate significantly increased the degree of saturation of urine with respect to brushite in five patients, probably by increasing the urinary excretion of phosphorus (P). (Urinary and serum orthophosphate is expressed in units of elemental phosphorus.) During the administration of cellulose phosphate the urine became less supersaturated in all nine patients tested; in six of them, it became undersaturated. These effects of cellulose phosphate probably resulted from a significant decrease in urinary calcium in the face of an only moderate increase in urinary phosphorus excretion. The administration of parathyroid extract greatly increased the activity product of Ca++ and HPO4-. Surgical removal of parathyroid adenoma or hyperplasia in three patients markedly lowered the degree of saturation of urine with respect to brushite.
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