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Hypercalcemia often causes polyuria by making the kidneys unresponsive to vasopressin, leading to nephrogenic diabetes insipidus. In this condition, the collecting ducts fail to concentrate urine because the ADH signal cannot effectively promote water reabsorption. Normally ADH binds V2 receptors in the collecting ducts, raising cAMP and driving aquaporin-2 channels to the membrane to reabsorb water. High calcium disrupts this signaling or the insertion of aquaporin-2, so water reabsorption falls and large volumes of dilute urine are produced. That fits the scenario of hypercalcemia with polyuria best.

Central diabetes insipidus would involve insufficient ADH production rather than renal insensitivity. SIADH causes inappropriately concentrated urine with hyponatremia. Hyperglycemia can cause osmotic diuresis from glucose in the filtrate, but the combination with hypercalcemia most characteristically points to nephrogenic diabetes insipidus due to renal unresponsiveness to ADH.