THE SEPARATE EFFECTS OF HYPERPARATHYROIDISM, HYPERCALCEMIA OF MALIGNANCY, RENAL FAILURE, AND ACIDOSIS ON THE STATE OF CALCIUM, PHOSPHATE, AND OTHER IONS IN PLASMA*

Abstract

Plasma from patients with primary and secondary hyperparathyroidism, hypercalcemia of malignancy, vitamin D intoxication and primary renal failure, with and without acidosis, has been analyzed for total, free, and complexed calcium, magnesium, phosphate and citrate. The ability of plasma protein to bind Ca, measured as KCaProt was unaltered in primary or secondary hyperparathyroidism or in the hypercalcemia of malignancy. Acidosis had only a minor effect. Renal failure itself had no effect except in some severe uremics, in whom calcium binding was decreased. Increased protein binding of phosphate, seen in one-fifth of the hypercalcemic samples, was eliminated by adding excess EDTA. Complexed Ca was increased only in severe uremia. Neither phosphate nor citrate accounted for the increase. The ion product [Ca2+] [HPO42-] was normal or low in primary hyperparathyroidism and was unaffected by parathyroidectomy in primary or secondary hyperparathyroidism. It was increased in severe renal failure but was unaffected by hypercalcemia itself. These results support the traditional concept of reciprocal adjustments in Ca and P concentrations to keep this product constant, with the modification that inhibitors of calcification accumulating in uremia may greatly increase the level about which these adjustments occur. In accordance with these findings, the percentage ionization of plasma calcium was normal in both primary and secondary hyperparathyroidism and also in other types of hypercalcemia. Some decrease was seen in severe uremia due to increased complexed calcium. Acidosis had only a minor effect and the absence of tetany in acidotic uremics with hypocalcemia cannot be attributed to an increase in ionization of plasma Ca.