Diagnosis of diabetes insipidus observed in Swiss Duroc boars.

BACKGROUND: Diabetes insipidus (DI) is a rare disease in humans and animals, which is caused by the lack of production, malfunction or dysfunction of the distal nephron to the antidiuretic effect of the antidiuretic hormone (ADH). Diagnosis requires a thorough medical history, clinical examination and further laboratory confirmation. This case report describes the appearance of DI in five Duroc boars in Switzerland. CASE PRESENTATION: Two purebred intact Duroc boars at the age of 8 months and 1.5 years, respectively, with a history of polyuric and polydipsic symptoms had been referred to the Swine Clinic in Berne. Based on the case history, the results of clinical examination and the analysis of blood and urine, a tentative diagnosis of DI was concluded. Finally, the diagnosis was confirmed by findings from a modified water deprivation test, macroscopic examinations and histopathology. Following the diagnosis, three genes known to be involved in inherited DI in humans were analyzed in order to explore a possible genetic background of the affected boars. CONCLUSION: The etiology of DI in pigs is supposed to be the same as in humans, although this disease has never been described in pigs before. Thus, although occurring only on rare occasions, DI should be considered as a differential diagnosis in pigs with polyuria and polydipsia. It seems that a modified water deprivation test may be a helpful tool for confirming a diagnosis in pigs. Since hereditary forms of DI have been described in humans, the occurrence of DI in pigs should be considered in breeding programs although we were not able to identify a disease associated mutation.

Hypernatremia in a Cat with Toxoplasma-Induced Panencephalitis.

A 12 yr old female neutered Carthusian crossbreed cat was presented due to progressive neurological signs. Clinical signs included dehydration, stupor, and anisocoria. Laboratory examination revealed severe hypernatremia, azotemia, hyperglobulinemia, and an erythrocytosis. Clinical signs and hypernatremia suggested an intracranial process. Imaging studies revealed a loss of structure in the cerebrum, hypothalamus, and pituitary gland. Due to a poor prognosis, the cat was euthanatized. Histopathological examination revealed a subacute granulomatous and necrotizing panencephalitis with Toxoplasma-typical protozoa. The Toxoplasma-induced dysfunction of the hypothalamus and pituitary gland led to diabetes insipidus, which was, in combination with insufficient water intake, the most likely cause for the hypernatremia.

Lymphocytic hypophysitis in a dog with diabetes insipidus.

An 8-year-old male German longhaired pointer was referred for diabetes insipidus responsive to treatment with desmopressin. The dog had polyuria and polydipsia, exercise intolerance and a dull hair coat. Plasma concentrations of thyroid-stimulating hormone, thyroxine, growth hormone (GH) and insulin-like growth factor-1 were decreased; plasma adrenocorticotropic hormone (ACTH) was slightly elevated and plasma α-melanocyte-stimulating hormone (MSH) was within the reference range. Computed tomography revealed a heterogeneously contrast-enhancing pituitary mass compressing the hypothalamus. Transsphenoidal hypophysectomy was performed and microscopical examination of the surgical biopsy samples revealed hypophysitis without evidence of pituitary adenoma. The hypophysitis was characterized by marked lymphocytic infiltration of the adenohypophysis that contained a mixed population of neuroendocrine cells expressing GH, ACTH or α-MSH. The lymphocytes were identified as T cells, resulting in a final diagnosis of lymphocytic hypophysitis strongly resembling human primary lymphocytic hypophysitis.

Water homeostasis and diabetes insipidus in horses.

Diabetes insipidus (DI) is a rare disorder of horses characterized by profound polyuria and polydipsia (PU/PD), which can be caused by loss of production of arginine vasopressin (AVP). This condition is termed neurogenic or central DI. DI may also develop with absence or loss of AVP receptors or activity on the basolateral membrane of collecting-duct epithelial cells. This condition is termed nephrogenic DI. Equine clinicians may differentiate true DI from more common causes of PU/PD by a systematic diagnostic approach. DI may not be a correctable disorder, and supportive care of affected horses requires an adequate water source.

Central diabetes insipidus in an African Grey parrot.

CASE DESCRIPTION: A 5.5-year-old sexually intact female African Grey parrot (Psittacus erithacus) was evaluated for a 1-year history of pronounced polyuria and polydipsia. The bird also had a 1-month history of signs of mild depression and mydriasis. CLINICAL FINDINGS: Physical examination revealed a thin body condition and incomplete bilateral mydriasis. Other examination findings as well as CBC and screening radiography results were unremarkable. Plasma biochemical analysis revealed mild hypernatremia. The bird had a 3.3% loss in body weight over 170 minutes during a water deprivation test, and urine osmolality remained low. After IM administration of 0.9 microg of desmopressin, the rate of weight loss decreased substantially and urine osmolality increased 300% over the following 200 minutes. TREATMENT AND OUTCOME: Initial attempts to treat the bird with orally administered desmopressin failed to correct the polydipsia and polyuria. Ultimately, IM administration of 24 microg of desmopressin/kg (10.9 microg/lb) every 12 hours yielded a noticeable reduction in water consumption and urine production over a 6- to 8-hour period. Eight months later, the bird was returned for a recheck examination, at which time it was in good health and continued to respond to the medication. Despite continued response to the medication, right-sided internal ophthalmoparesis was detected 16 months after the initial diagnosis. CLINICAL RELEVANCE: To the authors' knowledge, central diabetes insipidus in birds has not been reported. The condition should be considered in birds with clinical signs of disease similar to those in mammals. Long-term IM administration of desmopressin may be a viable treatment option.

[Diabetes insipidus in a Swiss Braunvieh heifer with internal hydrocephalus]. / Diabetes insipidus bei einem Braunviehrind mit Hydrocephalus internus.

This case report describes the findings in a seven-month-old heifer with diabetes insipidus attributable to internal hydrocephalus. The heifer was referred to the clinic because of reduced appetite, polydipsia, decreased faecal output and weight loss. The heifer was examined daily for 8 days. She was thin and weak and had a dull dry hair coat and decreased appetite. The heifer urinated frequently; the urine was clear and yel low, had a specific gravity of 1.015. A complete blood cell count, biochemical profile and blood gas analysis revealed increased serum urea, increased serum creatinine, hypernatraemia, hyperchloraemia, hypercalcaemia and hypophosphataemia. The heifer received 10 litres of water and 3 litres of ruminal fluid from a healthy cow per os daily for 5 days. The heifer had access to fresh water ad libitum. The general condition of the heifer did not improve after this treatment. Although the concentration of serum urea and creatinine decreased, the concentrations of sodium, chloride and calcium remained higher than normal. Based on the findings, a diagnosis of diabetes insipidus was made and the heifer was euthanatized. Postmortem examination revealed severe internal hydrocephalus, and a definitive diagnosis of central diabetes insipidus attributable to internal hydrocephalus was made.

Diabetes insipidus.

Diabetes insipidus is a metabolic disorder caused by a deficiency in the production of or response to arginine vasopressin (AVP). The lack of, or inability to appropriately respond to, AVP results in a lack of tubular reabsorption of water and urine of low specific gravity. Two main categories of diabetes insipidus are recognized in veterinary medicine: central and nephrogenic.

Development and performances of a Japanese quail line homozygous for the diabetes insipidus (di) mutation.

A strain of Japanese quail with the polyuria disorder (excessive urination) was developed from founders that regurgitated water spontaneously. A back-cross with a nonpolyuric quail line showed that the polyuric strain was fixed for an autosomal recessive mutation that also induced polydipsia (excessive drinking). Plasma levels and brain mRNA contents for avian Arg vasotocin were little affected by the mutation, but plasma avian Arg vasotocin was 13-fold higher and brain mRNA contents were significantly increased in both normal and mutant quail following a 24-h water deprivation. Affected and normal birds had similar performance traits (egg production and quality, feed intake, and gross carcass traits), but residual feed consumption was higher in polydipsic males. These results are consistent with the hypothesis that this strain was fixed for a mutation similar to the di gene described in the chicken and which induces nephrogenic diabetes insipidus. This new strain of Japanese quail might constitute a convenient model for the analysis of the underlying mechanisms of the disorder in birds and for comparative study with mammals.

Functional and morphological changes in the hypothalamus-pituitary posterior lobe system after hypophysectomy in the dog.

Acute diabetes insipidus-like symptoms have been reported as a complication after hypophysectomy in dogs. These symptoms are believed to be the consequence of deficiency of arginine vasopressin (AVP) secretion. The symptoms spontaneously resolve within 2 weeks, but the mechanism is unclear. In the present study, AVP secretion related to increases in Na+ concentration and serum osmotic pressure was measured, and immunohistochemical analysis in the paraventricular and supraoptic nuclei was performed after hypophysectomy in normal dog. In the hypertonic saline test, the plasma AVP concentration slightly increased in hypophysectomized dogs, although the increase was markedly smaller than that in normal dogs. An immunohistochemical study of the hypothalamus nucleus revealed that, AVP-positive cells tended to decrease after hypophysectomy. It suggests that excision of the posterior lobe by surgery injured the axon of magnocellular neuron in the hypothalamus. A decrease in the function and the number of AVP-producing and -secreting magnocellular neurons after hypophysectomy, suggests that the clinical improvement of postoperative diabetes insipidus-like symptoms may not be related to the recovery of AVP secretion.

Secondary hypothyroidism following head trauma in a cat.

An 18-month-old female neutered domestic short hair cat was examined because of marked polydipsia and stunted growth following head trauma when it was 8 weeks old. Diagnostic evaluation revealed hyposthenuric urine, low concentrations of thyroid hormone and undetectable thyroid stimulating hormone concentrations which did not rise following thyroid releasing hormone administration. Lateral radiographs of the left and right tibiae revealed incomplete mineralisation of the greater tubercle and open physis. An almost empty sella turcica and a greatly reduced pituitary were visible on magnetic resonance images of the brain. A presumptive diagnosis of secondary hypothyroidism and central diabetes insipidus following head trauma was made.

Feline endocrinopathies.

Feline endocrinopathies (excluding diabetes mellitus) include hyperthyroidism, hypothyroidism, acromegaly, hyposomatotropism, diabetes insipidus, hyperadrenocorticism, primary sex hormone-secreting adrenal tumors, primary hyperaldosteronism, pheochromocytoma, hypoadrenocorticism, hyperparathyroidism, and hypoparathyroidism. Each of these conditions will be discussed including their prevalence, cause, clinical signs, diagnosis, treatment options, and prognosis.

Traumatic partial hypopituitarism in a cat.

Traumatic hypopituitarism was diagnosed in an 11-month-old male neutered cat. The presenting complaints were polydipsia, polyuria and lethargy of three months' duration. Craniocerebral trauma, as a result of a road traffic accident, had preceded the onset of clinical signs by six weeks. Neurological examination revealed right-sided mydriasis, reduced visual and tactile left forelimb placing reflexes and decreased proprioception in both the left fore- and hindlimb. Initial laboratory findings included hypernatraemia, hyperchloraemia, mild azotaemia, eosinophilia and isosthenuria. Low basal cortisol, thyroxine, thyroid-stimulating hormone and insulin growth factor-1 were noted. Subsequent to treatment with prednisolone, a water deprivation test confirmed the presence of central diabetes insipidus and therapy with synthetic antidiuretic hormone successfully ameliorated the polydipsia.

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.

Prophylactic efficacy of desmopressin acetate for diabetes insipidus after hypophysectomy in the dog.

The prophylactic efficacy of desmopressin acetate (DDAVP) on diabetes insipidus (DI) after hypophysectomy was investigated in the dog. In the control group, hypernatremia with a plasma level of 155 mEq/l or higher persisted for 12 hr from the 4th to the 16th hour after hypophysectomy, and symptoms of DI developed within five days after surgery. In the DDAVP treatment group, these changes were not observed, showing that administration of DDAVP (4 microg, installation, twice daily) effectively prevented hypernatremia that develops immediately after surgery and DI-like symptoms that persists for about one week after surgery.

Polyuria and polydipsia. Diagnostic approach and problems associated with patient evaluation.

Primary disorders of water balance (central diabetes insipidus [DI], nephrogenic DI, and psychogenic polydipsia) should always be considered in the differential diagnosis of polyuria and polydipsia. In general, animals with these disorders have only one laboratory abnormality: a low urine specific gravity. In most instances, the more common causes of polyuria and polydipsia (e.g., hyperadrenocorticism, chronic renal failure, pyelonephritis, pyometra) have specific and obvious abnormalities associated with the complete blood cell count, the serum chemistry profile, and urinalysis. In some cases, however, a low urine specific gravity may be the only abnormality associated with these more common findings. The workup for polyuria and polydipsia can be tedious, time-consuming, expensive, confusing, and not without significant patient morbidity, especially in those cases with normal or near-normal blood work. This article focuses on the diagnostic approach and problems associated with diagnostic testing in patients with disorders of water balance.

Transient diabetes insipidus in a dog with acromegaly.

A nine-year-old female beagle with acromegaly and extreme polyuria and polydipsia during dioestrus is described. It was demonstrated that polyuria was related to an inadequate rise of arginine-vasopressin (AVP) levels after water deprivation and stimulation with hypertonic saline. Administration of AVP did not lead to a significant increase in urine osmolality or reduction of urine volume. Clinical signs, except for bony changes, completely disappeared following ovariohysterectomy.

Concurrent central diabetes insipidus and panhypopituitarism in a German shepherd dog.

This report describes a German shepherd dog that was presented with proportionate dwarfism and coat changes typical of hypopituitarism but that was also profoundly polydipsic and polyuric. Investigations established a diagnosis of concurrent central diabetes insipidus. Treatment with desmopressin was successful in managing the polyuria and polydipsia.

Central diabetes insipidus in dogs: 20 cases (1986-1995).

OBJECTIVE: To assess clinical signs, biochemical findings, results of modified water deprivation and other diagnostic tests, response to treatment, and survival time in dogs with central diabetes insipidus (CDI). DESIGN: Retrospective study. ANIMALS: 20 dogs with CDI. PROCEDURE: Signalment, history, physical examination, results of diagnostic tests, response to treatment, and survival time were extracted from the medical record of each dog and supplemented with information obtained from owners via telephone. RESULTS: Isosthenuria or hyposthenuria was a consistent finding. Seven dogs with complete CDI and 13 dogs with partial CDI were identified on the basis of results of a modified water deprivation test. Dogs treated with desmopressin acetate responded well to treatment. Seven dogs were alive 18 to 72 months (median, 36 months) after diagnosis, and 10 dogs died or were euthanatized 1 week to 2 years (median, 2 months) after diagnosis. Seven of 10 dogs that died developed neurologic signs after diagnosis of CDI. Computed tomography revealed a mass in the region of the pituitary gland in 5 of 7 dogs. Necropsy of 6 dogs, including 2 dogs on which computed tomography had been performed, revealed neoplasia in the pituitary gland. CLINICAL IMPLICATIONS: Onset of neurologic signs after diagnosis of CDI in middle- to old-aged dogs indicates that CDI may not be a benign disease that is treated easily. Brain imaging is recommended after diagnosis of CDI in middle- to old-aged dogs. Also, because many dogs are isosthenuric on initial examination, CDI cannot be ruled out as a cause of polyuria and polydipsia on the basis of lack of hyposthenuria.