Objective—To determine whether pamidronate disodium
can reduce cholecalciferol-induced toxicosis
in a dose-related manner.
Animals—20 clinically normal, 8- to 12-month-old
Procedure—All dogs were given 8 mg of cholecalciferol
(CCF)/kg of body weight once orally, then were randomly
assigned to 4 groups of 5 dogs each. Dogs were treated
with IV administration of 0.9% NaCl solution (SC
group), 0.65 mg of pamidronate/kg in 0.9% NaCl solution
(LP group), 1.3 mg of pamidronate/kg in
0.9% NaCl solution (MP group), or 2.0 mg of
pamidronate/kg in 0.9% NaCl solution (HP group) on
days 1 and 4 after administration of CCF. Dogs were
observed for 14 days, and serial blood samples were collected
for serum biochemical, electrolyte, and 25-hydroxyvitamin
D3 analyses. Urine samples were collected for
determination of specific gravity. Glomerular filtration rate
(GFR) was determined by plasma iohexol clearance.
Histologic examination of renal tissue was performed.
Results—One dog in the SC group was euthanatized 3
days after administration of CCF because of severe clinical
signs of toxicosis. Dogs in the HP group had significantly
higher mean GFR (day 3), serum potassium concentrations
(day 14), and urine specific gravity (days 7
and 14) and significantly lower mean serum creatinine
concentrations and total calcium × phosphorus concentration
product (days 4 and 7) than dogs in the SC
group. Dogs in the HP group had no abnormal findings
on histologic examination of renal tissue, dogs in the LP
and MP groups had trace to mild mineralization of renal
tissue, and dogs in the SC group had moderate mineralization
and cellular necrosis of proximal renal tubules.
Conclusions and Clinical Relevance—Pamidronate
disodium is a potentially useful drug to reduce CCFinduced
toxicosis and other causes of hypercalcemia
associated with increased bone resorption in dogs.
(Am J Vet Res 2000;61:9–13)