Equis ISSN 2398-2977


Contributor(s): Graham Munroe, Vetstream Ltd


  • Persistently raised serum calcium >13.5 mg/dl (3.375 mmol/l; 6.69 mEq/l).
  • Cause: multiple causes including neoplasia, renal failure, granulomatous disease, hypoadrenocorticism, hypervitaminosis D and others.
  • Diagnosis: serum biochemistry defines the syndrome, but other tests may be required to identify the underlying cause.
  • Signs: may include anorexia, lethargy, weight loss, poor performance, depression, sometimes polyuria/polydipsia, and other signs dependant upon cause. 
  • Treatment: fluid therapy, frusemide diuresis, glucocorticoids, or surgery, eg for parathyroid neoplasms. 
  • Prognosis: variable according to cause, but persistent untreated hypercalcemia may lead to renal failure and organ mineralization.




  • Calcium is measured as total serum calcium and ionized calcium (biologically active). 
  • Equine serum calcium levels are closely related to dietary intake.
  • Equines excrete a larger proportion of absorbed calcium in their urine than other mammals.
  • Parathyroid hormone (PTH), calcitonin and Vitamin D act in conjunction with the intestine, bone, kidneys and parathyroid glands to maintain calcium homeostasis.
  • Organ dysfunction or hormonal imbalance may disturb calcium homeostasis    →   hypercalcemia.
  • Vitamin D (calcitriol / 1,25 dihydroxycholecalciferol)   Vitamin D3  increases enteric calcium absorption, increases renal calcium resorption and increases calcium mobilization from bone via osteoblasts and osteoclasts. 
  • The kidney converts Vitamin D to its final active form. 
  • Hypercalcemia may arise from excess vitamin D or excess PTH activity, or from analogous molecules produced by neoplasms: 
    • Parathyroid hormone (PTH), released in response to low calcium or high phosphate, stimulates osteocyte activity, moving calcium from bone into the circulation. PTH also causes renal phosphate retention. 
    • Humoral hypercalcemia of malignancy - neoplasia may cause hypercalcemia via release of humoral factors such as osteoclast activating factor, calcitriol, prostaglandins, transforming growth factor, parathyroid hormone, and parathyroid hormone-related peptide. 
    • Excessive PTH-production may arise from parathyroid tumors in a primary fashion or from secondary hyperparathyroidism (chronic renal failure, via a complex process including phosphate retention amongst other mechanisms, leads to renal secondary hyperparathyroidism). 
    • Granulomatous disease may cause hypercalcemia via increased calcitriol release from macrophages. 
  • 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.
  • Renal concentrating ability is impaired under hypercalcemia   →    dehydration.
  • Renal tissue mineralization may   →    hypercalcemia + hyperphosphatemia.
  • Excess extracellular calcium reduces membrane excitability, resulting in dysrhythmias (bradycardia   →    tachycardia +/- extrasystole or ectopic beats   →    ventricular fibrillation   Heart: ventricular fibrillation  ) and muscle/smooth muscle weakness. 
  • Half of serum calcium is protein-bound, hence hypoalbuminemia will lower the total serum calcium measurement (and may mask high ionized calcium levels).
  • Hypercalcemia   →    calcitonin release   →    decreased plasma calcium.


  • Very variable according to cause: 
    • Vitamin D intoxication can be very rapid, with rapid tissue mineralization. 
    • Renal failure typically has a more chronic course.

Special risk factors

  • Fluid therapy in hypercalcemic horses should not contain any calcium.
  • Hypercalcemic horses should not be fed legume hays, eg Alfalfa, clover, calcium supplements or high calcium diets   Nutrition: minerals  .


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Further Reading


Refereed papers