From the Vets -- Published Comments - from Books, Papers, Articles, on the Web, etc.
From the July 2011 Presentation to the 63rd CVMA Convention -- Chronic Kidney Disease (CKD) in Dogs & Cats - The Pivotal Role of Phosphorus Control by Dennis J. Chew, DVM Dipl ACVIM.
Hormone replacement: Calcitriol
Calcitriol treatments help to decrease PTH or prevent its increase in those with renal secondary hyperparathyroidism. This occurs mostly by genomic effects to block PTH synthesis in addition to a mild calcemic effect, and antiproliferative effect that prevents parathyroid gland hyperplasia. During treatment of CRF patients with calcitriol, simultaneous monitoring of serum ionized calcium, serum phosphorus and PTH concentrations is the ideal way to document successful and safe control of renal secondary hyperparathyroidism.
Calcitriol should not be administered until hyperphosphatemia has been controlled. If the Ca X P solubility product exceeds 60-70, calcitriol should be avoided because of the risk of soft-tissue mineralization. The beneficial effects of calcitriol are also lessened within the parathyroid gland when ionized calcium remains low. Phosphorus restriction relieves phosphate-mediated inhibition of the renal 1α-hydroxylase system, resulting in enhanced endogenous synthesis of calcitriol and subsequent inhibition of PTH synthesis. The effectiveness of calcitriol in control of hyperparathyroidism has been noted to increase in patients in whom serum phosphate was lowered.
Supplementation with calcitriol in CRF was initially designed as a daily therapy for life in veterinary patients as long as serum phosphorus remains within the normal range and serum calcium does not become increased. An extremely low dosage of calcitriol (2 to 3 ng/kg/day) has been used in dogs and cats with stable CRF to reverse renal secondary hyperparathyroidism. Serum PTH concentrations decrease during calcitriol administration over a period of weeks to months. Calcitriol is manufactured in capsule (250 or 500 ng) and liquid (1000 ng/mL) forms. Reformulation by a compounding pharmacy may be necessary to provide accurate dosing. In a recent study, dogs with CRF treated with calcitriol survived for a median of 365 days compared to 250 days in dogs treated with placebo. Similar studies were done in cats by the same investigators who concluded that there is no advantage to calcitriol treatments in cats with CRF but the study followed cats for just one year. In order to show a difference in treatment effect if one exists, studies in cats with CRF must be conducted for at least 2 and possibly 3 years due to the inherently slow nature of the progression of chronic renal disease in this species.
Intermittent rather than daily dosing treatment protocols are likely to become the standard of care since less hypercalcemia occurs during this protocol. The equivalent dose given at 2.5 ng/kg daily is given instead every 3.5 days. This works out to a dose of 9 ng/kg (8.75 ng/kg rounded to 9 ng/kd). It is important to give the dose every 3.5 days, rather than on day 1 & 4. For example if a dose is given Tuesday PM the next dose should be given Saturday AM. This is the longest time in between dosing that will still suppress the parathyroid gland. This method of dosing is especially attractive for cat owners since medication will only be given twice weekly.
From the 2007 book "Your Cat - Simple New Secrets to a Longer, Stronger Life," by Elizabeth M. Hodgkins, DVM, Esq., former owner of the All About Cats Health & Wellness Center in Yorba Linda, CA, and nationally-known breeder of Ocicats.
Cats with CRD typically develop a condition known as renal secondary hyperparathyroidism. This means that when the kidneys become unable to do their normal work of controlling the levels of phosphorus and calcium in the bloodstream, the parathyroid glands, located right next to the thyroid glands in the neck, begin to work harder to keep the level of blood calcium in balance with rising blood phosphorus by secreting parathyroid hormone (PTH). Balance between the calcium and phosphorus in the blood is critical for the health of all animals. This balance requires the activation of vitamin D (a hormone as well as a vitamin) by the kidneys. When the cat's kidneys begin to fail, they lose the ability to activate vitamin D normally. They also lose the ability to excrete excess phosphorus. As active vitamin D levels drop, blood calcium also drops and blood phosphate levels start to climb. In response, the parathyroid gland secretes PTH.
But ailing kidneys may not have the ability to activate vitamin D no matter how much PTH is put out by the parathyroid glands. Even though more and more PTH is secreted, in CRD the kidney simply cannot respond. Soon there is so much circulating phosphate that it begins to combine with the blood calcium, and calcium phosphate crystals begin to form deposits in the body's soft tissues. This removal of calcium from the circulation causes the bones to release calcium to maintain the blood calcium level. As mineral leaves the bones, they become soft. The bone crystals deposited in the soft tissues, including the kidneys themselves, interfere with the normal functioning of those tissues.
To control this vicious cycle of imbalance and renal failure, veterinarians try to limit the normally high dietary phosphorus intake of the meat-eating carnivore by feeding protein and phosphorus-restricted diets or by adding a phosphorus binder to higher protein and phosphorus containing foods. This latter approach is by far the better one, because limiting protein intake in the cat creates additional problems.
Recently, scientists studying cats with CRD have also begun to recommend supplemental calcitriol to control renal secondary hyperparathyroidism (see https://groups.yahoo.com/neo/groups/Calcitriol/info). Calcitriol is the active form of vitamin D. Daily or intermittent supplementation with very small doses of calcitriol in mild to moderate CRD may be able to stop or greatly slow this overproduction of PTH, with its very serious consequences ... Used properly by the veterinarian prescribing appropriately low doses and sufficient patient monitoring to avoid excessive blood calcium levels, calcitriol supplementation promises to one of the most effective new CRD management tools in cats with this life threatening disease. (Pages 219-220)
Today, all of my CRD cats that are candidates for daily low-dose calcitriol supplementation receive this additional therapy as part of their CRD management. I am encouraged that this addition to my CRD protocol will provide even better long-term results for these patients. (Page 227)
What about calcitriol and kidney failure?
Calcitriol is a controversial treatment for cats with kidney failure – depending on where you live your vet may or may not advocate this treatment. For example, it is rarely used in the UK although quite common in certain practices in the USA.
Calcitriol is a naturally produced hormone that helps to control calcium levels in the body. It has been proposed as a treatment for cats with kidney failure as a method of normalising levels of parathyroid hormone which tend to be high in cats with this condition. Hyperparathyroidism (excessively high levels of parathyroid hormone) is common in cats with kidney failure and is thought to be harmful by exacerbating progression of their renal disease and making them feel ill (e.g. causing nausea and a poor appetite). Feeding a prescription kidney diet low in phosphate helps, as can phosphate binders, but calcitriol is also suggested by some clinicians to be useful in treating the hyperparathyroidism. Some vets feel that cats treated with calcitriol are brighter, have a better appetite, are more active and live longer. However, opinion is divided, there are some concerns over side-effects (mainly the risk of causing hypercalcaemia – an increase in blood calcium levels which can be very harmful) and there is no published hard evidence to back-up the claims made advocating the use of calcitriol in cats.
guidelines for conservatively treating chronic
kidney disease," Veterinary
Medicine, December 1, 2007,
#11 Provide calcitriol in dogs. Calcitriol is indicated in dogs with chronic kidney disease stages 3 and 4 to slow the progression of the disease and extend survival (evidence grade 1).18 However, do not begin calcitriol therapy until the patient's serum phosphorus concentration is 6 mg/dl or less. Unfortunately, evidence for or against calcitriol therapy in cats with chronic kidney disease is weak.
Calcitriol may be administered initially at a dose of 2.5 ng/kg/day. Monitor ionized calcium and parathyroid hormone (PTH) concentrations weekly until a treatment endpoint is reached. The dose of calcitriol may be adjusted to achieve a treatment endpoint of normalizing PTH concentrations without inducing hypercalcemia. Increase calcitriol doses about 0.75 to 1 ng/kg as needed to a maximum dose of 5 ng/kg. If hypercalcemia develops before PTH concentrations decline to normal, the dosage of calcitriol must be reduced to prevent adverse effects of hypercalcemia. An alternate approach is to attempt to provide two or three days total dose of calcitriol every second or third day. This dosage may mitigate the hypercalcemia and increase the effect on PTH concentrations.
Patients receiving calcitriol should have their serum calcium, ionized calcium, and phosphorus concentrations monitored at least every two to three months.
From Prolonging Life and Kidney Function - a paper presented at the 32nd Annual World Small Animal Veterinary Association (WSAVA) Conference in August 2007 in Sydney, Australia, by Dennis J. Chew, DVM, DACVIM (Internal Medicine), Professor, College of Veterinary Medicine, The Ohio State University; Stephen P. DiBartola, DVM, DACVIM (Internal Medicine), Professor and Associate Dean of Administration and Curriculum, College of Veterinary Medicine, The Ohio State University Columbus, OH, USA
Calcitriol as Treatment for Renal 2-HPTH
Calcitriol treatments help to decrease PTH or prevent its increase in those with renal secondary hyperparathyroidism. This occurs mostly by genomic effects to block PTH synthesis in addition to a mild calcemic effect and antiproliferative effect that prevents parathyroid gland hyperplasia. During treatment of CRF patients with calcitriol, simultaneous monitoring of serum ionized calcium, serum phosphorus and PTH concentrations is the ideal way to document successful and safe control of renal secondary hyperparathyroidism. Reformulation by a compounding pharmacy may be necessary to provide accurate dosing.
Calcitriol should not be administered until hyperphosphatemia has been controlled. If the Ca × P solubility product exceeds 60-70, calcitriol should be avoided because of the risk of soft-tissue mineralization. The beneficial effects of calcitriol are also lessened within the parathyroid gland when ionized calcium remains low. Phosphorus restriction relieves phosphate-mediated inhibition of the renal 1?-hydroxylase system, resulting in enhanced endogenous synthesis of calcitriol and subsequent inhibition of PTH synthesis. The effectiveness of calcitriol in control of hyperparathyroidism has been noted to increase in patients in whom serum phosphate was lowered.
Supplementation with calcitriol in CRF was initially designed as a daily therapy for life in veterinary patients as long as serum phosphorus remains within the normal range and serum calcium does not become increased. The majority of clinical patients with early CRF and creatinine concentrations between 2 and 2.5 mg/dL will have hyperparathyroidism effectively reversed or prevented by doses of calcitriol between 2.5 and 3.5 ng/kg/day. Doses lower than 2.5 ng/kg are rarely used, and occasionally a dose as high as 6 ng/kg/day is used when lower doses do not succeed in lowering PTH. After receiving the initial dose for 2 months, a recheck of serum PTH concentration will indicate if an incremental calcitriol dosage increase is necessary. A salutary effect of calcitriol treatment of CRF was recently shown in a placebo-controlled study of 37 dogs. The dose of calcitriol was adjusted according to serial ionized calcium and PTH determinations, and ranged from 0.75 to 5.0 ng/kg/day. Over the course of 1 year, there was a significant reduction in mortality rate in the group of dogs receiving calcitriol (28%) as compared to the placebo group (63% mortality). In dogs receiving calcitriol, the median survival time was 365 days, as compared to a median survival time of 250 days in those receiving a placebo (Polzin 2005). Thus, calcitriol therapy appears to have clinical benefit in dogs with chronic kidney disease. Similar studies were done in cats by the same investigators who concluded that there is no advantage to calcitriol treatments in cats with CRF but the study followed cats for just one year. In order to show a difference in treatment effect if one exists, studies in cats with CRF must be conducted for at least 2 and possibly 3 years due to the inherently slow nature of the progression of chronic renal disease in this species.
Based on recent evidence based medicine studies from clinical patients, control of renal secondary hyperparathyroidism should become a standard of care. Intermittent rather than daily dosing treatment protocols are likely to become the standard of care since less hypercalcemia occurs during this protocol.
In Consultations in Feline Internal Medicine, 5th Edition, (2007), Chapter 42, "Clinical Progression of Early Chronic Renal Failure and Implications for Management," written by Sheri J. Ross, DVM, David J. Polzin, DVM PhD, Dip. ACVIM, Professor of Internal Medicine at the University of Minnesota College of Veterinary Medicine, and Carl A Osborne, DVM PhD, Dip. ACVIM, Professor of Internal Medicine at the University of Minnesota College of Veterinary Medicine, write:
Renal Secondary Hyperparathyroidism
Renal secondary hyperparathyroidism is an important complication of CKD 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 CRF, the overall prevalence of renal secondary hyperparathyroidism was 84 per cent. Hyperparathyroidism was documented in 100 per cent of cats with end-stage CKD and 47 per cent of clinically normal cats with only biochemical evidence of CDK. Hyperparathyroidism was detected even in some cats with normal serum calcium and phosphorus concentrations.
Calcitriol (1,25-dihodroxycholecalciferol) 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 to dogs and
cats has been shown to decrease serum PTH
concentrations. Current evidence
Before initiation of therapy with calcitriol, the
serum phosphorus concentration should be stabilized
within the normal range (<6.0
Nagode, Chew, and Podell recommend that calcitriol be given at a dose of 2.5 to 3.5 ng/kg body weight PO per day to cats with CKD. Individual dosage adjustments must be based on serial evaluations of serum calcium, phosphorus, and PTH concentrations. The goal of calcitriol therapy is to normalize the serum PTH concentration without inducing hypercalcemia. After treatment is initiated, the patient's calcium, phosphorus, PTH, creatinine and serum urea nitrogen levels should be monitored serially (1 week, 1 month, and then every 1 to 2 months).
From a presentation to the Harris County Veterinary Medical Association by Alice M. Wolf, DVM, Diplomate ACVIM, dipABVP (Feline Practice), Texas A&M University College of Veterinary Medicine, College Station, TX, "Chronic Progressive Renal Disease in the Cat"
I am a proponent of the initiation of calcitriol therapy early in the course of CPRD [chronic progressive renal disease], in fact, even before azotemia becomes apparent. I have been impressed with the improvement in attitude, appetite, and sense of well-being in many of my patients with these subtle signs of early disease. A complete discussion of the many effects of calcitriol is beyond the scope of this discussion. In brief, it acts to lower PTH levels and help prevent the development of renal secondary hyperparathyroidism with its attendant negative effects. In order to use calcitriol, the serum calcium value should be normal and the serum phosphorus value < 6.0 mg/dl. I start at a calcitriol dose of 2.5 to 3.5 ng/kg PO q24h. Our pharmacy makes a suspension of calcitriol in a concentration of 25 ng/ml so it can be measured accurately and the volume administered is not excessive. Cats receiving calcitriol should have serum calcium/phosphorus levels monitored periodically to assure that the agent is working and that hypercalcemia has not occurred. If hypercalcemia persists or serum phosphorus levels rise above the normal range and cannot be managed with diet/phosphate binders, calcitriol treatment must be discontinued.
From Morris Animal Foundation, AnimalNews, VOLUME 5 NUMBER 4, December, 2005
Longer lives for dogs with kidney disease
A PROMISING DRUG FOR CRF
Chronic renal failure (CRF) is a common disease in older dogs, affecting about 10 percent of dogs over the age of 12.Typical clinical signs include increased thirst, increased urine (or, rarely, a decrease in urine), weight loss, decreased appetite, vomiting, muscle wasting, lethargy, bad breath, oral ulcers and sometimes diarrhea. One treatment option that has helped to prolong these dogs’ lives is diet therapy. Dogs with CRF who eat special diets live about three times longer than those who don’t, but there is still no cure. This is why more research is needed to understand the causes of the disease and ways to slow its progression. Dr. David Polzin is making great strides. With funding from Morris Animal Foundation, he recently completed a clinical trial at the University of Minnesota that points to a promising new treatment option.
When a dog’s kidney is functioning normally, it produces a hormone called calcitriol, which scientists believe helps to manage fluid and electrolyte balance and excrete waste as urine. In CRF, calcitriol levels drop, and the kidney can no longer adequately perform these functions. Based on this knowledge, Dr. Polzin wanted to determine whether providing small doses of calcitriol in addition to diet therapy would benefit dogs with kidney failure. His team gave calcitriol to a group of dogs with CRF while another group received a placebo of flavored olive oil. To eliminate bias, neither the researchers nor the pet owners knew which group was receiving the calcitriol. During the study, the dogs were monitored for changes in their kidney function, biochemical changes, decline in quality of life and survival.
Dr. Polzin’s team determined that a daily low dose of calcitriol stabilized kidney function, slowed the progression of the disease and prolonged survival. As recently as a decade ago, dogs with CRF often survived less than six months after diagnosis. Today the outlook is much more promising, thanks to treatment advances like this one. While there is no simple plan for preventing canine kidney disease, with good nutrition and calcitriol therapies, dogs with CRF can often enjoy many more years of high-quality life.
From a 6/1/05 article "Managing chronic diseases in cats," in DVM-the Newsmagazine for Veterinary Medicine, Dr. Susan Little, DVM, Diplomate of the ABVP (Feline Practice), President of the Winn Feline Foundation, co-owner of Bytown Cat Hospital and Merivale Cat Hospital in Ottawa, Canada, and Feline Internal Medicine Consultant for the Veterinary Information Network (VIN), writes :
Calcitriol (2 to 3 ng/kg orally every 24 hours) may help prevent and treat elevations in parathyroid hormone (PTH) concentrations associated with chronic renal insufficiency. Controlling PTH may reduce PTH toxicosis, slowing chronic renal insufficiency progression and improving appetite and well-being. It is only administered when phosphorus concentrations are normal and the calcium × phosphorus product is under 60. It's important to educate clients and ensure compliance when you use calcitriol because you must monitor patients' PTH and ionized calcium concentrations regularly. Serum calcium must be monitored at one and two weeks after the start of calcitriol therapy and every six months thereafter. PTH levels should be monitored monthly until normalized.
From a paper presented at the 30th annual World Small Animal Veterinary Association (WSAVA) in May 2005 in Mexico City, Mexico::
Sherry Sanderson, BS, DVM, PhD, DACVIM, DACVN
CALCITRIOL THERAPY IN CHRONIC RENAL FAILURE
In CRF, the number of functioning renal tubules progressively decreases, resulting in the loss of renal tubular cells that synthesize calcitriol. In addition to reduced synthesis of calcitriol due to loss of renal tubular cells, high levels of serum phosphorus that accumulate as glomerular filtration rate (GFR) decreases also impairs calcitriol synthesis by inhibiting 1-hydroxylation of 25-hydroxyvitamin D to produce 1,25-dihydroxyvitamin D (calcitriol). Calcitriol is the most biologically active form of vitamin D.
The initial effects of calcitriol deficiency are temporarily halted by a compensatory elevation in parathyroid hormone (PTH) concentrations (renal secondary hyperparathyroidism). The potent activation of calcitriol formation by parathyroid hormone (PTH) is due, in part, to its phosphaturic lowering of renal tubule cell phosphorus levels, thereby partially relieving the inhibition phosphorus has on calcitriol formation. Surprisingly, although high levels of serum phosphorus inhibit calcitriol, lowering serum phosphorus levels below normal does not raise serum calcitriol levels above normal in dogs. In addition, overt hyperphosphatemia is not a prerequisite for phosphorus to have an effect on PTH secretion. High dietary phosphorus intake may accentuate uremia-induced abnormal phosphorous metabolism, causing an increase in parathyroid cell phosphorous concentration, and dietary phosphorus restriction has been shown to decrease PTH secretion without changing serum calcitriol levels. In untreated human patients with mild to moderate CRF (serum creatinine concentration < 3.0 mg/dl), serum phosphorus concentrations correlated directly with PTH, independent of serum calcium and calcitriol levels, and this correlation was present despite the fact that most patients had serum phosphorous concentrations within the normal range.
Renal Secondary Hyperparathyroidism
Renal secondary hyperparathyroidism occurs to some extent in most dogs and cats with CRF. In a recent study in cats with spontaneous CRF, the overall prevalence of renal secondary hyperparathyroidism was 84%. The prevalence of renal secondary hyperparathyroidism in asymptomatic cats with CRF was 47%, and it was 100% in cats with end-stage CRF.
Relative or absolute deficiency of calcitriol is thought to play a central role in the development of renal secondary hyperparathyroidism. Excessive levels of PTH in CRF can have toxic effects on multiple tissues and organs. Some of these toxic effects include:
Excess PTH levels may also promote nephrocalcinosis and consequent progressive loss of renal function. Increased PTH causes damage to tissues by interacting with the PTH or PTHrP receptor in target cells to increase levels of intracellular ionic calcium. High cellular calcium is toxic by activating various enzymes that destroy cell membranes, proteins and nucleic acids. Ultimately, accumulation of intracellular calcium disrupts mitochondrial production of ATP, diminishing tissue energy.
Rationale for Calcitriol Therapy
The primary goal of calcitriol therapy is to prevent or correct renal secondary hyperparathyroidism and its adverse effects. Calcitriol decreases PTH levels in blood. Recommendations vary for when in the course of CRF to start calcitriol therapy. However, one potential argument for starting calcitriol supplementation in early CRF is the possibility of minimizing the toxic effects associated with renal secondary hyperparathyroidism. A potential adverse effect of calcitriol supplementation is the development hypercalcemia. Although hypercalcemia reportedly occurs in 30% to 57% of humans treated with calcitriol, hypercalcemia appears to be an uncommon side effect in dogs treated with calcitriol at the recommended doses. However, the potential benefits of calcitriol supplementation in patients with CRF must be balanced with the lack of randomized, controlled clinical trials to support its use. Clinical studies using calcitriol supplementation in both dogs and cats with naturally-occurring CRF are in progress, and results from these studies should help provide a clearer understanding of the pros and cons of its use. It is also important to provide careful medical care.
From a September 2003 lecture at the DC Academy of Veterinary Medicine, "Renal Disease / Urology," (2) by Sheri Ross, DVM, University of Minnesota (1)
Vitamin D supplementation may be considered for
dogs and cats with proven renal secondary
hyperparathyroidism. In mild renal failure,
calcitriol deficiency results predominantly from the
inhibitory effects of phosphate retention on renal
1a-hydroxylase activity. As renal failure
progresses, loss of viable renal tubular cells
limits calcitriol synthetic capacity. Therefore,
over time, phosphate restriction alone may fail to
prevent renal secondary hyperparathyroidism,
necessitating vitamin D supplementation for complete
In Consultations in Feline Internal Medicine, 4th Edition (2001), Chapter 44, "Medical Management of Chronic Renal Failure", Katherine M. James, DVM, PhD, DACVIM, Educational Director of the Veterinary Information Network (VIN) and Urology - Nephrology Consultant for VIN, writes:
Calcitriol synthesis is decreased in CRF owing to nephron loss and decreased 1 - hydroxylase enzyme activity, and also is inhibited by increased phosphorus concentration. In CRF, especially when hyperphosphatemia is present, calcitriol concentrations are low and insufficient to stimulate adequate intestinal calcium absorption. This effect leads to hypocalcemia, which further stimulates PTH production in an attempt to return serum calcium concentration to normal. Supplementation with calcitriol will interrupt this cycle and mitigate secondary renal hyperparathyroidism. In addition to inhibiting the development of nephrocalcinosis, calcitriol also may inhibit the development of glomerulosclerosis, and thereby delay progression of renal disease. No randomized clinical trials of calcitriol therapy have been reported in naturally occurring CRF in dogs or cats. My own clinical experience and that of others suggest that calcitriol therapy improves quality of life and can slow progression of renal failure in these patients. However, patient selection for calcitriol therapy is very important. Calcitriol should be used on in those patients being followed closely and in those with serum phosphorus concentrations consistently less than 6 mg/dl (preferably near 4 mg/dl). Calcitriol is a very potent agent and may cause hypercalcemia. When serum phosphorus concentration also is high, nephrocalcinosis can occur with devastating and potentially irreversible effects on the kidney. The recommended therapeutic dosage for calcitriol is 2.5 to 3.5 ng/kg/day. Currently, I recommend calcitriol therapy in appropriate patents as soon as CRF is detected. Preferably patients receiving calcitriol should be monitored by measuring serum ionized calcium concentration rather than serum total calcium concentration whenever possible. Patients initially are monitored once every 1 to 2 weeks, and this interval is increased is serum calcium and phosphorus concentrations are stable and within normal limits.
One of the most influential drugs to be used by our practice in the treatment of kidney disease is Calcitriol. Calcitriol is a vitamin D analog. Its role in the treatment of kidney disease is very complicated but its overall effect is to decrease the levels of a specific hormone (parathyroid hormone) that can be detrimental to the patient who is experiencing kidney problems. We have had excellent results with this drug. In fact, it is the single most important new treatment that we can offer our patients. This drug greatly improved the prognosis for our patients who have early kidney disease and has been very important in extending many of our patient’s lives. Calcitriol is administered once daily orally and is well tolerated by our patients. Even cat owners seem to be able to medicate their feline friends with minimal fuss.
Excerpted from the Clinic's web site
This web site is a product of me, David Jacobson, and is maintained for the benefit of members of the Feline Calcitriol User group, veterinarians, cat and dogs owners, and others interested in the use of compounded calcitriol to treat cats and dogs with chronic renal disease (CRD). My thanks to Drs. Larry Nagode and Dennis Chew for allowing me to post their professional work here and to Dr. Nagode for his assistance in creating and maintaining this site. If you are now using or have used calcitriol to treat your own CRF pet, please email me your personal story for posting here! Your comments, suggestions and criticisms about this site are welcome and appreciated. David Jacobson, Arlington, VA