Abstract

Hypoadrenocorticism is an important differential for hypercalcemia. The etiology of hypercalcemia in hypoadrenocorticism in dogs is unclear. To review the prevalence of hypercalcemia and use statistical models to identify clinical, demographic, and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism. One hundred ten dogs with primary hypoadrenocorticism; 107 with recorded total calcium (TCa), 43 recorded ionized calcium (iCa). Multicenter retrospective observational study at 4 UK referral hospitals. Univariable logistic regression analyses were performed to assess the association between independent variables of signalment, hypoadrenocorticism type (glucocorticoid only deficient hypoadrenocorticism [GHoC] vs glucocorticoid and mineralocorticoid deficient hypoadrenocorticism [GMHoC]), clinicopathological variables and hypercalcemia. Hypercalcemia was defined as elevated TCa, an elevated iCa, or both elevated TCa and iCa (Model 1) or as elevated iCa (Model 2). Overall prevalence of hypercalcemia was 34.5% (38/110). The odds of hypercalcemia (Model 1) were increased (P < .05) in dogs with GMHoC ([vs GHoC], OR [odds ratio] = 3.86, 95% confidence interval [CI] 1.105-13.463), higher serum creatinine (OR = 1.512, 95% CI 1.041-2.197), and higher serum albumin (OR = 4.187, 95% CI 1.744-10.048). The odds of ionized hypercalcemia (Model 2) were increased (P < .05) with reduced serum potassium concentration (OR = 0.401, 95% CI 0.184-0.876) and younger age (OR = 0.737, 95% CI 0.558-0.974). This study identified several key clinical and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism. These findings aid understanding of the pathophysiology and etiology of hypercalcemia in dogs with primary hypoadrenocorticism.

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