Results of the Multicenter Spaniel Trial (MUST): Taurine-and Carnitine-Responsive Dilated Cardiomyopathy in American Cocker Spaniels With Decreased Plasma Taurine Concentration

Fourteen American Cocker Spaniels (ACS) with dilated cardiomyopathy (DCM) were studied to determine if individuals of this breed with DCM are systemically taurine-or carnitine-deficient and to determine if they are responsive to taurine and carnitine supplementation. American Cocker Spaniels with DCM were identified using echocardiography, and plasma was analyzed for taurine and carnitine concentrations. Each dog was randomly assigned to receive either taurine and carnitine supplementation or placebos. Echocardiograms and clinical examinations were repeated monthly for 4 months. During this period, the investigators and owners were blinded with respect to the treatment being administered. Each dog was weaned off its cardiovascular drugs (furosemide, digoxin, and an angiotensin converting enzyme inhibitor) if an echocardio-graphic response was identified. At the 4-month time period, each investigator was asked to decide whether he or she thought his or her patient was receiving placebo or taurine/ carnitine, based on presence or absence of clinical and echocar-diographic improvement. Unblinding then occurred, and dogs receiving placebos were switched to taurine and carnitine supplementation and followed monthly for 4 additional months. All dogs were reexamined 6 months after starting supplementation; survival time and cause of death were recorded for each dog. Data from 3 dogs were not included because of multiple protocol violations. Each dog had a plasma taurine concentration <50 nmol/mL (mean ±SD for the group 15 ± 17 nmol/ mL) at baseline; normal range, 50–180 nmol/mL. The plasma taurine concentration did not exceed 50 nmol/mL at any time in the dogs receiving placebos (n = 5), but increased to 357 ± 157 nmol/mL (range 140–621 nmol/mL) during taurine and carnitine supplementation (n = 11). Plasma carnitine concentration was within, only slightly below, or slightly above reported limits of normality at baseline (29 ± 15 μmol/L); did not change during placebo administration; and increased significantly during supplementation (349 ±119 μmol/L; n = 11). Echocardiographic variables did not change during placebo administration. During supplementation, left ventricular end-dia-stolic and end-systolic diameters, and mitral valve E point-to-septal separation decreased significantly in both groups. Shortening fraction increased significantly but not into the normal range. Echocardiographic variables remained improved at 6 months. All dogs were successfully weaned off furosemide, an angiotensin converting enzyme inhibitor, and digoxin once an echocardiographic response was identified. Nine of the dogs have died since the onset of the study in 1992. One dog died of recurrence of DCM and heart failure 31 months after starting supplementation; six dogs died of noncardiac causes. Two dogs developed degenerative mitral valve disease and died of complications of this disease. Dogs less than 10 years of age lived for 46 ± 11 months, whereas dogs older than 10 years of age lived for 14 ± 7 months. Two of the 11 dogs were alive at the time of publication, having survived for 3.5 and 4.5 years, respectively. We conclude that ACS with DCM are taurine-deficient and are responsive to taurine and carnitine supplementation. Whereas myocardial function did not return to normal in most dogs, it did improve enough to allow discontinuation of cardiovascular drug therapy and to maintain a normal quality of life for months to years.     

Plasma Taurine Concentrations in Normal Dogs and in Dogs With Heart Disease

Plasma taurine concentrations were determined in 76 dogs with dilated cardiomyopathy (DCM), 28 dogs with acquired valvular disease (AVD), and 47 normal (control) dogs. The data were collected at 2 referral centers. The Animal Medical Center, New York, NY (AMC), and the University of California, Davis (UCD), and the studies were conducted independently. Different anticoagulants (sodium citrate at AMC and lithium heparin at UCD) were used to collect the plasma samples. Paired analysis of samples showed a significant difference in plasma taurine concentrations, depending on the anticoagulant used. Consequently, results from each clinic were analyzed separately. Plasma taurine concentrations were significantly higher in dogs with AVD (median, 133 nmol/mL; range, 25 to 229 nmol/mL) than in control dogs (median, 63 nmol/mL; range 44 to 224 nmol/mL) and dogs with DCM (median, 72 nmol/mL; range, 1 to 247 nmol/mL) at AMC (P= .001). The number of dogs with AVD at UCD was too small to draw meaningful conclusions. At UCD, the median plasma taurine concentration was 98 nmol/mL (range, 28–169 nmol/mL) in dogs with AVD, 75 nmol/mL (range, 0.1–184 nmol/mL) in dogs with DCM, and 88 nmol/mL (range 52–180 nmol/mL) in control dogs. There were no significant differences in plasma taurine concentrations between dogs with DCM and the control dogs at either hospital. Congestive heart failure and administration of cardiac medication had no significant effect on plasma taurine concentrations. Plasma taurine concentration was low (<25 nmol/mL) in 17% (13/76) of the dogs with DCM. Seven of the 13 dogs with low plasma taurine concentrations were Cocker Spaniels or Golden Retrievers. It was concluded that most dogs with DCM do not have low plasma taurine concentrations. However, certain breeds or individual dogs may have low plasma taurine concentrations in association with DCM. Whether this association is causal or not is unknown. The significance of the high plasma taurine concentrations in dogs with AVD is also unknown.     

Taurine deficiency in Newfoundlands fed commercially available complete and balanced diets

OBJECTIVE: To determine taurine status in a large group of Newfoundlands related by environment, diet, or breeding to a dog with dilated cardiomyopathy and taurine deficiency. DESIGN: Prospective study. ANIMALS: 19 privately owned Newfoundlands between 5 months and 11.5 years old that had been fed commercial dry diets meeting established nutrient recommendations. PROCEDURE: Diet histories were obtained, and blood, plasma, and urine taurine concentrations and plasma methionine and cysteine concentrations were measured. In 8 dogs, taurine concentrations were measured before and after supplementation with methionine for 30 days. Ophthalmic examinations were performed in 16 dogs; echocardiography was performed in 6 dogs that were taurine deficient. RESULTS: Plasma taurine concentrations ranged from 3 to 228 nmol/mL. Twelve dogs had concentrations < 40 nmol/mL and were considered taurine deficient. For dogs with plasma concentrations < 40 nmol/mL, there was a significant linear correlation between plasma and blood taurine concentrations. For dogs with plasma concentrations > 40 nmol/mL, blood taurine concentrations did not vary substantially. Taurine-deficient dogs had been fed lamb meal and rice diets. Retinal degeneration, dilated cardiomyopathy, and cystinuria were not found in any dog examined for these conditions. The taurine deficiency was reversed by a change in diet or methionine supplementation. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate a high prevalence of taurine deficiency among an environmentally and genetically related cohort of Newfoundlands fed apparently complete and balanced diets. Blood taurine concentrations indicative of taurine deficiency in Newfoundlands may be substantially less than concentrations indicative of a deficiency in cats.     

Taurine depletion and cardiovascular disease in adult cats fed a potassium-depleted acidified diet.

Although low plasma taurine concentrations have been associated with congestive cardiomyopathy in cats, the cause of taurine depletion in cats consuming adequate quantities of taurine is unknown. Taurine depletion and cardiovascular disease (cardiomyopathy and thromboembolism) developed unexpectedly in 3 of 6 healthy adult cats during a potassium-depletion study. Plasma taurine concentration decreased significantly (P less than 0.05) and rapidly over an 8-week period (from 98 to 36 nmol/ml) in 6 cats that consumed a potassium-deficient diet (0.20% potassium, dry matter basis) that was acidified with 0.8% ammonium chloride, despite containing dietary taurine concentrations (0.12% dry matter basis) in excess of amounts currently recommended. Taurine concentrations were significantly lower in cats fed the acidified diet than in 6 cats fed a potassium-deficient diet that was not acidified (36 nmol/ml vs 75 nmol/ml) after 8 weeks. In addition, plasma taurine concentrations did not decrease over a 6-month period in 8 cats that were fed a potassium-replete diet with acidifier. Plasma taurine concentrations were lowest in 3 cats that died of cardiovascular disease in the group receiving potassium-deficient, acidified diets. These data indicated an association between taurine and potassium balance in cats and suggested that development of taurine depletion and cardiovascular disease may be linked to concurrent potassium depletion.     

Effect of nonthyroidal illness on serum thyroxine concentrations in cats: 494 cases (1988)

We reviewed the medical records of 494 cats with a variety of nonthyroidal diseases in which serum thyroxine (T4) concentration was determined as part of diagnostic evaluation. The cats were grouped by category of disease (ie, renal disease, congestive heart failure, diabetes mellitus, focal neoplasia, systemic neoplasia, hepatopathy, inflammatory bowel disease, inflammatory pulmonary disease, miscellaneous diseases, or undiagnosed disease), degree of illness (ie, mild, moderate, or severe), survival (ie, lived, died, or euthanatized), and presence or absence of a palpable thyroid gland. The mean (+/- SD) serum T4 concentrations in all 10 groups of cats, which ranged from 10.5 +/- 11.1 nmol/L in cats with diabetes mellitus to 18.7 +/- 7.8 nmol/L in cats with focal neoplasia, were significantly (P less than 0.001) lower than those of normal cats (27.0 +/- 10.4 nmol/L). The number of ill cats with low serum T4 concentrations (less than 10 nmol/L) was highest in the cats with diabetes mellitus (59%), hepatopathy (54%), renal failure (48%), and systemic neoplasia (41%). When the serum T4 concentrations in cats with mild, moderate, and severe illness were compared, mean concentrations were progressively lower (21.3 +/- 6.8, 14.8 +/- 8.1, and 6.5 +/- 5.8 nmol/L, respectively) as degree of illness increased. Severity of illness had a more significant (P less than 0.001) effect in lowering serum T4 concentrations than did disease category. Mean serum T4 concentrations in the cats that died (7.8 +/- 9.8 nmol/L) or were euthanatized (10.0 +/- 7.0 nmol/L) were also significantly (P less than 0.001) lower than those of cats that survived (15.2 +/- 8.8 nmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)     

Incidence and prognostic value of low plasma ionized calcium concentration in cats with acute pancreatitis: 46 cases (1996-1998).

OBJECTIVE: To determine the incidence and prognostic significance of low plasma ionized calcium concentration in cats with clinical signs of acute pancreatitis (AP). DESIGN: Retrospective study. ANIMALS: 46 cats with AP and 92 control cats with nonpancreatic diseases. PROCEDURE: Medical records were reviewed, and results of clinicopathologic testing, including plasma ionized and total calcium concentrations, acid-base values, and electrolyte concentrations, were recorded. Cats with AP were grouped on the basis of outcome (survived vs died or were euthanatized), and plasma ionized calcium concentrations, acid-base values, and electrolyte concentrations were compared between groups. RESULTS: Serum total calcium concentration was low in 19 (41%) cats with AP, and plasma ionized calcium concentration was low in 28 (61%). Cats with AP had a significantly lower median plasma ionized calcium concentration (1.07 mmol/L) than did control cats (1.12 mmol/L). Nineteen (41%) cats with AP died or were euthanatized; these cats had a significantly lower median plasma ionized calcium concentration (1.00 mmol/L) than did cats that survived (1.12 mmol/L). Ten of the 13 cats with AP that had plasma ionized calcium concentrations < or = 1.00 mmol/L died or were euthanatized. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that low plasma ionized calcium concentration is common in cats with AP and is associated with a poorer outcome. A grave prognosis and aggressive medical treatment are warranted for cats with AP that have a plasma ionized calcium concentration < or = 1.00 mmol/L.     

Taurine deficiency in dogs with dilated cardiomyopathy: 12 cases (1997-2001)

OBJECTIVE: To determine signalment, history, clinical signs, blood and plasma taurine concentrations, electrocardiographic and echocardiographic findings, treatment, and outcome of dogs with low blood or plasma taurine concentrations and dilated cardiomyopathy (DCM). DESIGN: Retrospective study. ANIMALS: 12 client-owned dogs with low blood or plasma taurine concentrations and DCM. PROCEDURE: Medical records were reviewed, and clinical data were obtained. RESULTS: All 12 dogs were being fed a commercial dry diet containing lamb meal, rice, or both as primary ingredients. Cardiac function and plasma taurine concentration improved with treatment and taurine supplementation. Seven of the 12 dogs that were still alive at the time of the study were receiving no cardiac medications except taurine. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that consumption of certain commercial diets may be associated with low blood or plasma taurine concentrations and DCM in dogs. Taurine supplementation may result in prolonged survival times in these dogs, which is not typical for dogs with DCM. Samples should be submitted for measurement of blood and plasma taurine concentrations in dogs with DCM, and taurine supplementation is recommended while results of these analyses are pending.     

Plasma homocysteine, B vitamins, and amino acid concentrations in cats with cardiomyopathy and arterial thromboembolism

Arterial thromboembolism (ATE) is a common complication of cats with cardiomyopathy (CM), but little is known about the pathophysiology of ATE. In people, high plasma concentrations of homocysteine and low B vitamin concentrations are risk factors for peripheral vascular disease. In addition, low plasma arginine concentrations have been linked to endothelial dysfunction. The purpose of this study was to compare concentrations of homocysteine, B vitamins, and amino acids in plasma of normal cats to those of cats with CM and ATE. Plasma concentrations of homocysteine, vitamin B6, vitamin B12, folate, and amino acids were measured in 29 healthy cats, 27 cats with CM alone, and 28 cats with both CM and ATE. No differences were found between groups in homocysteine or folate. Mean vitamin B12 concentration (mean +/- standard deviation) was lower in cats with ATE (866 +/- 367 pg/mL) and cats with CM (939 +/- 389 pg/mL) compared with healthy controls (1,650 +/- 700 pg/mL; P < .001). Mean vitamin B6 concentration was lower in cats with ATE (3,247 +/- 1.215 pmol/mL) and cats with CM (3,200 +/- 906 pmol/mL) compared with healthy control animals (4,380 +/- 1,302 pmol/mL; P = .005). Plasma arginine concentrations were lower in cats with ATE (75 +/- 33 nmol/mL) compared with cats with CM (106 +/- 25 nmol/mL) and healthy control animals (96 +/- 25 nmol/ mL; P < .001). Vitamin B12 concentration was significantly correlated with left atrial size. We interpret the results of this study to suggest that vitamin B12 and arginine may play a role in CM and ATE of cats.     

Myocardial taurine concentrations in cats with cardiac disease and in healthy cats fed taurine-modified diets.

Myocardial taurine concentrations were measured in cats with cardiac disease and in healthy cats fed diets with various concentrations of taurine. Group 1 was composed of 26 cats with 3 categories of naturally developing cardiac disease: dilatative cardiomyopathy (group 1A), 10 cats; hypertrophic cardiomyopathy (group 1B), 9 cats; and volume overload (group 1C), 7 cats. These cats had been fed various commercial diets. Group 2 was composed of 40 healthy cats that had been fed diets varying in taurine concentration (0 to 1% taurine) for at least 2 years. Mean myocardial taurine concentrations did not differ significantly between group-1 cats with dilatative cardiomyopathy and those with hypertrophic cardiomyopathy or volume overload. Cats in group 1A had a mean myocardial taurine concentration 3 times higher than healthy cats fed a taurine-free diet (P less than 0.002). Mean myocardial taurine concentrations did not differ significantly between group-1A cats and healthy cats fed a diet containing 0.02% taurine; group-1A cats had significantly lower mean myocardial taurine concentrations than did healthy cats fed a synthetic diet containing 0.05 or 1.0% taurine (P less than 0.001). Acute oral administration of taurine in 5 group-1A cats appeared to increase mean myocardial taurine concentrations, compared with similar cats not given taurine during treatment for cardiac failure. In group-2 cats, mean myocardial taurine concentrations increased directly with percentage of dietary taurine.     

Effects of dietary fat and L-carnitine on plasma and whole blood taurine concentrations and cardiac function in healthy dogs fed protein-restricted diets

OBJECTIVE: To evaluate plasma taurine concentrations (PTC), whole blood taurine concentrations (WBTC), and echocardiographic findings in dogs fed 1 of 3 protein-restricted diets that varied in fat and L-carnitine content. ANIMALS: 17 healthy Beagles. DESIGN: Baseline PTC and WBTC were determined, and echocardiography was performed in all dogs consuming a maintenance diet. Dogs were then fed 1 of 3 protein-restricted diets for 48 months: a low-fat (LF) diet, a high-fat and L-carnitine supplemented (HF + C) diet, or a high-fat (HF) diet. All diets contained methionine and cystine concentrations at or above recommended Association of American Feed Control Officials (AAFCO) minimum requirements. Echocardiographic findings, PTC, and WBTC were evaluated every 6 months. RESULTS: The PTC and WBTC were not significantly different among the 3 groups after 12 months. All groups had significant decreases in WBTC from baseline concentrations, and the HF group also had a significant decrease in PTC. One dog with PT and WBT deficiency developed dilated cardiomyopathy (DCM). Taurine supplementation resulted in significant improvement in cardiac function. Another dog with decreased WBTC developed changes compatible with early DCM. CONCLUSIONS AND CLINICAL RELEVANCE: Results revealed that dogs fed protein-restricted diets can develop decreased taurine concentrations; therefore, protein-restricted diets should be supplemented with taurine. Dietary methionine and cystine concentrations at or above AAFCO recommended minimum requirements did not prevent decreased taurine concentrations. The possibility exists that AAFCO recommended minimum requirements are not adequate for dogs consuming protein-restricted diets. Our results also revealed that, similar to cats, dogs can develop DCM secondary to taurine deficiency, and taurine supplementation can result in substantial improvement in cardiac function.     

Pharmacokinetics of tacrolimus after multidose oral administration and efficacy in the prevention of allograft rejection in cats with renal transplants

OBJECTIVE: To describe pharmacokinetics of multi-dose oral administration of tacrolimus in healthy cats and evaluate the efficacy of tacrolimus in the prevention of allograft rejection in cats with renal transplants. ANIMALS: 6 healthy research cats. PROCEDURE: Cats received tacrolimus (0.375 mg/kg, PO, q 12 h) for 14 days. Blood tacrolimus concentrations were measured by a high performance liquid chromatography-mass spectrometry assay. Each cat received an immunogenically mismatched renal allograft and native kidney nephrectomy. Tacrolimus dosage was modified to maintain a target blood concentration of 5 to 10 ng/mL. Cats were euthanatized if plasma creatinine concentration exceeded 7 mg/dL, body weight loss exceeded 20%, or on day 50 after surgery. Kaplan-Meier survival curves were plotted for 6 cats treated with tacrolimus and for 8 cats with renal transplants that did not receive immunosuppressive treatment. RESULTS: Mean (+/- SD) values of elimination half-life, time to maximum concentration, maximum blood concentration, and area under the concentration versus time curve from the last dose of tacrolimus to 12 hours later were 20.5 +/- 9.8 hours, 0.77 +/- 0.37 hours, 27.5 +/- 31.8 ng/mL, and 161 +/- 168 hours x ng/mL, respectively. Tacrolimus treated cats survived longer (median, 44 days; range, 24 to 52 days) than untreated cats (median, 23 days; range, 8 to 34 days). On histologic evaluation, 3 cats had evidence of acute-active rejection, 1 cat had necrotizing vasculitis, and 2 cats euthanatized at study termination had normal appearing allografts. CONCLUSIONS AND CLINICAL RELEVANCE: Tacrolimus may be an effective immunosuppressive agent for renal transplantation in cats.     

Hemostatic Disorders in Feline Immunodeficiency Virus-Seropositive Cats

The hemostatic function of 40 feline immunodeficiency virus (FlV) seropositive and 8 FIV and feline leukemia virus (FeLV) seropositive cats was evaluated and compared with reference values from 30 clinically healthy cats. The FIVpositive cats were divided into 3 groups: group I included asymptomatic carriers; group II comprised sick FIV-infected cats with illnesses not likely to influence the hemostatic system; and group III included FIV-positive cats with diseases potentially associated with coagulopathies. Platelet counts in FIV/FeLV-infected cats were significantly lower than in healthy cats (P < .003), whereas the differences in the 3 groups of FIV-positive cats were variable (group I, P= .009; II, P= .05; III, P= .09). Thrombocytopenia (< 145,000 platelets/μL) was present in 4 FIV-positive and 3 FIV/FeLV-positive cats. Platelet aggregation induced by collagen (0.5 and 0.25 μg/mL), adenosine diphosphate (ADP) (1 and 0.6 μmol/L), and thrombin (0.4 and 0.25 IU/mL) was not significantly different from that of healthy cats. The plasma coagulation system was evaluated by measuring one-stage prothrombin time (OSPT), activated partial thromboplastin time (APTT), thrombin time, fibrinogen concentration, coagulation factor assays, fibrinogen and fibrin degradation products (FDP), and plasma exchange test. The OSPT was similar in FlV-seropositive cats and in the healthy control group. Cats with FIV infection, however, had markedly shorter clotting times than healthy cats when using a modified test system (P < .05). In all groups of FIV-infected cats and in those with FIV/FeLV infection, APTT measured with 2 different commercially available tests, and a modified plasma assay was markedly prolonged compared with healthy cats (APTT1 and 2:3 modification: P < .01; APTT2: P < .05 except group III). In 22 of 40 cats with FIV and in 5 of 8 cats with FIV/FeLV infection, plasma samples were beyond the reference range. The thrombin time was also significantly prolonged in cats with FIV and FIV/FeLV infection (P < .01); values in 17 of 40 FIV-positive cats were above reference range. The mean fibrinogen concentration of cats with FIV and FIV/FeLV infection was higher than in the healthy control group (P < .001). Factor VIII activity of 4 cats with FIV infection was 1.5 times higher than that of healthy cats. Factor XII activity of 3 cats from a group of 20 cats with prolonged APTT was between 20% and 35%. Factor IX and XI activities ranged between 70% and 120%. The markedly prolonged APTT in 2 FIV-positive cats could be shortened considerably in a plasma exchange test using 20% feline pooled plasma. The alterations in the coagulogram of FIV-seropositive cats were not related to a clinical stage or concurrent diseases. A definite explanation of the distinct disorder within the intrinsic plasma coagulation system in FIV-infected cats was not found.     

Correlation between activation of the sympathetic nervous system estimated by plasma concentrations of norepinephrine and Doppler echocardiographic variables in dogs with acquired heart disease

OBJECTIVE: To evaluate correlations between plasma concentrations of norepinephrine and Doppler echocardiographic variables for dogs with degenerative mitral valve disease (DMVD) or dilatative cardiomyopathy (DCM) to better understand the time course and magnitude of sympathetic activation in dogs with heart failure (HF). ANIMALS: 15 healthy dogs, 15 dogs with DMVD, and 15 dogs with DCM. PROCEDURES: Dogs were positioned in lateral recumbency with minimal restraint for at least 20 minutes. Plasma samples were obtained and assayed by use of high-performance liquid chromatography. Concentrations were correlated with HF classification and with the main Doppler echocardiographic variables for each group. RESULTS: Mean +/- SD norepinephrine concentration was significantly higher in dogs with DMVD (494.4 +/- 204.8 pg/mL) or DCM (655.7 +/- 652.5 pg/mL) than in healthy dogs (205.8 +/- 78.9 pg/mL), but concentrations did not differ significantly between the 2 groups with HF. Correlations were not detected between norepinephrine and heart rate or any M-mode echocardiographic variables evaluated, except for fractional shortening (FS) in DCM dogs. In that group, norepinephrine was inversely correlated with FS values. In DMVD dogs, no significant correlation was found between norepinephrine and the left atrium-to-aortic root ratio or mitral regurgitation. CONCLUSIONS AND CLINICAL RELEVANCE: A proportional inverse correlation exists between norepinephrine and FS values in dogs with DCM. However, norepinephrine concentration was not correlated with the evaluated echocardiographic variables in dogs with DMVD. Sympathetic antagonists should be evaluated as a treatment option because of the increased plasma concentrations of norepinephrine detected in dogs with HF.     

Plasma and whole blood taurine in normal dogs of varying size fed commercially prepared food

The objective of the present study was to examine the effect of signalment, body size and diet on plasma taurine and whole blood taurine concentrations. A total of 131 normal dogs consuming commercially prepared dog food had blood drawn 3-5 h post-prandially to be analysed for plasma amino acids and whole blood taurine. Body weight and morphometric measurements of each dog were taken. Plasma and whole blood taurine concentrations were 77 +/- 2.1 nmol/ml (mean +/- SEM) and 266 +/- 5.1 nmol/ml (mean +/- SEM), respectively. No effect of age, sex, body weight, body size, or diet was seen on plasma and whole blood taurine concentrations. Mean whole blood taurine concentrations were lower in dogs fed diets containing whole grain rice, rice bran or barley. The lowest whole blood concentrations were seen in dogs fed lamb or lamb meal and rice diets. Plasma methionine and cysteine concentrations were lower in dogs fed diets with animal meals or turkey, and whole grain rice, rice bran or barley. Fifteen of 131 dogs had plasma taurine concentrations lower than, or equal, to the previously reported lowest mean food-deprived plasma taurine concentration in normal dogs of 49 +/- 5 nmol/ml (mean +/- SEM) (Elliott et al., 2000). These findings support the theory that taurine deficiency in dogs may be related to the consumption of certain dietary ingredients. Scientific and clinical evidence supports the hypothesis that dilated cardiomyopathy is associated with low blood taurine concentration in dogs; therefore, further work is indicated to determine the mechanism by which diet can affect taurine status in dogs.     

Cats discriminate between cholecalciferol and ergocalciferol

A comparison was made of the ability of ergocalciferol and cholecalciferol to elevate plasma concentrations of vitamin D and 25-hydroxyvitamin D in cats. Cholecalciferol, given as an oral bolus in oil, resulted in a rapid elevation of plasma concentration of cholecalciferol followed by a rapid decline. In contrast, 25-hydroxyvitamin D concentration in plasma increased until day 3 after administration and remained elevated for a further 5 days. When 337 microg of both cholecalciferol and ergocalciferol in oil were given as an oral bolus to 10 cats, the peak plasma concentrations of cholecalciferol and ergocalciferol occurred at 8 or 12 h after administration. Peak concentrations of cholecalciferol were over twice those of ergocalciferol (570 +/- 80 vs. 264 +/- 42 nmol/l). The area under the curve 0-169 h for cholecalciferol was also more than twice that for ergocalciferol. When ergocalciferol and cholecalciferol were administered in a parenteral oil-based emulsion, higher concentrations of 25-hydroxyvitamin D3 than 25-hydroxyvitamin D2 were maintained in plasma. When both vitamins were included in the diet in the nutritional range, plasma concentrations of 25-hydroxyvitamin D2 were 0.68 of those of 25-hydroxyvitamin D3. Discrimination against ergocalciferol by cats appears to result from differences in affinity of the binding protein for the metabolites of the two forms of vitamin D. These results indicate that cats discriminate against ergocalciferol, and use it with an efficiency of 0.7 of that of cholecalciferol to maintain plasma 25-hydroxyvitamin D concentration.     

Relationships between Low Serum Cobalamin Concentrations and Methlymalonic Acidemia in Cats

Background: Serum cobalamin concentrations below reference range are a common consequence of gastrointestinal disease in cats. Serum cobalamin ≤ 100 ng/L is associated with methylmalonic acidemia.
Objectives: To determine the prevalence of cobalamin deficiency, defined by elevated serum methylmalonic acid (MMA), in cats with serum cobalamin ≤ 290 ng/L, and the optimum serum cobalamin concentration to predict cobalamin deficiency in cats.
Sample Set: Residual serum samples (n = 206) from cats with serum cobalamin ≤ 290 ng/L.
Methods: Retrospective, observational study. Serum cobalamin and folate were measured with automated assays. Serum MMA was determined by gas chromatography-mass spectrometry. Cobalamin deficiency was defined as serum MMA > 867 nmol/L. Sensitivity and specificity of serum cobalamin concentrations ≤290 ng/L for detecting MMA > 867 nmol/L were analyzed using a receiver-operator characteristic curve.
Results: There was a negative correlation between serum cobalamin and MMA concentrations (Spearman's r =−0.74, P < 0.0001). The prevalence of MMA ≥ 867 nmol/L in cats with serum cobalamin ≤ 290 ng/L was 68.4%. Serum cobalamin ≤ 160 ng/L had a 74% sensitivity and 80% specificity for detecting MMA > 867 nmol/L. No significant difference in serum folate concentrations was detected between affected and unaffected cats.
Conclusions and Clinical Importance: Elevated MMA concentrations, suggesting cobalamin deficiency, are common in cats with serum cobalamin ≤ 290 ng/L. Cobalamin deficiency is clinically significant, and supplementation with parenteral cobalamin is recommended for cats with gastrointestinal disease and low serum cobalamin concentrations.     

Evaluation of the Clinical and Histologic Features of Renal Allograft Rejection in Cats

OBJECTIVES: To describe the clinical signs and histopathologic features of renal allograft rejection in cats, and to provide a historical, untreated control group for use in future studies of feline renal allograft rejection. ANIMALS: Fourteen adult research cats. METHODS: Renal transplantation and bilateral nephrectomy were performed in pairs of immunogenically mismatched cats. A physical examination was performed, and packed cell volume, total protein, and plasma creatinine concentrations were measured each day after surgery. The cats were euthanatized when plasma creatinine concentration exceeded 7 mg/dL or when weight loss exceeded 20%. Renal histopathology was scored according to the Banff 97 criteria by 3 pathologists. RESULTS: Nine cats completed the study. Plasma creatinine exceeded 7 mg/dL in 5 cats, weight loss exceeded 20% in 3 cats, and 1 cat was found dead. Clinical signs in cats with rejection were nonspecific or absent. Rectal temperature decreased by 0.8 +/- 0.5 degrees C in the 24 hours before euthanasia. The pathologists agreed on the allograft histopathologic category in 6 of 9 cats. The histologic consensus was acute/active rejection in 8 cats and normal in 1 cat. Median survival time of the 8 cats with histologically confirmed allograft rejection was 23 days (range, 8-34 days). CONCLUSIONS AND CLINICAL RELEVANCE: Renal allograft rejection is associated with minimal clinical signs. Therefore, plasma creatinine concentration should be measured routinely in patients with a functioning allograft. An increase in plasma creatinine concentration is highly suspicious for allograft rejection, although a biopsy of the renal allograft is needed for definitive diagnosis.     

Diagnosis of hyperthyroidism in cats with mild chronic kidney disease

OBJECTIVES: In cats with concurrent hyperthyroidism and non-thyroidal illnesses such as chronic kidney disease, total thyroxine concentrations are often within the laboratory reference range (19 to 55 nmol/l). The objective of the study was to determine total thyroxine, free thyroxine and/or thyroid-stimulating hormone concentrations in cats with mild chronic kidney disease. METHODS: Total thyroxine, free thyroxine and thyroid-stimulating hormone were measured in three groups. The hyperthyroidism-chronic kidney disease group (n=16) had chronic kidney disease and clinical signs compatible with hyperthyroidism but a plasma total thyroxine concentration within the reference range. These cats were subsequently confirmed to be hyperthyroid at a later date. The chronic kidney disease-only group (n=20) had chronic kidney disease but no signs of hyperthyroidism. The normal group (n=20) comprised clinically healthy senior (>8 years) cats. RESULTS: In 4 of 20 euthyroid chronic kidney disease cats, free thyroxine concentrations were borderline or high (> or =40 pmol/l). In the hyperthyroidism-chronic kidney disease group, free thyroxine was high in 15 of 16 cats, while thyroid-stimulating hormone was low in 16 of 16 cats. Most hyperthyroidism-chronic kidney disease cats (14 of 16) had total thyroxine greater than 30 nmol/l, whereas all the chronic kidney disease-only cats had total thyroxine less than 30 nmol/l. CLINICAL SIGNIFICANCE: The combined measurement of free thyroxine with total thyroxine or thyroid-stimulating hormone may be of merit in the diagnosis of hyperthyroidism in cats with chronic kidney disease.     

Plasma-glucose concentrations in dogs and cats before and after surgery: comparison of healthy animals and animals with sepsis

Various surgical procedures were performed in healthy dogs and cats and in dogs and cats with sepsis. Plasma-glucose concentrations after surgery were usually increased over presurgical values. After surgery, cats had significantly higher plasma-glucose concentrations (P less than 0.05) than did dogs. Postsurgical concentrations for healthy dogs were between 100 to 200 mg/dl, whereas the concentrations for dogs with sepsis ranged from 66 to 356 mg/dl. Of 8 dogs with sepsis that developed postsurgical plasma-glucose concentrations of greater than 150 mg/dl, 4 (50%) died, whereas of 7 dogs with sepsis that developed postsurgical concentrations of less than 150 mg/dl, only 1 (14%) died; however, the difference between these 2 mortality percentages was not significant (P = 0.08).     

Echocardiographic evidence for myocardial failure induced by taurine deficiency in domestic cats.

Dietary taurine-deficiency is a cause of dilated cardiomyopathy (DCM) in cats. While the incidence of clinical cases of feline DCM has markedly decreased since the association between DCM and taurine-deficiency was first recognized, not all cats maintained on taurine-deficient diets develop DCM. The objective was to temporally evaluate left ventricular (LV) function using M-mode echocardiography in 23 cats maintained on a taurine-deficient diet; 20 time-matched, taurine-supplemented cats served as controls. The duration of feeding trials ranged from 6-15 months. No diminution of myocardial function was recorded in a small number of taurine-deficient cats whereas cardiac performance in some taurine-deficient cats diminished to levels characteristic of DCM. Of the taurine-deficient cats, 17 (74%) experienced a greater than 25% reduction in fractional shortening and 21 (91%) had a greater than 25% increase in LV end-systolic short-axis diameter. On average, LV end-systolic short-axis diameter increased by 70% and fractional shortening decreased by 37% in taurine-deficient cats. Mean velocity of circumferential fiber shortening was similarly reduced in taurine-deficient cats. The greatest rate of change in M-mode echocardiographic variables occurred during the first four months on the taurine-deficient diet. Dietary taurine deficiency leads to a spectrum of changes in myocardial function in domestic cats. While DCM is observed in some cats, decreased systolic pump function and increased LV end-systolic short-axis diameter are more consistent findings.