One of the most common diseases we treat as small animal veterinarians is renal failure and renal insufficiency in cats and dogs. We are desperate to do more for these patients – to keep them eating and comfortable with minimal intervention for as long as possible. In the past 10 years, there has been much controversy regarding the use of calcitriol (1,25 dihydroxyvitamin D) to slow the progression of renal failure in cats and dogs.
In lab animal research and years of human use, calcitriol has been used to reduce renal secondary hyperparathyroidism. However, evidence suggests that it is most effective before the onset of excess parathyroid hormone secretion and the hyperphosphatemia that results. Newer synthetic vitamin D analogs may have other actions besides vitamin D receptor activation that benefit ill kidneys, although their injectable, short-acting formulations limit their use in veterinary medicine. A recent study of calcitriol use in cats showed no decrease in PTH concentrations in either normal or renal failure cats. This suggests that if the goal is to reduce PTH, the doses used in this study were not adequate, the sample size was too small, or the trial length too short.
The key question for veterinarians and clients, is whether the use of calcitriol will benefit an individual patient. While mulling over this question, the motto “DO NO HARM” lurks inevitably in the foreground. I have seen many patients, particularly cats, who lived far long and better on calcitriol than expected. Although the same can be said of some animals with renal failure NOT on calcitriol, especially those on a phosphorus-restricted renal diet.
What are the risks?
· Animals can become hypercalcemic at any time during therapy (days, weeks, months, years). Since this cannot be predicted, frequent blood calcium & phosphorus monitoring is essential. Once detected, stopping calcitriol and later reducing the dose typically resolves the hypercalcemia. However, if the animal has had a Ca x P > 60 for a prolonged period this may result in permanent dystrophic mineralization and reduced GFR.
· Dystrophic mineralization is also a risk for patients who are hyperphosphatemic.
What are the benefits?
· Delayed onset of renal secondary hyperparathyroidism and signs of uremia.
· Improved quality of life.
Which animal is a candidate?
· Renal failure or insufficiency with normal total and ionized calcium and phosphorus <>
· The animal must have an owner willing to commit to the time and expense of frequent monitoring – q 1 week initially, then q 1-2 months for the duration of Calcitriol therapy.
o I typically Rx only 1 month’s worth of calcitriol at a time. I put no refills on the 1st Rx and only 1 refill on subsequent Rx’s to encourage the owner to return for recheck blood work. No refills will be given until the patient returns.
o Warn owners of the potential for hypercalcemia and worsening of renal disease, even despite close monitoring.
Monitoring
· Obtain baseline chemistry panel (must include total calcium, phosphorus, BUN, creatinine) and baseline PTH and ionized calcium.
· Start calcitriol at the low end of the dose if PTH is elevated. Recheck calcium, phosphorus, BUN, creatinine in 1 week. If values are stable, continue for 3 more weeks.
· At 1 month, repeat chemistry panel (must include total calcium, phosphorus, BUN, creatinine) and baseline PTH and ionized calcium.
· If PTH is within normal limits, continue at the same dose of calcitriol and recheck q 1-2 months. If PTH remains above normal limits, increase the dose (up to 3.5 ng/kg/day) and recheck in 1 week and in 4 weeks.
· If hypercalcemia occurs, stop calcitriol and recheck total calcium, phosphorus, BUN, creatinine in 1 week. If the hypercalcemia has resolved and phosphorus remains below 6 mg/dl, consider restarting calcitriol at 50% the previous dose. Others discontinue calcitriol altogether at this point.
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