The way in which the body processes calcium and phosphate, the function of vitamin D (which acts more like a hormone than a vitamin), and the formation of bone are all tied together into a system that involves 2 other hormones—parathyroid hormone and calcitonin—that are secreted by the parathyroid glands.

Disorders of calcium and phosphorus metabolism that affect the skeletal system are discussed in the chapter on bone, joint, and muscle disorders (see Bone, Joint, and Muscle Disorders of Cats: Disorders Associated with Calcium, Phosphorus, and Vitamin D in Cats).

Calcium-regulating Hormones

Calcium is an essential component of the skeleton, and it has important functions in muscle contraction, blood clotting, enzyme activity, the nervous system, and hormone release, among others. Precise control of calcium in the body is vital to health. Parathyroid hormone, vitamin D, and calcitonin all interact to keep the level of calcium steady, despite variations in intake and excretion. Other hormones may also contribute to maintaining the balance of calcium in the body.

Parathyroid hormone is created and stored in the parathyroid glands, which are located on either side of the thyroid gland in the neck. The creation of this hormone is regulated by a feedback mechanism that involves the level of blood calcium. The primary function of parathyroid hormone is to control the level of calcium by affecting the movement of calcium into and out of bone, the retention of calcium by the kidneys, and absorption of calcium from the digestive tract.

Vitamin D is the second major hormone involved in the regulation of calcium metabolism. In several species, including horses and people, vitamin D is formed in the skin after exposure to ultraviolet light (such as sunshine). In contrast, cats are not able to form enough vitamin D in the skin and depend on dietary intake. Parathyroid hormone and conditions that stimulate its secretion, as well as reduced phosphate levels, increase the formation of vitamin D.

Calcitonin is a hormone secreted by certain cells of the thyroid gland in mammals. When the level of blood calcium increases, calcitonin is released to prevent hypercalcemia (abnormally high levels of calcium).

Hypocalcemia

Hypocalcemia is an abnormally low level of calcium in the blood, leading to twitching, muscle tremors, and seizures. The causes of hypocalcemia include previous surgical removal of the parathyroid glands (leading to hypoparathyroidism), kidney disease or failure, and calcium imbalance in nursing females.

Hypoparathyroidism is characterized by low calcium levels, high phosphate levels, and either temporary or permanent insufficiency of parathyroid hormone. It is uncommon in cats, but can be caused by previous removal of the parathyroid glands as a treatment for hyperthyroidism or for a parathyroid tumor. Common signs of hypocalcemia include muscle tremors and twitches, muscle contraction, and generalized convulsions. Diagnosis is based on history, signs, low calcium and high phosphorus levels, and the serum parathyroid hormone level. Other causes of hypocalcemia must be eliminated.

The goal of treatment is to return the level of blood calcium to normal and to eliminate the underlying cause. If a cat is having muscle spasms or seizures because of low calcium levels, immediate treatment with intravenous calcium is needed. Dietary supplements of calcium, often along with vitamin D, are prescribed for longterm treatment.

Chronic kidney failure is probably the most common cause of hypocalcemia. However, the hypocalcemia that occurs with kidney failure does not tend to lead to the nervous system signs that are seen in hypoparathyroidism. Treatment usually involves dietary restriction and treatment to lower phosphate concentration in the blood.

Several other diseases can also cause hypocalcemia (see Hormonal Disorders of Dogs: Causes and Treatment of Low Blood Calcium Levels (Hypocalcemia)).

Hypercalcemia

Hypercalcemia is an abnormally high level of calcium in the blood. The signs associated with this condition depend on how high the calcium level is, how quickly it develops, and how long it lasts. The most common signs are increased thirst and urination, followed by reduced appetite, vomiting, constipation, weakness, depression, muscle twitching, and seizures.

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Causes and Treatment of Hypercalcemia (Increased Blood Calcium Levels) in Cats Cause Mechanism Treatment Primary hyperparathyroidism (relatively rare in cats) Parathyroid glands are overactive (often due to a tumor) and secrete excessive parathyroid hormone Removal or destruction of tumor Hypercalcemia caused by cancer (malignant hypercalcemia) Increased bone breakdown and resorption triggered by cancer cells causes higher levels of calcium in blood Depends on specific type of cancer Chronic kidney failure Exact mechanism is unknown; most common cause of hyper-calcemia in cats Supportive care Vitamin D toxicity (hypervitaminosis D) Vitamin D supplements taken in excess (for example, to treat hypo-parathyroidism); accidental ingestion of human psoriasis medicine calcipotriene (tacalcitol) or rodent poisons containing calcitriol Adjustment of vitamin D dosage (if from medication) Granulomatous disease Inflammation activates the type of white blood cells that can increase levels of active vitamin D Treatment of underlying disease, for example, antifungal drugs or surgery Idiopathic hypercalcemia of cats Unknown cause; affects cats 2 to 13 years old (either sex) High-fiber diet and/or medication (prednisone)

In cats, kidney failure, tumors, and a newly recognized syndrome called idiopathic hypercalcemia are the most common causes of hypercalcemia (see Hormonal Disorders of Cats: Causes and Treatment of Hypercalcemia (Increased Blood Calcium Levels) in Cats).

Hypercalcemia is treated by identifying and treating the condition causing it. However, the cause may not always be apparent. Supportive treatment, including fluids, diuretics (“water pills”), sodium bicarbonate, and glucocorticoids, is often needed to lower the level of calcium in the blood.

Last full review/revision July 2011 by Deborah S. Greco, DVM, PhD, DACVIM; David Bruyette, DVM, DACVIM; Robert J. Kemppainen, DVM, PhD; Mark E. Peterson, DVM, DACVIM