Since Greenwald,1 in 1915, reported the observation of an increase in the concentration of inorganic phosphorus in the blood serum of patients with nephritis, many investigators have studied the inorganic constituents of the blood and other body fluids in renal disease. Marriott and Howland2 appear to have been the first to report the occurrence of hypocalcemia in renal failure, a phenomenon they attributed to the increase in the concentration of serum phosphate. They also suggested that the latter factor is of importance in the production of nephritic acidosis. The intimate relationship between hyperphosphatemia and hypocalcemia was soon after demonstrated by Binger,3 who showed that the intravenous injection of phosphates is followed by a diminution in the concentration of serum calcium. Subsequent studies have confirmed these observations and have in part supported the conception of the etiologic relation of hyperphosphatemia to hypocalcemia in nephritis. Halverson, Mohler and Bergeim
CANTAROW A. CALCIUM STUDIES: VII. THE CALCIUM AND INORGANIC PHOSPHORUS CONTENT OF CEREBROSPINAL FLUID AND BLOOD SERUM IN CHRONIC GLOMERULONEPHRITIS WITH UREMIA. Arch Intern Med (Chic). 1932;49(6):981–993. doi:10.1001/archinte.1932.00150130104009
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