https://www.kidney-international.org/article/S0085-2538(15)32803-9/pdf

Importance of dietary sodium in the hypercalciuria syndrome.

It has long been known that oral or intravenous administration of phosphate salts lowers the serum calcium concentration in normal animals (1, 2) and in hypercalcemic human subjects (3-5). Recently , interest has been renewed in the clinical use of phosphate therapy to control life-threatening hypercalcemia because of the relative in-effectiveness or toxicity of other modes of therapy (6, 7). In 1962, Dent (5) reported dramatic lowering of the serum calcium concentration in a patient with hyperparathyroidism during the intravenous infusion of sodium phosphate and sustained lowering of serum calcium by continuing oral doses of phosphate in another patient with hyperpara-thyroidism. Since then, Goldsmith and Ingbar (8) have demonstrated the clinical effectiveness and apparent safety of both oral and intravenous phosphate therapy in the management of hyper-calcemia accompanying a variety of diseases. Most of the investigators who have shown that phosphate administration lowers serum calcium concentration have suggested that this effect is the result of the precipitation of calcium phosphate salts in the body. The present studies were carried out to further test this hypothesis. If phosphate infusion lowers serum calcium concentration by causing calcium phosphate salt precipitation, then. a) phosphate infusion should * tend to lower serum calcium concentration in all subjects, regardless of the presence or absence of those endocrine organs normally involved in the regulation of the serum calcium; b) a simultaneous increase in calcium excretion should not account for the fall in serum calcium occurring during phosphate infusion; and c) the degree by which serum calcium concentrations fall should be a function of the extent to which the solubility product of some calcium phosphate salt is exceeded during the infusion of phosphate. The results of the present experiments satisfy all of these postulates and strongly support the hypothesis that phosphate infusion lowers serum calcium concentration as a result of CaHPO4 precipitation. Methods Studies were carried out in 22 patients divided into four groups: 1) eight control subjects without disorders of calcium homeostasis, 2) three patients with hypopara-thyroidism on adequate calcium and vitamin D therapy, 3) four patients with primary hyperparathyroidism, and 4) seven patients with hypercalcemia in association with malignant tumors of the breast or lung or with multiple myeloma. All were hospitalized in the Marquette University Clinical Research Center, where they received constant diets. Calcium and phosphorus intakes were constant for each subject but varied from subject to subject, ranging from 10 to 26 mmoles …

/pdf/studies-of-the-mechanism-by-which-phosphate-infusion-lowers-os5ud56wnp.pdf

Studies of the mechanism by which phosphate infusion lowers serum calcium concentration

DUARTE, CRISTOBAL G., AND JOHN F. WATSON. Calcium reabsorption in proximal tubule of the dog nephron. Am. J. Physiol. 212(6): 1355-1360. Ig67.This experiment was performed to study the reabsorption of calcium in the dog proximal tubule and further evaluate the relationship between sodium and calcium transport. A microadaptation of a fluorometric method was developed to determine the concentration of calcium in tubule fluid. Calcium concentration was measured in tubule fluid samples and compared with simultaneous values in serum ultrafiltrates in normal, and in mannitoland saline-loaded dogs. No correlation was found between TF/UF calcium ratio and location along the proximal tubule. The mean TF/ UF calcium concentration ratio in nondiuretic dogs was 1.08 (SD & o. I 2). The mean TF/UF calcium concentration ratios obtained in mannitoland saline-loaded dogs was 0.92 (SD =t 0.14) and 0.91 (SD rf= 0.05), respectively, both of which are significantly less than that observed in nondiuretic dogs. It was also demonstrated that the urinary excretion of calcium is dependent on the filtered load and closely follows the pattern of sodium excretion. Tubular inhibition of sodium transport in the proximal tubule during isotonic saline loading was accompanied by a smaller but significant inhibition of calcium reabsorption which was sufficient to account for the increase in calcium excretion in the urine.

Calcium reabsorption in proximal tubule of the dog nephron.

P
i, Ca, Mg, Na, Cl and K handlings by the rat kidney tubules were analysed before, during, and after an acute phosphate plasma loading, using the tubular fluid recollection technique and electron microprobe analysis. As compared to the control period, hyperphosphatemia resulted in: a) a drop in plasma ultrafiltrate calcium concentration; b) some increase in GFR; c) a 20% decrease in (TF/P) Inulin in both late proximal and early distal fluid samples; d) fractional proximal reabsorptions of Na, Cl and K were reduced to about the same proportion. All these effects partly reversed after stopping the phosphate perfusion; e) as a mean value, both relative and even (to a lesser extent) absolute proximal phosphate reabsorption decreased during the loading and the recovery periods; f) the observed change in overall kidney phosphate reabsorption as a function of the filtered load was entirely accounted for by a change in the reabsorption taking place along the terminal segments; g) (TF/P

 f
 ) mean value for calcium in late proximal samples dropped to 0.78 during the loading period and to 0.83 during the third period; h) (TF/P

 f
 ) mean value for magnesium was 1.66 during the control period, and only 1.12 during the last period; accordingly fractional proximal Mg reabsorption increased from 13 (control) to 35% (recovery period); this delayed effect of hyperphosphatemia on proximal Mg handling accounted for the reduction in urinary Mg output noted during the last period. The possible role of hyperphosphatemia, extracellular expansion, hypocalcemia and maximal PTH release is discussed in order to explain these different observations.

Simultaneous Mg, Ca, P, K, Na and Cl analysis in rat tubular fluid

Tubular reabsorption and excretion of calcium were studied at different levels of filtered calcium by means of calcium infusion in normal and hypercalciuric subjects and in patients with idiopathic nephrolithiasis Calcium reabsorption and excretion rose linearly with filtered load and in no case was a maximum tubular reabsorptive capacity for calcium reached No decrease in tubular reabsorption of calcium was found in hypercalciuric as compared with normocalciuric subjects, and no difference in tubular reabsorption was found between patients with idiopathic nephrolithiasis and normal subjects Calcium excretion and reabsorption calculated from the endogenous creatinine clearance during calcium infusion were virtually identical with the corresponding values calculated from the inulin clearance

https://jcp.bmj.com/content/jclinpath/21/3/353.full.pdf

Tubular reabsorption of calcium in normal and hypercalciuric subjects

Renal excretion of calcium by the dog.

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Renal excretion of calcium by the dog.