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

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.

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.

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.