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Archive for the ‘Laboratory Tests’ Category

Practical Recent Abstracts

September 29, 2008 Leave a comment

Edited by Jennifer S. Fryer, DVM

The influence of crystalloid type on acid-base and electrolyte status of cats with urethral obstruction

Drobatz KJ, Cole SG. JVECCS 2008; 18: 355 – 361.

To compare the effect of a balanced isotonic crystalloid solution with that of 0.9% sodium chloride on the acid[ndash]base and electrolyte status of cats with urethral obstruction. Randomized prospective clinical trial. Academic veterinary emergency room.

Sixty-eight cats with naturally occurring urethral obstruction. Cats were randomized to receive either a balanced isotonic crystalloid solution (Normosol-R, n=39) or 0.9% sodium chloride (n=29) for fluid therapy. Baseline venous blood gas and blood electrolyte values were obtained at the time of admission and at intervals during the course of therapy. Baseline values were similar between groups.

Cats receiving Normosol-R had a significantly higher blood pH at 12 hours, a significantly greater increase in blood pH from baseline at 6 and 12 hours, as well as a significantly higher blood bicarbonate concentration at 12 hours and a significantly greater increase in blood bicarbonate from baseline at 6 and 12 hours. Conversely, the increase in blood chloride from baseline was significantly higher at 2, 6, and 12 hours in cats receiving 0.9% sodium chloride. There were no significant differences in the rate of decline of blood potassium from baseline between groups. Subgroup analysis of hyperkalemic cats (K+>6.0 mmol/L) and acidemic cats (pHEfficacy and tolerability of once-daily cephalexin in canine superficial pyoderma: an open controlled study

Toma S, Colombo S, Cornegliani L, Persico P, Galzerano M, Gianino MM, Noli C. Journal of Small Animal Practice 2008; 49: 384 – 39.

Objectives: The aims of this study were to evaluate the efficacy and tolerability of oral cephalexin given at 30 mg/kg once daily in dogs with superficial pyoderma and to compare them with those of oral cephalexin given at 15 mg/kg twice daily.

Methods: Twenty dogs with superficial pyoderma were treated with cephalexin at 30 to 60 mg/kg orally once daily (group A) and compared with 20 dogs treated at a dose of 15 to 30 mg/kg orally twice daily (group B). Dogs were treated until 14 days after clinical remission. Type and distribution of lesions, pruritus and general health status were assessed every 14 days using a numerical scale until 14 days after treatment discontinuation. Total scores for each evaluation day were compared between the two groups as well as time to obtain resolution and percentage of relapses.

Results: Resolution of superficial pyoderma was obtained in all dogs in 14 to 42 days (median 28 days for both groups), with no difference between groups. Six dogs experienced vomiting or diarrhoea but did not require discontinuation of the treatment. Only one dog (in group A) relapsed nine days after treatment discontinuation.
Clinical Significance: Once-daily cephalexin is as effective as twice-daily cephalexin in the treatment of canine superficial pyoderma.

****
Evaluation of antibodies against feline coronavirus 7b protein for diagnosis of feline infectious peritonitis in cats

Kennedy MA, Abd-Eldaim M, Zika SE, Mankin JM, Kania SA. AJVR 2008; 69: 1179-1182.

Objective—To determine whether expression of feline coronavirus (FCoV) 7b protein, as indicated by the presence of specific serum antibodies, consistently correlated with occurrence of feline infectious peritonitis (FIP) in cats.

Sample Population—95 serum samples submitted for various diagnostic assays and 20 samples from specific-pathogen–free cats tested as negative control samples.

Procedures—The 7b gene from a virulent strain of FCoV was cloned into a protein expression vector. The resultant recombinant protein was produced and used in antibody detection assays via western blot analysis of serum samples. Results were compared with those of an immunofluorescence assay (IFA) for FCoV-specific antibody and correlated with health status.

Results—Healthy IFA-seronegative cats were seronegative for antibodies against the 7b protein. Some healthy cats with detectable FCoV-specific antibodies as determined via IFA were seronegative for antibodies against the 7b protein. Serum from cats with FIP had antibodies against the 7b protein, including cats with negative results via conventional IFA. However, some healthy cats, as well as cats with conditions other than FIP that were seropositive to FCoV via IFA, were also seropositive for the 7b protein.

Conclusions and Clinical Relevance—Expression of the 7b protein, as indicated by detection of antibodies against the protein, was found in most FCoV-infected cats. Seropositivity for this protein was not specific for the FCoV virulent biotype or a diagnosis of FIP.

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Small Animal Test Guide

July 7, 2008 Leave a comment


In this guide, we answer the following questions on all the most common small animal tests:
Why do it?
What samples do I need and at what time should they be collected?
Does the animal need to be fasted?
What unique things should I know about this test?

ACTH Stimulation Test
B12/Cobalamin & Folate
Bile Acids Test
Bromide Concentration
Digoxin Concentration
Fructosamine
High-dose Dexamethasone Suppression Test
Endogenous ACTH
Free T4 by Equilibrium Dialysis
Insulin/Glucose
Low-Dose Dexamethasone Suppression Test
Parathyroid Hormone
Phenobarbital Concentration
PLI or cPL
T3 Suppression Test
TLI
Urine Cortisol:Creatinine Ratio
Urine Protein:Creatinine Ratio
von Willebrand’s Factor

Emergency Management of the Blocked Ferret

April 29, 2008 Leave a comment

By Christal Pollock, DVM, DABVP-Avian

Diagnosis of urethral obstruction in the male ferret is rarely a diagnostic challenge, but the need to place a urinary catheter in a 1-kg patient can be intimidating.

Urinary catheter placement can be challenging in the male ferret because of its small size and its J-shaped os penis. Locate the prepuce on the ventral abdomen just caudal to the umbilicus. The os penis is palpable. After gently extruding the penis, it may help to grasp the base with a gauze square. Aseptically prepare the penis, and use a 24-gauge catheter with the needle removed to find and dilate the urethral opening. The urethral opening is located on the ventral surface of the penis just proximal to the J-shaped curve.

After the urethral opening is found and dilated, pass a urinary catheter. A 3.5 Fr red rubber catheter may be used in a very large male, however most individuals require a smaller tube. A 3-Fr 11-in urinary catheter specifically designed for ferrets is available (Slippery Sam, Global Veterinary Products; New Buffalo, MI) or a 22- or 20-gague jugular catheter may be used. Pre-measure red rubber catheters and jugular catheters. Leave the jugular catheter stylet in place to facilitate passage, but manipulate the catheter carefully. Resistance most often occurs as the catheter travels around the pelvic flexure. Gently flush the urethra with sterile saline to facilitate catheter passage.

· Anesthesia is required for adequate muscle relaxation. Most individuals should be intubated and maintained on isoflurane or sevoflurane when anesthetized for extended periods. Avoid ketamine in ferrets with urethral obstruction.

· When urinary catheterization proves difficult, remove a small amount of urine once via cystocentesis to reduce pressure and allow passage of the urinary catheter. Repeated cystocentesis is not recommended because of thin bladder wall. In rare cases, percutaneous cystostomy may be performed when catheter placement fails.

· Suture butterfly tape strips near the prepuce to secure the catheter. Use tape to fasten the catheter or attached tubing to the tail base to minimize tension on the line. Bandaging the abdomen may also minimize the risk of rotation. Create a closed collection system by attaching a small intravenous bag and monitor urine production. The average 1-kg ferret produces 26-28 ml of urine over a 24-hour period (range: 8-48 ml).

· To catheterize the female ferret, place her in ventral recumbency and elevate the rear with a rolled towel. Aseptically prepare the vulva and perivulvar region, and then insert a sterile vaginal speculum or otoscope. Locate the urethral opening on the vestibule floor 1-cm cranial to the clitoral fossa. Insert a 3.5-Fr red rubber catheter, which may be fitted with a wire stylet.

The most important cause of dysuria or stranguria in the male ferret is prostatomegaly secondary to adrenal disease. Struvite urolithiasis may also cause urethral obstruction, however the incidence is relatively low now that ferret food is commercially available. (Cystitis and prostatic abscesses are uncommon but potential causes of stranguria and dysuria in the ferret). History and physical examination may provide clues to the underlying cause of urethral obstruction, but signalment is not particularly helpful. Most affected ferrets are middle aged to older, although any age may be affected.

Adrenal disease

Struvite urolithiasis

Diet

Good diet (Animal protein-based)

Bad diet (Plant protein-based)

Exam findings

Dorsal symmetrical alopecia

—–

Laboratory results

+/- Urinary tract infection

Non-regenerative anemia

Urinary tract infection

Crystalluria

Radiographs

Unremarkable

Radiopacity

Ultrasonography

Prostatomegaly

Adrenomegaly

—–

· Ferret adrenal disease is associated with an elevation in sex steroid hormones, and elevated androgen levels can leads to prostatomegaly. Dorsal symmetrical alopecia is also a common clinical sign.

· Ferrets require high quality, animal-based dietary protein. Therefore a low quality, plant protein-based diet promotes development of alkaline urine and struvite crystalluria.

· Ferrets normally have relaxed abdomens that are easy to palpate. Although pain will cause the abdominal muscles to tense, the over distended bladder is still palpable. There may also be evidence of urine dribbling and the prepuce may be red from excessive licking.

· Normal ferret biochemistry is similar to that in other mammals with a few exceptions. Creatinine in the ferret generally ranges from 0.1-0.3 mg/dL with values almost always less than 0.5 mg/dL. Creatinine from 0.7-1.0 mg/dL signifies azotemia.

· Obtain whole body survey radiographs using tabletop technique, high-speed film, and fine screen cassettes. Contrast radiography may be useful in identifying urethral stones. Enlarged adrenal glands are rarely visible on radiographs, and ultrasonography is needed. Note that renal cysts are a common incidental finding.

· Ferrets are relatively stoic animals, but do not ignore pain management. Provide preemptive analgesia, and monitor ferrets carefully for signs of discomfort. Signs of pain may include anorexia, lethargy, crying, stiff movements, squinting, and an inability to sleep in a natural, curled position.

References & Further Reading

Castanheira de Matos RE, Morrisey JK. Common procedures in the pet ferret. Vet Clin North Am Exot Anim Pract 2006; 9: 347-365.

Esteves MI, Marini RP, Ryden EB, et al. Estimation of glomerular filtration rate and evaluation of renal function in ferrets (Mustela putorius furo). Am J Vet Res 1994;55:166-172.

Pollock CG. Emergency medicine of the ferret. Veterinary Clinics of North America: Exotic Animal Practice. 10(2): 463-500, 2007.

Quesenberry KE, Carpenter JW, eds. Ferrets, rabbits, and rodents: clinical medicine and surgery. 2nd ed. St. Louis: WB Saunders Co, 2003: 2-134.

EHV-1 the neuropathogenic strain

April 29, 2008 Leave a comment

by Natalie Carrillo, MV, DVM, Dip ACVIM-LA

Recent outbreaks of myeloencephalopathy caused by equine herpesvirus (EHV-1) have generated new research that provides better information about diagnosis, treatment and outbreak management. The objective of this article is to summarize this information in a practical and applicable manner.

Clinical signs

The onset of EHV-1 myeloencephalopathy is characterized by a biphasic fever. In several outbreaks2 it has been observed that only horses younger than 5 years displayed fevers and respiratory signs, whereas the older horses were febrile, but had no signs of respiratory disease. It has also been observed that older horses develop neurologic deficits more frequently and of greater severity than younger horses (<5 y) 2. The reason for this bias is unknown, but may be explained by the role the horse’s immune system plays in the extent and severity of vasculitis and vascular thrombosis2.

The neurologic deficits appear approximately 4-6 days after the onset of fever2 and develop as the result of vasculitis, thrombosis and secondary ischemic degeneration of the neuropil1. The neurologic signs reflecting spinal cord involvement range from mild ataxia to recumbency, the pelvic limbs are more frequently involved and bladder atony is common. The brainstem may also be affected and therefore deficits of the cranial nerves may also be observed.

Epidemiology and outcome

The clinical signs are of rapid onset, but they also stabilize quickly. Most non recumbent animals do well, but the prognosis for recumbent horses is poor. In an outbreak of EHV-1 approximately 20-30 % of horses will be affected by the neuropathogenic strain, and of these the mortality will be approximately 30%1, 2.

Diagnosis

If you suspect a horse has EHV-1 due to an unexplained fever after being at an event, for example. A nasal swab and an EDTA purple top tube should be collected and submitted on ice packs overnight for real-time TaqMan® PCR on both samples to diagnose and differentiate the neuropathogenic vs non neuropathogenic strains. Results will be ready in 24h post arrival3. (See references for mailing addresses).

Outbreaks and treatment

In the event of a suspected outbreak there are guidelines on the AAEP website http://www.aaep.org/control_guidelines_nonmember.htm that pertain to biosecurity and quarantine. They are to extensive to cover, and are not the objective of this article. What I do want to incur into are treatment guidelines.

On the onset of fever of a suspected animal:

First implement biosecurity measures including stall confinement. Collect pertinent samples for diagnosis and then initiate therapy with NSAIDs such as flunixin meglumine 1.1 mg/kg or phenylbutazone 4.4mg/kg to manage the fevers.

Once the disease is confirmed or clinical signs of the disease progress to a working diagnosis of EHV-1, then more aggressive therapy and prophylaxis of surrounding animals should be initiated. All animals possibly exposed should be treated with Valacyclovir (Valtrex®) 205-403 mg/kg PO every 8 hours. Acyclovir despite clinical reports of effectivity2 has shown not to reach adequate serum levels to inhibit viral replication6 therefore should not be the first drug of choice. Valtrex® is an expensive drug and this option should be thoroughly discussed with the owner.

Management for the horses displaying clinical signs of the neuropathogenic form of EHV-1:

· NSAIDs – continue flunixin meglumine 1.1mg/kg for 10 d (monitor serum creatinine every 3-5d depending on hydration status of the horse).

· DMSO (if you are a believer) 1g/kg at 20% sol IV every 24h for 3 days, as a free radical scavenger.

· Valacyclovir (Valtrex®) 205-403 mg/kg PO every 8 hours for 10 days or until clinical signs stabilize.

· Vitamin E 10.000 IU PO every 24h for 10 days7 as an antioxidant.

· Dexamethasone 0.1 mg/kg IV for 3 days then taper for a total of 10d. This therapy is controversial. On one hand it is a potent anti-inflammatory, but on the other it does suppress the immune system at these doses. And never forget the potential for laminitis. I would reserve this choice of therapy for horses showing neurological deficits, I would not administer to horses with just a fever, even if it is a confirmed case.

· If at any point a horse should become recumbent or needs assistance standing, or in general deteriorates to the point of requiring constant monitoring please talk to the client about referral to a hospital with facilities for critical care.

Vaccination in an outbreak

From http://www.vetmed.ucdavis.edu/ceh/topics-EHV-1-vaccinations.htm

· On premises with confirmed clinical EHV-1 infection, booster vaccination of horses likely to be exposed is not recommended.

· Non-exposed horses or horses that have to enter the premises should have a booster vaccination if they have not been vaccinated within the past 90 days. This does not guarantee protection against the disease; the hope is that reduced nasal shedding of infectious EHV-1 by these horses will help reduce the magnitude of challenge experienced by other horses and potentially help reduce spread.

· A current publication8 showed that recent vaccination with Rhinomune (modified live vaccine) may provide some protection against EHV-1 myeloencephalopathy. These results should be interpreted with caution because the number of animals used in the study was small.

· Vaccines that provide the highest levels of viral neutralizing titers are Pneumabort, Prodigy, Calvenza and Rhinomune. The high levels of antibodies have been shown to reduce viral shedding. It is important to warn clients of the potential side effects of the modified live vaccine such as swelling of the injection site, fever and swelling of the limbs.

I hope this article has been helpful, if you should have any further questions about a case please do not hesitate to contact me.

References:

1.- Julia H. Kydd and K.C. Smith, Equine Herpesvirus Neurologic Disease: Reflections from across the pond. J Vet Intern Med. 2006 May-June;20(3):467-68.

2.- Henninger RW, et al, Outbreak of neurologic disease caused by equine herpesvirus-1 at a university equestrian center. J Vet Intern Med. 2007 Jan-Feb;21(1):157-65.

3.- Allen GP, Development of a real-time polymerase chain reaction assay for rapid diagnosis of neuropathogenic strains of equine herpesvirus-1.J Vet Diagn Invest. 2007 Jan;19(1):69-72. M.H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546.

4.- Garré B, et al, Pharmacokinetics of acyclovir after intravenous infusion of acyclovir and after oral administration of acyclovir and its prodrug Valacyclovir in healthy adult horses. Antimicrob Agents Chemother. 2007 Dec;51(12):4308-14. Epub 2007 Sep 10.

5.- BG Bentz, et al, Pharmacokinetics of Valacyclovir in the adult horse. Abstract #108 J Vet Intern Med. 2007 May-June;21(3):601.

6.- BG Bentz et al, Pharmacokinetics of Acyclovir after Single Intravenous and Oral Administration to Adult Horses. J Vet Intern Med. 2006 May-June;20(3):467-68.

7.- J.K. Higgins, et al, Vitamin E levels in serum and cerebrospinal fluid of healthy horses following oral supplementation. Abstract #340 J Vet Intern Med. 2007 May-June;21(3):666.

8.- Goodman LB, et al, Comparison of the efficacy of inactivated combination and modified-live virus vaccines against challenge infection with neuropathogenic equine herpesvirus type 1 (EHV-1).

Vaccine. 2006 Apr 24;24(17):3636-45. Epub 2006 Feb 13.

Emergency Management of the Blocked Ferret

April 29, 2008 Leave a comment
By Christal Pollock, DVM, DABVP-Avian

Diagnosis of urethral obstruction in the male ferret is rarely a diagnostic challenge, but the need to place a urinary catheter in a 1-kg patient can be intimidating.

Urinary catheter placement can be challenging in the male ferret because of its small size and its J-shaped os penis. Locate the prepuce on the ventral abdomen just caudal to the umbilicus. The os penis is palpable. After gently extruding the penis, it may help to grasp the base with a gauze square. Aseptically prepare the penis, and use a 24-gauge catheter with the needle removed to find and dilate the urethral opening. The urethral opening is located on the ventral surface of the penis just proximal to the J-shaped curve.

After the urethral opening is found and dilated, pass a urinary catheter. A 3.5 Fr red rubber catheter may be used in a very large male, however most individuals require a smaller tube. A 3-Fr 11-in urinary catheter specifically designed for ferrets is available (Slippery Sam, Global Veterinary Products; New Buffalo, MI) or a 22- or 20-gague jugular catheter may be used. Pre-measure red rubber catheters and jugular catheters. Leave the jugular catheter stylet in place to facilitate passage, but manipulate the catheter carefully. Resistance most often occurs as the catheter travels around the pelvic flexure. Gently flush the urethra with sterile saline to facilitate catheter passage.

· Anesthesia is required for adequate muscle relaxation. Most individuals should be intubated and maintained on isoflurane or sevoflurane when anesthetized for extended periods. Avoid ketamine in ferrets with urethral obstruction.

· When urinary catheterization proves difficult, remove a small amount of urine once via cystocentesis to reduce pressure and allow passage of the urinary catheter. Repeated cystocentesis is not recommended because of thin bladder wall. In rare cases, percutaneous cystostomy may be performed when catheter placement fails.

· Suture butterfly tape strips near the prepuce to secure the catheter. Use tape to fasten the catheter or attached tubing to the tail base to minimize tension on the line. Bandaging the abdomen may also minimize the risk of rotation. Create a closed collection system by attaching a small intravenous bag and monitor urine production. The average 1-kg ferret produces 26-28 ml of urine over a 24-hour period (range: 8-48 ml).

· To catheterize the female ferret, place her in ventral recumbency and elevate the rear with a rolled towel. Aseptically prepare the vulva and perivulvar region, and then insert a sterile vaginal speculum or otoscope. Locate the urethral opening on the vestibule floor 1-cm cranial to the clitoral fossa. Insert a 3.5-Fr red rubber catheter, which may be fitted with a wire stylet.

The most important cause of dysuria or stranguria in the male ferret is prostatomegaly secondary to adrenal disease. Struvite urolithiasis may also cause urethral obstruction, however the incidence is relatively low now that ferret food is commercially available. (Cystitis and prostatic abscesses are uncommon but potential causes of stranguria and dysuria in the ferret). History and physical examination may provide clues to the underlying cause of urethral obstruction, but signalment is not particularly helpful. Most affected ferrets are middle aged to older, although any age may be affected.

Adrenal disease

Struvite urolithiasis

Diet

Good diet (Animal protein-based)

Bad diet (Plant protein-based)

Exam findings

Dorsal symmetrical alopecia

—–

Laboratory results

+/- Urinary tract infection

Non-regenerative anemia

Urinary tract infection

Crystalluria

Radiographs

Unremarkable

Radiopacity

Ultrasonography

Prostatomegaly

Adrenomegaly

—–

· Ferret adrenal disease is associated with an elevation in sex steroid hormones, and elevated androgen levels can leads to prostatomegaly. Dorsal symmetrical alopecia is also a common clinical sign.

· Ferrets require high quality, animal-based dietary protein. Therefore a low quality, plant protein-based diet promotes development of alkaline urine and struvite crystalluria.

· Ferrets normally have relaxed abdomens that are easy to palpate. Although pain will cause the abdominal muscles to tense, the over distended bladder is still palpable. There may also be evidence of urine dribbling and the prepuce may be red from excessive licking.

· Normal ferret biochemistry is similar to that in other mammals with a few exceptions. Creatinine in the ferret generally ranges from 0.1-0.3 mg/dL with values almost always less than 0.5 mg/dL. Creatinine from 0.7-1.0 mg/dL signifies azotemia.

· Obtain whole body survey radiographs using tabletop technique, high-speed film, and fine screen cassettes. Contrast radiography may be useful in identifying urethral stones. Enlarged adrenal glands are rarely visible on radiographs, and ultrasonography is needed. Note that renal cysts are a common incidental finding.

· Ferrets are relatively stoic animals, but do not ignore pain management. Provide preemptive analgesia, and monitor ferrets carefully for signs of discomfort. Signs of pain may include anorexia, lethargy, crying, stiff movements, squinting, and an inability to sleep in a natural, curled position.

References & Further Reading

Castanheira de Matos RE, Morrisey JK. Common procedures in the pet ferret. Vet Clin North Am Exot Anim Pract 2006; 9: 347-365.

Esteves MI, Marini RP, Ryden EB, et al. Estimation of glomerular filtration rate and evaluation of renal function in ferrets (Mustela putorius furo). Am J Vet Res 1994;55:166-172.

Pollock CG. Emergency medicine of the ferret. Veterinary Clinics of North America: Exotic Animal Practice. 10(2): 463-500, 2007.

Quesenberry KE, Carpenter JW, eds. Ferrets, rabbits, and rodents: clinical medicine and surgery. 2nd ed. St. Louis: WB Saunders Co, 2003: 2-134.

Calcitriol?

January 2, 2008 Leave a comment

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 < 6 mg/dl.

· 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.

 

Jennifer S. Fryer, DVM

Calcitriol?

January 2, 2008 Leave a comment
By Jennifer S. Fryer, DVM

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.