Calcium and phosphate homeostasis in dogs with newly diagnosed naturally occurring hypercortisolism

Abstract

Abstract Background Hypercortisolism affects calcium and phosphate metabolism in dogs; however, the exact mechanisms are not completely understood. Objectives To evaluate circulating concentrations of whole parathormone (wPTH), 25‐hydroxyvitamin D (25‐(OH)D), calcitriol, and fibroblast growth factor‐23 (FGF‐23) in dogs with naturally occurring hypercortisolism (NOHC) and healthy dogs, and their association with calcium and phosphate homeostasis. Animals Twenty‐three client‐owned dogs with NOHC, and 12 client or staff‐owned healthy dogs. Methods Prospective cross‐sectional study. The circulating concentrations of total calcium, ionized calcium (iCa), phosphate, wPTH, 25‐(OH)D, calcitriol and FGF‐23, and the urinary fractional excretion of phosphate (FEP) and calcium (FECa) were compared between dogs with NOHC before treatment and healthy dogs. Results Dogs with NOHC had higher mean serum phosphate concentrations (4.81 mg/dL, SD ± 0.71 vs 3.86 mg/dL, SD ± 0.60; P < .001), median FECa (0.43%, range, 0.03‐2.44 vs 0.15%, range, 0.06‐0.35; P = .005), and median serum wPTH concentrations (54.6 pg/mL, range, 23.7‐490 vs 24.6 pg/mL, range, 5.5‐56.4; P = .003) as compared to the controls. Circulating concentrations of total calcium, iCa, and calcitriol and the FEP did not differ between groups, whereas the serum 25‐(OH)D concentrations were lower in dogs with NOHC as compared to the controls (70.2 pg/mL, SD ± 42.3 vs 106.3 pg/mL, SD ± 35.3; P = .02). The dogs with NOHC had lower plasma FGF‐23 concentrations than controls (316.6 pg/mL, range, 120.8‐575.6 vs 448.7 pg/mL, range, 244.8‐753; P = .03). Conclusions and Clinical Importance Urine loss of calcium and hyperphosphatemia could contribute to the adrenal secondary hyperparathyroidism.

Keywords

• calcitriol
• FGF‐23
• hyperadrenocorticism
• parathyroid hormone
• urinary calcium excretion
• vitamin D