Effects of hypercalcemia on serum concentrations of magnesium, potassium, and phosphate and urinary excretion of electrolytes in horses.
OBJECTIVE
To determine effects of experimentally induced hypercalcemia on serum concentrations and urinary excretion of electrolytes, especially ionized magnesium (iMg), in healthy horses.


METHODS
21 clinically normal mares.


METHODS
Horses were assigned to 5 experimental protocols (1, hypercalcemia induced with calcium gluconate; 2, hypercalcemia induced with calcium chloride; 3, infusion with dextrose solution; 4, infusion with sodium gluconate; and 5, infusion with saline [0.9% NaCl] solution). Hypercalcemia was induced for 2 hours. Dextrose, sodium gluconate, and saline solution were infused for 2 hours. Blood samples were collected to measure serum concentrations of electrolytes, creatinine, parathyroid hormone, and insulin. Urine samples were collected to determine the fractional excretion of ionized calcium (iCa), iMg, sodium, phosphate, potassium, and chloride.


RESULTS
Hypercalcemia induced by administration of calcium gluconate or calcium chloride decreased serum iMg, potassium, and parathyroid hormone concentrations; increased phosphate concentration; and had no effect on sodium, chloride, and insulin concentrations. Hypercalcemia increased urinary excretion of iCa, iMg, sodium, phosphate, potassium, and chloride; increased urine output; and decreased urine osmolality and specific gravity. Dextrose administration increased serum insulin; decreased iMg, potassium, and phosphate concentrations; and decreased urinary excretion of iMg. Sodium gluconate increased the excretion of iCa, sodium, and potassium.


CONCLUSIONS
Hypercalcemia resulted in hypomagnesemia, hypokalemia, and hyperphosphatemia; increased urinary excretion of calcium, magnesium, potassium, sodium, phosphate, and chloride; and induced diuresis. This study has clinical implications because hypercalcemia and excessive administration of calcium have the potential to increase urinary excretion of electrolytes, especially iMg, and induce volume depletion.
Toribio
Ramiro E
RE
Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210, USA.
Kohn
Catherine W
CW
Rourke
Kelly M
KM
Levine
Andrea L
AL
Rosol
Thomas J
TJ
D000818:Animals; D002118:Calcium / Q000097:blood; D002122:Calcium Chloride / Q000633:toxicity; D002125:Calcium Gluconate / Q000633:toxicity; D004573:Electrolytes / Q000652:urine*; D005260:Female; D005942:Gluconates / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D006734:Horse Diseases / Q000097:blood* / Q000139:chemically induced / Q000652:urine*; D006736:Horses / Q000097:blood* / Q000652:urine*; D006934:Hypercalcemia / Q000097:blood / Q000652:urine / Q000662:veterinary*; D008274:Magnesium / Q000097:blood; D010710:Phosphates / Q000097:blood; D011188:Potassium / Q000097:blood; D013997:Time Factors
D004573:Electrolytes; D005942:Gluconates; D010710:Phosphates; D008274:Magnesium; D005947:Glucose; D002122:Calcium Chloride; C030691:gluconic acid; D011188:Potassium; D002125:Calcium Gluconate; D002118:Calcium