ISSN 2398-2969      

Hypercalcemia: overview


Kyle Braund

Audrey K Cook


  • Uncommon syndrome characterized by increased ionized calcium concentrations.
  • Cause: variety of underlying causes, but most common is neoplasia.
  • Diagnosis: defined by measurement of ionized calcium concentrations, but other tests may be required to identify the underlying cause.
  • Signs: polydipsia/polyuria, muscular weakness, dehydration, collapse, may be asymptomatic.
  • Treatment: determined by underlying cause; hypercalcemia may be temporarily managed with fluids, frusemide, bisphosphonates or glucocorticoids.
  • Prognosis: variable according to cause, but persistent untreated hypercalcemia may lead to renal failure, urolithiasis and organ mineralization.
    Follow the diagnostic tree for Elevations in Total Serum Calcium Elevations in Total Serum Calcium.



  • Paraneoplastic (hypercalcemia of malignancy): parathyroid hormone (PTH) mimetics - released from neoplastic cells, including PTH-related peptide (PTH-rp) and TFG alpha:
  • Primary hyperparathyroidism: inappropriate secretion of parathyroid hormone (PTH) by a functional parathyroid tumor, usually an adenoma (fairly uncommon; Keeshonds predisposed).
  • Local osteolysis: invasion of bone by tumor cells or infectious agents.
  • Hypoadrenocorticism Hypoadrenocorticism (Addison's disease): may result in mild to moderate hypercalcemia.
  • Hypervitaminosis D(dietary over-supplementation, rodenticide ingestion Vitamin D poisoning (cholecalciferol) ).
  • Granulomatous diseases, such as fungal infections, may be associated with hypercalcemia, through release of vitamin D Vitamin D like substances.
  • Advanced chronic renal disease Kidney: chronic kidney disease (CKD) may result in tertiary hyperparathyroidism, characterized by sustained hyperplasia of the parathyroid resulting in loss of sensitivity to calcium and autonomous release of PTH PTH assay.


  • Hypercalcemia is the result of increased uptake from gastrointestinal system, excessive release of from bone, or decreased renal excretion.
  • PTH and PTH-rp activate osteoclasts, with release of clacium from bone. These agents also promote renal conservation of calcium and stimulate the synthesis of active Vitamin D by the kidneys.
  • Vitamin D and its analogues increase gastrointestinal uptake of calcium. At high levels, calcium is also released from bone.
  • Osteolytic processes result in release of calcium and phosphorous from bone.
  • Hypercalcemia impairs renal responsiveness to anti-diuretic hormone (ADH), resulting in poorly concentrated urine, and compensatory polydipsia.
  • Excess extracellular calcium reduces membrane excitability, resulting in dysrhythmias and muscle weakness.
  • Sustained hypercalcemia is associated with urolithiasis Urolithiasis and subsequent dysuria, hematuria and urinary tract obstruction Urinary obstruction.
  • Excessive circulating calcium, on exceeding a critical Ca x P solubility product, leads to calcium deposition in tissues such as lungs, kidney, gastric mucosa, blood vessel walls, and myocardium (metastatic calcification).
  • Kidney and lung damage from such metastatic calcification can prove fatal.


  • Depends on underlying cause and severity of hypercalcemia.
  • Lymphoma → sudden onset, rapid course.
  • Primary hyperparathyroidism → insidious onset, gradual progressive hypercalcemia.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Messinger J S, Windham W R & Ward C R (2009) Ionized hypercalcemia in dogs: a retrospective study of 109 cases (1998-2003). JVIM 23 (3), 514-519 PubMed.
  • Mellanby R J et al (2006) Plasma concentrations of parathyroid hormone-related protein in dogs with potential disorders of calcium metabolism. Vet Rec 159 (25), 833-838 PubMed.
  • Hostutler R A et al (2005) Uses and effectiveness of pamidronate disodium for treatment of dogs and cats with hypercalcemia. JVIM 19 (1)29-33 PubMed.
  • Mellanby R J, Mee A P, Berry J L & Herrtage M E (2005) Hypercalcaemia in two dogs caused by excessive dietary supplementation of vitamin D. JSAP 46 (7), 334-338 PubMed.

Other sources of information

  • Schenick P A & Chew D J (2012)Investigation of hypercalcemia and hypocalcemia.In:BSAVA Manual of Canine and Feline Endocrinology.C T Mooney & M E Peterson (eds), BSAVA, England, pp 221-233,

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