Hyperparathyroidism, an abnormal increase in the production of the parathyroid hormone, robs the bones of calcium. These bones become weak and brittle and are easily broken. Parathyroid hormone is normally released in response to low blood calcium and maintains a normal blood calcium/phosphorus ratio. However, in diseased dogs the mineral balance is askew.

The parathyroid hormone (PTH) secretion is stimulated to maintain serum calcium concentrations at some specific level. The system functions as if there were a "calciostat" that operates at a serum calcium concentration set point of about 10.5 to 11.5 mg/dL. When serum calcium concentrations decrease below these levels, the rate of PTH secretion increases; when the serum calcium concentration exceeds the set point (as might occur after consumption of a meal high in calcium), PTH secretion is suppressed. 1

There are two types of hyperparathyroidism: primary and secondary. Primary hyperparathyroidism (PHPT) is one of the most common endocrine conditions and is accompanied by hypertension and increased cardiovascular mortality.3 The condition is caused by a benign tumor that grows on one or more of the four parathyroid glands. It has often been seen in Keeshonden. If a Keeshond that has the defective autosomal dominant PHPT gene is used for breeding, 50% of the offspring will also have the gene, while 50% will not. If a Keeshond with the defective gene is bred to another Keeshond who also has the defective gene, 50% of the offspring will have one copy of the defective gene, 25% will have two copies of the normal gene and 25% will have two copies of the defective PHPT gene.3 Secondary hyperparathyroidism may result from chronic kidney failure or calcium deficiency during growth.


Surgical removal of the diseased, hyperactive parathyroid gland, followed by intensive post-operative care, yields a good prognosis for a return to active life. Therapies include injectable and oral administration of calcium, vitamin D and magnesium until the previously suppressed remaining parathyroid glands are strong enough to support the dog. New therapies have been introduced lately including percutaneous ultrasound-guided radiofrequency heat ablation. Heat destroys tissue by causing thermal necrosis. Radiofrequency waves are converted to heat at the tip of an insulated needle. This form of therapy has several advantages as compared with surgery or ethanol ablation, it does not require surgery, only necessitates a brief period of anesthesia (usually less than 20 minutes), and is relatively inexpensive. 1

Secondary Renal Hyperparathyroidism

Secondary renal hyperparathyroidism can also compromise bone health. The clinical signs of renal disease will often be dominant; however, young, growing dogs with congenital renal disease may demonstrate more obvious signs of a bone disease such as lameness, pain, and fractures. Skeletal changes may be most apparent in the structure of the head, seen as a pliable "rubber jaw" or loosened teeth. Treatment is focused on the primary renal disease process, and crate rest is enforced to prevent skeletal damage or fracture. Dietary changes are made to control protein intake, for the kidney disease, and to possibly supplement dietary calcium.

Nutritional Secondary Hyperparathyroidism

Nutritional secondary hyperparathyroidism can result from a diet low in calcium, high in phosphorus, or deficient in vitamin D. An all-meat diet, for example, lacks the nutrient balance found in commercial dog foods.2 Secondary hyperparathyroidism may also be caused by gastrointestinal malabsorption of calcium or glucocorticoid excess. Gastrointestinal malabsorption can be caused by agents that bind calcium in the GI tract, preventing absorption. Something as seemingly harmless as mineral oil has been implicated as such an agent. Treatment is based on correcting the diet and guarding against fractures during the rehabilitation period.


  1. Stephen J. Ettinger, DVM, DACVIM and Edward C. Feldman, DVM, DACVIM. Textbook of Veterinary Internal Medicine
  2. Clinical and computed tomography features of secondary renal hyperparathyroidism
  3. Laboratory of Richard E. Goldstein, DVM. Canine Primary Hyperparathyroidism
Hyperparathyroidism in dogs