1,25-dihydroxycholecalciferol (calcitriol; 1,25-dihydroxyvitamin D) is a fat soluble pro-hormone produced in the cells of the proximal tubule of the nephron in the kidneys by the action of 25-hydroxyvitamin D3 1-alpha-hydroxylase. The principle action of calcitriol is to increase circulating blood calcium in response to decreased calcium caused by milk fever, rickets, nutritional secondary hyperparathyroidism, etc.
There are two major forms of vitamin D, D2 (or ergocalciferol) and vitamin D3 (or cholecalciferol). It is responsible for promoting the mineralisation of bones. It also aids the absorption of calcium and phosphorous by increasing absorption from the digestive tract and reducing urinary calcium loss and regulates blood calcium levels. It is produced in the fur (or skin in humans) upon exposure to sunlight and also ingested in small quantities via food. Foods containing vitamin D include fish, liver, dairy products and egg yolk.
Vitamin-D deficiency has been recorded as a genetic disease in cats, leading to rickets (nutritional secondary hyperparathyroidism). Vitamin-D responsive therapy is well-known in cats with chronic renal disease.
Vitamin D toxicosis (also known as hypervitaminosis D) is caused by the accumulation of toxic levels of vitamin D. The most common causes are cholecalciferol rodenticide poisoning, over-supplementing with vitamin D3, over-supplementation with vitamin D3 in the diet, and ingestion of plants containing calcitriol glycosides.
Vitamin D intoxication is sometimes seen in kittens and young cats due to overenthusiastic use of vitamin D supplements. Calcitriol, the active hormone synthesised from Vitamin D causes increased absorption of calcium and phosphorus from the gut, and its use is to stimulate bone growth in rapidly growing animals. Calcitriol also causes reabsorption of calcium in the kidneys; enabling normal mineralization of bone and preventing hypocalcemic tetany. It is also necessary for bone growth and bone remodeling by osteoblasts and osteoclasts. Its use in feline diets is questionable if the diet is nutritionally balanced.
Clinical signs are referrable to mineralisation of multiple organs, including lungs (chronic non-responsive cough), heart (cardiac murmurs, cardiomyopathy) and gastrointestinal signs (intestinal damage due to mineralisation of intestinal smooth muscle
Serum chemistry often shows very high levels of calcium and phosphorus but normal levels of creatinine and moderately high levels of blood urea nitrogen. The increased serum levels of calcium and phosphorus with no indication of renal failure was suggestive of chronic vitamin D toxicosis.
Excess vitamin D and its active metabolites will increase the absorption of calcium and phosphorus from the intestines. The level of calcium absorption from the intestine is dependent on the serum levels of calcium binding protein (CBP) which is usually elevated in excess vitamin D. The excess amount of calcium and phosphorus in the serum will precipitate in the lungs, kidneys, aorta, gastric mucosa and submucosa among others.
Symptomatic management of secondary disease is often the primary palliative treatment.
Reversal of organ mineralisation is gradual if the removal of vitamin D from diet is instigated soon enough. Permanent organ damage is common.
In severe cases, chelation drugs such as Desferoxamine are an option.
- Geisen V et al (2009) Vitamin D-dependent hereditary rickets type I in a cat. J Vet Intern Med 23(1):196-299