Felipedia

Secondary Hyperparathyroidism (Renal) See also Parathyroid gland

Renal secondary hyperparathyroidism is an important complication of chronic renal insufficiency (CRI) and may occur early in the course of the disease. It results presumably from the combined influence of phosphorus retention and decreased production of 1,25-dihydroxyvitamin D (calcitriol). In a recent study of cats with spontaneous CRI, the overall prevalence of renal secondary hyperparathyroidism was 84 per cent. Hyperparathyroidism was documented in 100% of cats with end-stage CRI and 47% of clinically normal cats with only biochemical evidence of CRI. Hyperparathyroidism was detected even in some cats with normal serum calcium and phosphorus concentrations.

Calcitriol (1,25-dihydroxycholecalciferol) is the most biologically active form of vitamin D and is produced by 1-alpha hydroxylation of 25-hydroxycholecalciferol in the kidneys. As functioning renal mass declines, the ability of the kidneys to produce 1-alpha-hydroxylase is impaired, which results in decreased calcitriol concentrations. This leads to a decrease in calcium and phosphorus absorption and ultimately elevated serum parathyroid hormone (PTH) concentrations. PTH is a uremic toxin.; elevated serum concentrations have been associated with a variety of physiological abnormalities.

Exogenous administration of calcitriol in dogs and cats has been shown to decrease serum PTH concentrations. Current evidence supporting the use of calcitriol in cats with CRI is limited to a survey of veterinarians who use the drug routinely in the management of their CRI patients. Results of this survey were favourable and imply that patients treated with calcitriol seemed brighter, were more active, has better appetites, and lived longer than cats not treated with the drug. Randomised, controlled clinical trials examining the use of calcitriol in the management of feline CRI currently are in progress.

Before initiation of therapy with calcitriol, the serum phosphorus concentration should be stabilised within the normal range (<6.0 mg/dl). Controlling hyperphosphatemia increases the effectiveness of calcitriol therapy and minimises the potential for dystrophic mineralisation should hypercalcemia occur after therapy has been initiated. Although hypercalcaemia apparently does not occur as commonly in veterinary patients as it does in human beings, it is a serious complication that could lead to further renal impairment. Calcium-containing phosphorus binding agents (such as calcium carbonate) must be avoided when using calcitriol, because this combination could potentiate the development of hypercalcaemia.

The recommended dose of calcitriol is 2.5 to 3.5 ng/kg PO daily to cats with CRI. Individual dosage adjustments must be based on serial evaluations of serum calcium, phosphorus, and PTH concentrations. The goal of calcitriol therapy is to normalise the serum PTH concentration without inducing hypercalcaemia. After treatment is initiated, the patient's calcium, phosphorus, PTH, creatinine and serum urea nitrogen levels should be monitored serially (1 week, 1 month, then every 2 months).