Metabolic and renal effects of acute hypercalcemia in dogs

¹ Department of Medicine, State University of New York College of Medicine at New York City; and Medical Service (Service B), Kings County Hospital, Brooklyn, New York

The acute metabolic and renal effects of exogenously produced hypercalcemia were studied in hydrated dogs ingesting high- and low-calcium diets, in parathyroidectomized dogs and in dogs receiving vitamin D₂. Under all these conditions, elevation of the plasma calcium concentration to 18 mg/100 ml resulted in solute diureses containing all major cations and in hyperphosphatemia. No change in free water clearance or net tubular transport of phosphorus occurred. Further elevation of levels of the plasma calcium caused marked reductions of glomerular filtration, renal plasma flow, and solute excretion and an increase in free water clearance. The increment in cation excretion exceeded the quantity of calcium retained. Less than 50% of the calcium load could be located in the extracellular space and urine at the end of the infusions. Erythrocyte calcium content increased two- to fourfold but erythrocyte concentrations of magnesium and acid-soluble phosphorus did not change. These data suggest that the solute diuresis of hypercalcemia is primarily renal in origin. Displacement of cations from osseous and intracellular sites by calcium may also occur and contribute to the solute diuresis. The hyperphosphatemia is independent of changes in parathyroid function, glomerular filtration and tubular transport of phosphorus and constitutes an unexplained consequence of induced hypercalcemia.

Note:
With the Technical Assistance of Albert Schaffer and Jack Schorr