A puppy resting with its turtle toy.

Nutritional Secondary Hyperparathyroidism in Pets

New puppy and kitten owners may feel overwhelmed with information about raising a young pet to adulthood. There seems to be advice coming from everywhere: friends, family, the internet, and your veterinarian. Fads come and go, sometimes to the detriment of your pet’s health. Incorrect advice regarding feeding your puppy or kitten may be harmful, leading to potentially severe abnormalities in growth. One such nutritionally-related disease is nutritional secondary hyperparathyroidism.

What Is Nutritional Secondary Hyperparathyroidism?

Nutritional secondary hyperparathyroidism is a disease that occurs as a direct result of feeding diets either too low in calcium or too high in phosphorus. The resulting mineral imbalance leads to demineralization of the bones (osteopenia). Osteopenic bones are weak, painful, and prone to fractures resulting in a host of severe clinical signs. The disease may be accompanied by other metabolic issues.

Pathophysiology of the Disease

Although we mostly associate calcium with bones and teeth, calcium actually plays a vital role in muscle contraction (even the heart muscle), blood clotting, transmission of nerve impulses, and cell membrane stability and permeability.

When an animal, especially a growing one, eats a diet low in calcium or high in phosphorus, a cascade of hormones is set into action to maintain the level of calcium in the blood. Low blood calcium causes serious physiological disorders, including loss of heart muscle function and seizures. Therefore, the body will do all it can to avoid having low calcium levels, even if that means taking calcium from the bones.

Here is the progression of physiological changes caused by low or high calcium intake:

Low dietary intake of calcium —> low blood calcium —-> stimulation of PTH (parathyroid hormone) —-> release of calcium from bone into the bloodstream, kidneys increase reabsorption of calcium and excrete more phosphorus, GI tract increases absorption of calcium and phosphorus, thus normalizing blood calcium levels.

High dietary intake of phosphorus —> causes high blood phosphorus—> leads to lowering of blood calcium levels— > triggers release of PTH (parathyroid hormone)—> release of calcium from bone into the bloodstream, kidneys increase reabsorption of calcium and excrete more phosphorus, GI tract increases absorption of calcium and phosphorus, thus normalizing blood calcium levels.

What Types of Diets Cause Secondary Hyperparathyroidism?

Diets should be 0.8 – 1.2% calcium on a dry matter basis. The calcium to phosphorus ratio should not exceed 1:1 to 2:1 in puppies (large-breed puppies should be on the lower end of this range). Kitten foods should fall closer to a 1:1 ratio. Homemade diets that consist of all meat, or conversely, all grain, will fail to meet these guidelines. If feeding a brand name, pre-made diet that meets AAFCO requirements, the proper dietary calcium to phosphorus ratio will be met. It is always safer to feed young puppies and kittens high-quality, pre-made puppy or kitten food for this reason.

What Are the Signs of Nutritional Secondary Hyperparathyroidism?

In both puppies and kittens, clinical signs of nutritional secondary hyperparathyroidism are usually related to decreased bone density and osteopenia. Affected animals will be reluctant to move and their limbs will be painful when palpated. Pathologic, painful fractures of the limbs may occur as the bones become weak from lack of calcium. Neurological signs directly related to low blood calcium, such as seizures or muscle twitching, may also be seen. Vertebral body fractures occasionally occur and the resulting instability within the vertebral canal may directly affect the spinal cord, resulting in paresis or paralysis.

How Will My Veterinarian Diagnose Hyperparathyroidism?

This disease is often diagnosed based upon observation of clinical signs and discussion of diet alone, but often other diagnostics are recommended. If your pet is showing signs of lameness or is in pain when a limb is palpated, radiographs of the affected limb are in order to rule out pathologic fractures. Signs of osteopenia (bone loss) are easily noted on radiographs of affected animals.

Blood tests may also be utilized to confirm a diagnosis. Blood levels of calcium may be normal or low while phosphorus levels may be low to high. Serum PTH levels may also be elevated. Other biochemical parameters are usually normal, with the exception of a mild increase in alkaline phosphatase.

How Is Hyperparathyroidism Treated?

Thankfully, the addition of proper nutrition will allow most affected animals to recover completely. Consuming a diet with the proper calcium and phosphorus ratio will allow bones to once again sequester calcium, resulting in normalization of growth and healing of pathologic fractures. Radiographic improvement may be seen in as little as 3 – 4 weeks after starting an appropriate diet. Cage rest to restrict a puppy or kitten’s activity while recovering is recommended, as well as giving pain medications to improve comfort. On occasion, additional calcium supplements are given for short periods, if blood calcium levels are severely low.

If a young animal has suffered from spinal cord paralysis secondary to a pathologic vertebral fracture, they are unlikely to recover complete limb function, even after the vertebra has healed due to the initial spinal cord damage. Kittens or puppies with severely misshapen bones due to a chronic, late-treated disease, may also never appear to recover completely. Nutritional secondary hyperparathyroidism, although rare, is a totally preventable disease that no pet should ever endure.