Valerie J. Parker

Exogenous thyrotoxicosis in dogs attributable to consumption of all-meat commercial dog food or treats containing excessive thyroid hormone: 14 cases (2008-2013)

OBJECTIVE To describe findings in dogs with exogenous thyrotoxicosis attributable to consumption of commercially available dog foods or treats containing high concentrations of thyroid hormone. DESIGN Retrospective and prospective case series. ANIMALS 14 dogs. PROCEDURES Medical records were retrospectively searched to identify dogs with exogenous thyrotoxicosis attributable to dietary intake. One case was found, and subsequent cases were identified prospectively. Serum thyroid hormone concentrations were evaluated before and after feeding meat-based products suspected to contain excessive thyroid hormone was discontinued. Scintigraphy was performed to evaluate thyroid tissue in 13 of 14 dogs before and 1 of 13 dogs after discontinuation of suspect foods or treats. Seven samples of 5 commercially available products fed to 6 affected dogs were analyzed for thyroxine concentration; results were subjectively compared with findings for 10 other commercial foods and 6 beef muscle or liver samples. RESULTS Total serum thyroxine concentrations were high (median, 8.8 μg/dL; range, 4.65 to 17.4 μg/dL) in all dogs at initial evaluation; scintigraphy revealed subjectively decreased thyroid gland radionuclide in 13 of 13 dogs examined. At ≥ 4 weeks after feeding of suspect food or treats was discontinued, total thyroxine concentrations were within the reference range for all dogs and signs associated with thyrotoxicosis, if present, had resolved. Analysis of tested food or treat samples revealed a median thyroxine concentration for suspect products of 1.52 μg of thyroxine/g, whereas that of unrelated commercial foods was 0.38 μg of thyroxine/g. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that thyrotoxicosis can occur secondary to consumption of meat-based products presumably contaminated by thyroid tissue, and can be reversed by identification and elimination of suspect products from the diet.

Association of Vitamin D Metabolites with Parathyroid Hormone, Fibroblast Growth Factor-23, Calcium, and Phosphorus in Dogs with Various Stages of Chronic Kidney Disease.

Background Hypovitaminosis D is associated with progression of renal disease, development of renal secondary hyperparathyroidism (RHPT), chronic kidney disease‐mineral bone disorder (CKD‐MBD), and increased mortality in people with CKD. Despite what is known regarding vitamin D dysregulation in humans with CKD, little is known about vitamin D metabolism in dogs with CKD. Objectives The purpose of our study was to further elucidate vitamin D status in dogs with different stages of CKD and to relate it to factors that affect the development of CKD‐MBD, including parathyroid hormone (PTH), fibroblast growth factor‐23 (FGF‐23), calcium, and phosphorus concentrations. Methods Thirty‐seven dogs with naturally occurring CKD were compared to 10 healthy dogs. Serum 25‐hydroxyvitamin D [25(OH)D], 1,25‐dihydroxyvitamin D [1,25(OH)2D], and 24,25‐dihydroxyvitamin D [24,25(OH)2D], and PTH and FGF‐23 concentrations were measured. Their association with serum calcium and phosphorus concentrations and IRIS stage was determined. Results Compared to healthy dogs, all vitamin D metabolite concentrations were significantly lower in dogs with International Renal Interest Society (IRIS) stages 3 and 4 CKD (r [creatinine]: −0.49 to −0.60; P < .05) but not different in dogs with stages 1 and 2 CKD. All vitamin D metabolites were negatively correlated with PTH, FGF‐23, and phosphorus concentrations (r: −0.39 to −0.64; P < .01). Conclusions and Clinical Importance CKD in dogs is associated with decreases in all vitamin D metabolites evaluated suggesting that multiple mechanisms, in addition to decreased renal mass, affect their metabolism. This information could have prognostic and therapeutic implications.

Fibroblast Growth Factor-23 Concentration in Dogs with Chronic Kidney Disease

Background Chronic kidney disease (CKD) is associated with hyperphosphatemia, decreased vitamin D metabolite concentrations, and hyperparathyroidism. This syndrome is known as CKD‐mineral bone disorder (CKD‐MBD). Recently, it has been shown that an increase in fibroblast growth factor‐23 (FGF‐23) concentration is an early biomarker of CKD in people. It is an independent risk factor for both progression of renal disease and survival time in humans and cats with CKD. Information about FGF‐23 in healthy dogs and those with CKD is lacking. Objectives To measure FGF‐23 concentration in dogs with different stages of CKD and determine its association with factors involved in CKD‐MBD, including serum phosphorus and parathyroid hormone (PTH) concentrations. A secondary aim was to validate an ELISA for measurement of plasma FGF‐23 concentration in dogs. Animals Thirty‐two client‐owned dogs with naturally occurring CKD and 10 healthy control dogs. Methods Prospective cross‐sectional study. An FGF‐23 ELISA was used to measure plasma FGF‐23 concentration in dogs and their association with serum creatinine, phosphorus, calcium, and PTH concentrations. Results Plasma FGF‐23 concentrations increased with severity of CKD and were significantly different between IRIS stages 1 and 2 versus stages 3 and 4 (P < .0001). Increases in FGF‐23 concentrations were more frequent than hyperparathyroidism or hyperphosphatemia in this cohort. Serum creatinine and phosphorus concentrations were the strongest independent predictors of FGF‐23 concentration. Conclusions and clinical importance Plasma FGF‐23 concentrations increase in dogs with CKD as disease progresses. Plasma FGF‐23 concentrations appear to be useful for further study of the pathophysiology of CKD‐MBD in dogs.

Feline hyperparathyroidism Pathophysiology, diagnosis and treatment of primary and secondary disease

Practical relevance: Hyperparathyroidism exists in primary and secondary forms. Primary hyperparathyroidism has typically been considered a disease that uncommonly affects cats, but this condition is more prevalent than previous diagnoses would suggest. Secondary hyperparathyroidism may be caused by either nutritional influences (ie, nutritional secondary hyperparathyroidism) or chronic kidney disease (ie, renal secondary hyperparathyroidism). Tertiary hyperparathyroidism has yet to be documented in veterinary medicine, but it is possible that this condition occurs in some cats following longstanding renal secondary hyperparathyroidism. Clinical challenges: Diagnosis of this group of calcium metabolic disorders presents a number of challenges for the clinician. For example, clinical signs can be non-specific and, especially in the case of primary hyperparathyroidism, there is often a low index of suspicion for the disease; careful sample handling is required for testing of parathyroid hormone (PTH) and ionized calcium levels; and there is currently no feline-specific assay for PTH, which has implications for test sensitivity and interpretation of results. Aims: This article briefly outlines PTH and calcium physiology by way of introduction to a review of PTH measurement and interpretation. Various forms of feline hyperparathyroidism are then described, encompassing diagnosis and treatment options.

Update on Feline Ionized Hypercalcemia

Hypercalcemia in cats is recognized with increased frequency, especially idiopathic hypercalcemia, which is the most common cause. Idiopathic hypercalcemia seems to be unique to the cat, not occurring in the dog as a specific syndrome. There are many causes of hypercalcemia, and diagnosis relies on evaluation of clinical signs, physical examination, diagnostic imaging, serum biochemistry, urinalysis, and evaluation of calcium metabolic hormones. With an accurate diagnosis, treatment options can be tailored to the individual.

Dietary management of presumptive protein-losing enteropathy in Yorkshire terriers

OBJECTIVES To describe the clinical outcome of dietary management of Yorkshire terriers with protein-losing enteropathy without immunosuppressive/anti-inflammatory medications. METHODS Records were searched for Yorkshire terriers with hypoalbuminaemia and a clinical diagnosis of protein-losing enteropathy that were managed with diet and without immunosuppressive/anti-inflammatory medications. Serum albumin changes were compared using a one-way repeated measures ANOVA. Canine chronic enteropathy clinical activity index scores were compared using a Wilcoxon signed-rank test. RESULTS Eleven cases were identified. Clinical signs were variable including: diarrhoea, respiratory signs, vomiting, lethargy and weight loss. Diets fed included home cooked (n=5); Royal Canin Gastrointestinal Low Fat (n=4); Hills Prescription Diet i/d Low Fat (n=1); or Purina HA Hypoallergenic (n=1). Clinical signs resolved completely in eight dogs, partially resolved in two dogs and failed to respond in one dog. In dogs that responded, albumin significantly improved from baseline (mean 14·9 g/L, sd ±3·7), at 2 to 4 weeks (mean 24·2 g/L, sd ±5·5, P=0·01), and at 3 to 4 months (mean 27·0 g/dL, sd ±5·9, P=0·01). CLINICAL SIGNIFICANCE These results indicate that dietary management of protein-losing enteropathy is a potential management strategy in Yorkshire terriers. Randomised clinical trials in Yorkshire terriers with protein-losing enteropathy are necessary to compare success rate, survival and quality of life with dietary management versus combined dietary and immunosuppressive/anti-inflammatory therapy.

Factors associated with survival in dogs with chronic kidney disease

Background: Chronic kidney disease (CKD) is associated with morbidity and mortality in dogs. Plasma fibroblast growth factor‐23 (FGF‐23) concentration is an independent predictor of CKD progression and survival in cats and people with CKD. Objectives: To investigate the relationship among FGF‐23, parathyroid hormone (PTH), vitamin D metabolites, and other clinical variables with survival time in dogs with CKD. Animals: Twenty‐seven azotemic CKD dogs. Methods: Dogs were recruited prospectively into the study and followed until death or study conclusion. Dogs were International Renal Interest Society (IRIS) staged into stage 2 (n = 9), stage 3 (n = 12), and stage 4 (n = 6) CKD. Survival times were calculated from the date of study inclusion. Univariable Cox regression was used to assess variables associated with survival including body condition score (BCS), muscle condition score, hematocrit, creatinine, CKD stage, serum phosphorus, urine protein:creatinine ratio (UPC), calcium phosphorus product (CaPP), PTH, 25‐hydroxyvitamin D, 1,25‐‐dihydroxyvitamin D, and FGF‐23 concentrations. Results: Significant hazard ratios (hazard ratio; 95% confidence interval; P value) were as follows: BCS < 4/9 (1.579; 1.003‐2.282; P = .05), muscle atrophy (2.334; 1.352‐4.030; P = .01), increased creatinine (1.383; 1.16‐1.64; .01), hyperphosphatemia (3.20; 1.357‐7.548; P = .005), increased UPC (3.191; 1.310‐7.773; P = .01), increased CaPP (4.092; 1.771‐9.454; P = .003), and increased FGF‐23 (2.609; 1.090‐6.240; P = .05). Survival times for each IRIS CKD stage were significantly different (P = .01). Conclusions and Clinical Importance: Multiple variables, including FGF‐23, were associated with duration of survival in CKD dogs. FGF‐23 could be a prognostic marker in dogs with CKD.

Dietary Aspects of Weight Management in Cats and Dogs

The optimal weight loss diet for cats and dogs is best determined by obtaining a full dietary history and performing a detailed assessment of the pet, pet owner, and environment in which the pet lives. Incorporating information about pet and owner preferences allows for individualization of the weight management plan and has the potential to increase adherence. Calorie density, macronutrients, and micronutrient concentrations should be considered as part of a weight management plan. Owners should play an active role in the weight loss plan to have the best outcome.