Vitamin D intoxication caused by ingestion of commercial cat food in three kittens

Abstract

Hypervitaminosis D in cats has been reported from ingestion of vitamin D 3 -containing rodenticide and pet food. Affected animals present with lethargy, chronic weight loss, anorexia, polyuria, episodic vomiting and signs of respiratory disturbance, such as cough and difficulty in breathing. Laboratory changes in cats with hypervitaminosis D included hypercalcaemia, hyperphosphataemia, alkalosis, high urea and creatinine concentrations, hypercalciuria and a decrease in urine concentrating ability. 1-4 Case descriptionsA 6-month-old sexually intact male British Shorthair cat (cat 1) weighing 2.5 kg presented to the Veterinary Teaching Hospital of the Ludwig Maximilian University of Munich for a 3-week history of polyuria, lethargy and laboured breathing breathing. The cat's littermate (2.3 kg sexuallyintact female -cat 2) also living in their household, showed similar, but less severe, signs. One year previously, a sibling of the two cats (cat 3) (same parents, but from a previous litter) had been presented by the same owners because of similar, yet more severe, clinical signs (polyuria, polydipsia, lethargy, anorexia, coughing for 3 months) at the age of 5 months. This cat had been euthanased owing to his overall bad condition, poor prognosis and financial constraints after the initial diagnostic evaluation had revealed renal failure with marked renal azotaemia, metabolic acidosis, hyperphosphataemia, marked anaemia and severe hypercalcaemia, as well as severe radiographic lung changes characterised by a generalised bronchointerstitial pattern and peribronchial cuffing.On physical examination cat 1 was lethargic and moderately dehydrated. It showed polypnoea with AbstractTwo siblings, a 6-month-old sexually intact male weighing 2.5 kg (cat 1) and a sexually intact female (cat 2) British Shorthair cat weighing 2.3 kg, were examined because of a 3-week history of polyuria, lethargy and laboured breathing. One year previously, another sibling (cat 3) had been presented because of similar, yet more severe, clinical signs at the age of 5 months. Physical examination revealed lethargy, dehydration and polypnoea with slightly increased inspiratory effort. Diagnostic investigation revealed severe hypercalcaemia (cats 1-3), renal azotaemia (cats 1 and 3) and a radiologically generalised miliary interstitial pattern of the lungs (cats 1-3) attributable to hypervitaminosis D caused by ingestion of commercial cat food. Cat 3 was euthanased. Cats 1 and 2 were treated with isotonic saline solution (180 ml/kg IV daily), sucralfate (30 mg/kg PO q12h), terbutaline (only cat 1: 0.1 mg/kg SC q4h), furosemide (1.5 mg/kg IV q8h) and tapering doses of prednisolone. Cat 2 was normal on day 14. Cat 1 had stable renal disease and was followed up to day 672. The radiological generalised military interstitial pattern of the lungs had improved markedly. Excessive cholecalciferol-containing commercially available cat food poses a great hazard to cats. Supportive treatment may result in long-term survival and improvement of radiological pul...

Chronic Vitamin D Intoxication in Captive Iberian Lynx (Lynx pardinus)

“…In the lynx with subclinical toxicosis this moderate degree of hypercalcemia was not surprising and the absence of marked hypercalcemia may be explained by the hormonal adjustments after chronic exposure to high doses of vitamin D as backed up by low PTH. In captive lynx with renal disease calcium concentrations were higher but still lower than what has been reported in vitamin D intoxicated cats [ 6 , 17 – 19 ]. In these lynx, renal failure may have influenced plasma calcium since cats with renal disease tend to show hypocalcemia [ 20 ].…”

“…An increase in extracellular calcium is the main feature of vitamin D toxicity in many species [ 3 – 5 , 10 ]. Captive lynx showed elevated plasma calcium concentrations when compared with free range lynx, however the magnitude of hypercalcemia was moderate and much lower than what has been reported in clinical cases of vitamin D toxicosis in domestic cats [ 6 , 17 – 19 ]. Previous reports of vitamin D intoxication in cats have mostly described acute toxicosis due to ingestion of vitamin D-containing rodenticides [ 6 , 17 , 18 ], which is different to the prolonged exposure to supplements with high vitamin D concentrations to which captive lynx were subjected.…”

Treatment of Ionized Hypercalcemia in 12 Cats (2006–2008) Using PO‐Administered Alendronate

“…Therefore, inhibiting osteoclast activity should decrease serum iCa concentrations and improve clinical signs if this hypothesis is true. Possible explanations for increased bone resorption include feeding an acidifying,12 magnesium‐restricted diet13; increased vitamin D14 intake with or without increased vitamin A15 intake; decreased copper intake16; increased aluminum intake17; and, acquired or genetic abnormalities in the calcium‐sensing receptor 18…”

Clinical Management of Avian Renal Disease

“…14 In cases of hypervitaminosis D associated with hypercalcemia, fluid therapy and treatments stimulating calciuresis, such as bisphosphonates and corticosteroids, are recommended in dogs and cats. 120,121 Unfortunately, the use of corticosteroids is controversial in birds owing to the risk of associated immunosuppression and safe doses of bisphosphonate have not been described in birds. Because metastatic calcifications are irreversible, prognosis is guarded.…”