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Disorders Associated with Calcium, Phosphorus, and Vitamin D in Cats

By Russell R. Hanson, DVM, DACVS, DACVECC, Professor of Equine Surgery, Department of Clinical Sciences, College of Veterinary Medicine, Auburn University ; Joerg A. Auer, DrMedVet, Dr h c, MS, DACVS, DECVS, Professor and Director, Equine Department, Vetsuisse Faculty, University of Zürich ; Joseph Harari, MS, DVM, DACVS, Veterinary Surgeon, Veterinary Surgical Specialists, Spokane, WA ; Dale A. Moore, MS, DVM, MPVM, PhD, Associate Professor, Veterinary Medical Teaching and Research Center, University of California-Davis ; Sheldon Padgett, DVM, MS, DACVS

Also see professional content regarding disorders associated with calcium, phosphorus, and Vitamin D.

Defective bone formation is called osteodystrophy. It is caused in most cases by deficiencies or imbalances of calcium, phosphorus, and vitamin D, all of which are important in creating and maintaining strong, healthy bones.


Rickets is a disease of young, growing animals that causes soft and deformed bones. It is commonly caused by insufficient phosphorus or vitamin D in the diet. More rarely, calcium deficiencies are to blame. As in most diets causing defective bone formation, the cause is typically an imbalance in the ratio of calcium to phosphorus. Animals fed all-meat diets are commonly affected.

In affected kittens, the most common signs are a reluctance to move, lameness in the hind legs, bowing of the legs, and the inability to control muscle movements. The skeletal disease becomes progressively more severe after 5 to 14 weeks. The kittens become quiet and reluctant to play; they assume a sitting position or lie down with the hind legs stretched out away from the body. Normal activities may result in the sudden onset of severe lameness due to incomplete or folding fractures of one or more bones. In folding fractures, pressure on the bones causes them to slowly “fold” over and deform instead of fracturing. Joints may also appear swollen.

The outlook for treating rickets is good if there are no broken bones or irreversible damage to the bone. The primary treatment is to correct the diet. Exposure to sunlight (ultraviolet radiation) will also increase the production of vitamin D.

Recent studies show that many homemade diets for cats are deficient in minerals and fail to achieve a proper calcium-to-phosphorus ratio. Therefore a high-quality commercial food, or one designed by a credentialed veterinary nutritionist, is recommended.

Adult Rickets (Osteomalacia)

Osteomalacia develops similarly to rickets but in mature bones. It may be seen in cats that remain indoors and that consume an all-meat diet. The signs are similar to those seen in kittens but may be less severe. Over time, the bones become brittle and fracture easily. Because bones mature at different rates, both rickets and osteomalacia can be seen in the same animal.

Affected animals should be confined for the first few weeks while the diet is corrected. The response to proper nutrition is rapid. Within 1 week the animals become more active and show an improved attitude. Jumping or climbing must be prevented because the skeleton is still susceptible to fractures. Restrictions can usually be relaxed after 3 weeks, but confinement with limited movement is recommended until the skeleton returns to normal. Response to treatment can be monitored using x-rays.

Metabolic Osteodystrophies (Defective Bone Formation due to Metabolic Abnormalities)

In both primary hyperparathyroidism (see Disorders Associated with Calcium, Phosphorus, and Vitamin D in Dogs : Primary Hyperparathyroidism) and renal secondary hyperparathyroidism (see Disorders Associated with Calcium, Phosphorus, and Vitamin D in Cats : Rubber Jaw Syndrome (Renal Secondary Hyperparathyroidism)), defective bone formation results from metabolic abnormalities.

Rubber Jaw Syndrome (Renal Secondary Hyperparathyroidism)

A disorder seen occasionally in cats, rubber jaw syndrome is caused by an excess of parathyroid hormone (hyperparathyroidism) due to longterm kidney disease or failure. With progressive kidney disease, excess phosphate in the blood leads to lower calcium levels. Decreased calcium levels in turn trigger an increase in parathyroid hormone levels. In addition, the kidneys are necessary to produce the active form of vitamin D (calcitriol). Too little calcitriol leads to further increases in parathyroid hormone levels.

The most obvious signs include those related to kidney malfunction (vomiting, dehydration, excessive thirst and urination, depression), loose teeth that may fall out while chewing, and jawbones that become softened and pliable (rubber jaw syndrome) and fail to close properly.

This type of hyperparathyroidism is diagnosed when laboratory test results show abnormalities consistent with kidney malfunction. Tests will also reveal increased levels of parathyroid hormone in the blood.

Treatment options include modifying the diet, supplementing it with active vitamin D (calcitriol), and giving medication that binds phosphate. Any underlying kidney disease must be managed as well. Prescription diets with restricted dietary phosphorus are available. Your veterinarian can give you specific recommendations for proper treatment options for your cat. Be sure to follow those recommendations and any prescriptions precisely as directed.