Evaluation of a modified water-deprivation test for diagnosis of polyuric disorders in dogs.

A modified water-deprivation test was performed on 12 polyuric and 4 clinically normal dogs. Immediately after maximal urine osmolality had been achieved with water deprivation, antidiuretic hormone was injected to test further renal concentrating ability. The test provided accurate diagnosis of severe hypothalamic-neurohypophyseal diabetes insipidus in 3 dogs, partial diabetes insipidus in 2 dogs, and primary (psychogenic) polydipsia in 2 dogs. Five polyuric dogs with hyperadreno corticism had a response to the modified water-deprivation test similar to that of dogs with partial diabetes indipidus.     

Successful long-term treatment of congenital nephrogenic diabetes insipidus in a dog

A two-year-old intact male shiba inu dog with excessive polyuria and polydipsia (PU-PD) was diagnosed as having congenital nephrogenic diabetes insipidus based on clinical findings, the results of urinalysis, blood examinations, a modified water deprivation test and a low dose dexamethasone suppression test. The owner was advised to provide adequate access to drinking water, and treatment with a low dose of hydrochlorothiazide (2 mg/kg, twice daily) together with a low sodium diet was initiated. As a result, the daily water intake decreased significantly from 6500 to 7500 ml/day (800 to 980 ml/kg/day) to 1400 to 1900 ml/day (170 to 230 ml/kg/day) and the clinical signs associated with the PU-PD and dehydration improved over the following two years.     

Acquired nephrogenic diabetes insipidus in a dog with leptospirosis

A 5 year old male neutered Cairn Terrier was evaluated for signs of polyuria and polydipsia. Initial hematology and chemistry panels were unremarkable and urinalysis showed a persistent hyposthenuria. Eleven days later, the dog became lethargic, inappetent and had developed acute renal failure. The dog was ultimately euthanized due to a poor response to treatment. Microscopic agglutination titres were consistent with a diagnosis of leptospirosis. The initial hyposthenuria in this case was consistent with acquired nephrogenic diabetes insipidus. This is an uncommon presentation of leptospirosis that has not previously been described to progress to acute renal failure. Leptospirosis should be considered as a differential diagnosis in any dog presenting with polyuria and polydipsia and these patients should be treated as a zoonotic risk.     

Water transport in the kidney and nephrogenic diabetes insipidus

Nephrogenic diabetes insipidus is caused by an inability of the kidney to concentrate urine despite adequate concentration of vasopressin in blood and is characterized by polyuria, polydipsia, and hyposthenuria in the presence of plasma hyperosmolality. Nephrogenic diabetes insipidus is the result of defects in water homeostasis in the kidney. Nephrogenic diabetes insipidus occurs when the kidneys cannot or do not respond to vasopressin. There are 2 categories of nephrogenic diabetes insipidus. Congenital nephrogenic diabetes insipidus is a rare, inherited, irreversible cause of polyuria and polydipsia in humans that is even rarer in animals. Acquired nephrogenic diabetes insipidus is more common and is often secondary to illness or medication that interferes with the action of vasopressin in the renal tubules. Unlike congenital nephrogenic diabetes insipidus, acquired or secondary nephrogenic diabetes insipidus is often reversible with correction of the associated or causative problem.     

Diagnostic approach to polydipsia and polyuria

A variety of metabolic disturbances account for the majority of cases of polydipsia and polyuria. This chapter presents guides to differential diagnosis as well as a discussion of the etiology and clinical features of the primary causes--central diabetes insipidus, nephrogenic diabetes insipidus, and psychogenic polydipsia.     

Diabetes insipidus and hyperadrenocorticism associated with high plasma adrenocorticotropin concentration and a hypothalamic/pituitary mass in a dog

Central diabetes insipidus was diagnosed in association with a dexamethasone-insuppressible adrenocorticotropin-secreting tumor in a dog. Over the 3 years before the dog's death, the combination of specific pituitary function tests, peptide hormone radioimmunoassays, and visualization of the tumor by use of x-ray computed tomography of the skull, allowed an etiologic diagnosis. Because initial signs of glucocorticoid excess were questionable and adrenolytic therapy was not allowed by the owners, treatment consisted only of administration of synthetic vasopressin, which was successful in the management of the diabetes insipidus.     

The role of vasopressin in dogs with polyuria

Polyuria and polydipsia (PUPD) occur frequently in dogs and may be caused by a variety of endocrine, metabolic, and renal disturbances. The studies described in this PhD Thesis, which was defended in January 2004 in Utrecht, investigated the role of the antidiuretic hormone vasopressin (VP) in the pathogenesis of different forms of canine polyuria. Experiments in healthy dogs demonstrated that the ranges of urine specific gravity and urine osmolality are much larger than previously thought. A water deprivation test is not required in all polyuric dogs, because serial measurements of urine osmolality may already lead to the diagnosis of primary polydipsia, in some cases. In dogs with primary polydipsia a wide variation in VP responses to hypertonic stimulation can be found, including a hyperresponse, a hyporesponse, and a non-linear response. The significance of the VP response to hypertonic saline infusion as the 'gold standard' for a diagnosis of canine polyuria is discussed. In the dog, VP is secreted in a pulsatile fashion with a wide variation in the number of VP pulses, VP pulse duration, and VP pulse amplitude and height. The occurrence of spontaneous VP pulses may severely hamper the interpretation of the curve describing the relationship between plasma osmolality and plasma VP concentration during osmotic stimulation. A radioimmunoassay to measure the VP-dependent water channel aquaporin-2 (AQP2) in urine was developed in dogs. In healthy dogs, urinary AQP2 excretion closely reflects changes in collecting duct exposure to VP. Measurement of urinary AQP2 excretion in polyuric dogs may be helpful to distinguish between central diabetes insipidus, nephrogenic diabetes insipidus, and primary polydipsia.     

A case of central diabetes insipidus in the cat: diagnosis and treatment

A case of diabetes insipidus is described in a two-year-old entire male short-haired domestic cat. The clinical signs included a marked polyuria associated with secondary polydipsia and a urine specific gravity of 1–005. Diagnosis was confirmed by water deprivation test and response to desmopressin. Treatment with chlorothiazide diuretics is also described.     

Magnetic resonance imaging,clinicopathologic findings,and clinical progression of a puppy with confirmed Eastern equine encephalitis virus

A 5-month-old puppy was evaluated for rapidly progressive neurologic signs and pyrexia. Magnetic resonance imaging showed multifocal meningoencephalitis with transtentorial and foramen magnum herniation. A cerebrospinal fluid tap revealed highly cellular fluid, and the puppy was euthanized. Histopathology showed lymphoplasmacytic and neutrophilic meningoencephalitis. Viral polymerase chain reaction testing for Eastern equine encephalitis was positive. Rapid progression of neurologic signs and respiratory arrest necessitated mechanical ventilation. Severe hypernatremia, most consistent with central diabetes insipidus, developed.Key clinical message:Transtentorial and foramen magnum herniation and high cerebrospinal fluid cell counts may be indicators of poor prognosis. Brain death, respiratory arrest, and central diabetes insipidus may also ensue with Eastern equine encephalitis infection.     

Nephrogenic Diabetes lnsipidus—in Sibling Colts

Nephrogenic diabetes insipidus was diagnosed in two full sibling Thoroughbred colts. Each colt had a history of excessive urination. Extreme polydipsia (greater than 80 L per day) was documented in both colts. Inability to concentrate urine in response to water deprivation, infusion of hypertonic saline, or exogenous vasopressin administration indicated insensitivity of the collecting duct epithelial cells to vasopressin. A diagnosis of nephrogenic diabetes insipidus was further supported by a normal increase in plasma vasopressin concentration after water deprivation in the one colt in which such testing was pursued.     

Cryptococcal pyelonephritis in a dog

A 5-year-old castrated male Golden Retriever was evaluated for polyuria, polydipsia, and progressive regurgitation thought to be a result of bacterial pyelonephritis and megaesophagus. Bacteriologic culture of urine failed to yield clinically relevant growth, and results of a urine sediment examination were normal. With time, intention tremors and progressive neurologic dysfunction were also observed. At necropsy, a diagnosis of cryptococcal disease was confirmed histologically and immunohistochemically. Findings in the dog of this report were indicative of nephrogenic diabetes insipidus with polyuria and polydipsia caused by cryptococcal pyelonephritis. Neurologic manifestations of systemic cryptococcus infection included megaesophagus, esophageal hypomotility, and regurgitation attributed to localization of cryptococcal organisms in the brain stem in the region of the dorsal motor nucleus of the vagus nerve. To the authors' knowledge, this is the first report of polyuria secondary to cryptococcal pyelonephritis.     

Intestinal malabsorption and cryptosporidiosis in an adult dog

Chronic intestinal cryptosporidiosis was diagnosed as the cause of chronic diarrhea and weight loss in an adult dog without obvious signs of immunosuppression. Results of tests for digestive function suggested that the dog had impaired intestinal absorption or bacterial overgrowth. The nutrient malabsorption might have resulted in or have been caused by the cryptosporidiosis. Temporary clinical improvement without reduction in fecal oocyst concentration was noticed following treatment with clindamycin. The dog was euthanatized. At necropsy, the dog was found to have chronic lymphoplasmacytic enteritis and cryptosporidiosis. A veterinary student that worked in the ward where the dog was kept developed cryptosporidal diarrhea.     

Multiple endocrine abnormalities in Basenji dogs with renal tubular dysfunction

Three Basenji dogs with renal tubular dysfunction were studied. Hyposthenuria and diminished urine concentrating ability, indicative of nephrogenic diabetes insipidus, were documented. Metabolic acidosis, hyperchloremia, and reduction in glomerular filtration rate also were detected in all dogs. In addition, an exaggerated response to the adrenocorticotropin test and hyperaldosteronism, believed to be secondary to decreased effective circulating blood volume, were detected in all 3 dogs. Thyroxine values were decreased in all dogs and could be correlated with histopathologic changes of the thyroid gland in 2 dogs. Gastropathy and hypergastrinemia were identified in 2 dogs. Diffuse lymphocytic-plasmacytic enteritis was evident in 2 dogs. It was concluded that a urine concentrating defect that may be secondary to hypercortisolism exists in Basenji dogs with renal tubular dysfunction.     

Intestinal permeability testing in dogs with diet-responsive intestinal disease

Fifteen dogs with signs of small and, or, large bowel disease that responded clinically to an exclusion diet were studied, using differential sugar absorption as an objective parameter of the mucosal response to the diet. Intestinal permeability and function were assessed by determining the urinary excretion ratios of lactulose/rhamnose and xylose/3-O-methylglucose, respectively, following oral administration of a mixture of these four sugars. Five dogs, all retrievers, were tentatively diagnosed as having dietary hypersensitivity, based upon resolution of clinical signs and normalisation of high intestinal permeability following an exclusion diet and recurrence of signs (in four of five dogs) upon challenge with the original diet. The fifth dog did not become symptomatic when challenged, but intestinal permeability increased. The remaining 10 dogs were diagnosed as having food intolerance, based upon clinical improvement on an exclusion diet, relapse on challenge with their original diet, but lack of improvement in intestinal permeability. These findings suggest that a differential sugar absorption test may be useful to determine the reasons for clinical response to exclusion diets. Demonstration of increased intestinal permeability with subsequent normalization following an exclusion diet may be useful in the diagnosis of dietary hypersensitivity, while persistent abnormalities in intestinal permeability are suggestive of underlying intestinal disease and food intolerance.     

Vasopressin response to osmotic stimulation in 18 young dogs with polyuria and polydipsia

Common disorders of water homeostasis leading to polyuria include a variety of endocrine, metabolic, and renal disturbances. After exclusion of most of these conditions, the diagnostic dilemma of differentiating between central diabetes insipidus, primary polydipsia, and nephrogenic diabetes insipidus may remain. Here, we report on 18 young dogs with polyuria that had been present in most cases since the dogs were puppies. The conditions were categorized according to the plasma vasopressin (VP) response to hypertonicity. The VP response to osmotic stimulation was tested by IV infusion of 20% NaCl for 2 hours. The VP response in all dogs was abnormal. Three categories could be distinguished: an exaggerated response (n = 3), a subnormal response (n = 4), and a nonlinear response with high plasma VP concentrations unrelated to increases in plasma osmolality (n = 11). The VP response to hypertonicity did not consistently distinguish among different clinical entities. In the 9 dogs with variations in urine osmolality compatible with primary polydipsia, exaggerated, subnormal, and nonlinear responses were observed. Examination of the present data questions the generally accepted notion that VP measurements during hypertonic saline infusion are the "gold standard" for the diagnostic interpretation of causes of polydipsia and polyuria. Studies of the peripheral reflection in plasma of the pulsatile VP release in healthy and polyuric individuals, with and without osmotic provocation, should be performed.     

Pituitary tumour causing multiple endocrinopathies in a dog

A 9-year-old male Boxer with signs of lethargy, weight gain, polyuria, polydipsia, eosinopaenia and lymphopaenia was diagnosed as having hyperadrenocorticism. Concurrent central diabetes insipidus was diagnosed using a water deprivation test and antidiuretic hormone response test. A contrast radiographic technique was used to outline a pituitary mass. A chromophobe adenoma and secondary hypothyroidism were found on post-mortem examination.     

Keratoconjunctivitis sicca and diabetes mellitus in a dog.

Diabetes mellitus and keratoconjunctivitis sicca were diagnosed in a female Poodle. The dog was treated for diabetes and keratoconjunctivitis sicca until blood glucose concentrations were within normal limits. Treatment for keratoconjunctivitis sicca was suspended then, and signs of this disorder did not appear again. Most of the factors known to predispose to keratoconjunctivitis sicca were not applicable to this dog. On the basis of observations made in this dog, we suggest that diabetes mellitus and keratoconjunctivitis sicca may be linked. Clinical signs of the disorders developed simultaneously and resolved when diabetes mellitus was controlled with insulin.     

Sand impaction of the small intestine in eight dogs

Objective : To describe signalment, clinical findings, imaging and treatment of intestinal sand impaction in the dog. Methods : Medical records of dogs with radiographic evidence of small intestinal sand impaction were reviewed. Results : Sand impaction resulting in small intestinal obstruction was diagnosed in eight dogs. All dogs presented with signs of vomiting. Other clinical signs included anorexia, lethargy and abdominal pain. Radiographs confirmed the presence of radio-opaque material consistent with sand causing distension of the terminal small intestine in all dogs. Four dogs were treated surgically for their impaction and four dogs were managed medically. Seven of the eight dogs survived. Clinical Significance : Both medical and surgical management of intestinal sand impaction in the dog can be effective and both afford a good prognosis for recovery.     

Isolation of a rotavirus from a newborn dog with diarrhea

A rotavirus was isolated from a newborn dog that died after having clinical signs of diarrhea. Virus particles with rotaviral morphologic features were observed by transmission electron microscopy in the intestinal homogenate collected at necropsy. Cytopathic effects were observed, and rotaviral antigens were detected by indirect immunofluorescence in MA-104 monolayer cultures (a fetal rhesus macaque kidney cell) inoculated with intestinal homogenate. This rotavirus isolate, designated LSU 79C-36, may be a specific canine rotavirus or a rotavirus from another species.