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.     

Renal concentrating ability in dehydrated hyponatremic dogs

Eleven hyponatremic dogs were unable to concentrate their urine during periods of severe dehydration and azotemia. When normonatremia was reestablished in eight of the dogs, their renal concentrating ability returned. Six dogs, including the 3 dogs in which normonatremia was not reestablished, died or were euthanatized; renal lesions were not found during postmortem examination. Two dogs had hypoadrenocorticism, which has been documented as a cause of hyponatremia and impaired renal concentrating ability. Two dogs had gastrointestinal disease, which has been documented as a cause of hyponatremia, but not of impairment of renal concentrating ability. All dogs without hypoadrenocorticism had clinical and clinicopathologic indications of blood loss, which has not been documented as a cause of hyponatremia or impairment of renal concentrating ability. Hyponatremia (less than 120 mEq/L) was induced by chronic blood removal in a dog maintained on a low-sodium diet. During the period of hyponatremia, the dog became azotemic, hypotensive, and severely dehydrated; renal concentrating ability was impaired. We conclude that hyponatremia may be caused by hemorrhage, but irrespective of the cause, hyponatremia impairs renal concentrating ability.     

Disturbed Vasopressin Release in 4 Dogs with So-Called Primary Polydipsia

Primary polydipsia is characterized by a marked increase in water intake and secondary polyuria, and in dogs often is described as a behavioral problem or a psychological disorder. We describe 4 dogs with primary polydipsia, diagnosed on the basis of a modified water deprivation test, in which further examination included serial measurements of urine osmolality (UOsm) and plasma vasopressin (VP) measurements during water deprivation and hypertonic saline infusion. The dogs, ranging in age from 4 months to 4 years, all were presented for evaluation of polyuria and polydipsia. Physical examination, routine blood chemistry, and urinalysis disclosed no specific cause for the polyuria and polydipsia. During serial measurements UOsm spontaneously reached high concentrations in 2 dogs, whereas in the other 2 dogs UOsm also fluctuated but on no occasion exceeded 1,000 mosm/kg. Primary polydipsia was diagnosed when UOsm exceeded 1,000 mosm/kg at the end of the modified water deprivation test and plasma osmolality did not exceed the upper limit of the reference range during testing. During water deprivation, plasma VP concentrations remained relatively low. The VP response to hypertonic saline infusion was abnormal, with an increased threshold value in 3 dogs, an increased sensitivity in 2 dogs, and an exaggerated response in 1 dog. It is concluded that some dogs fulfilling current criteria for primary polydipsia produce concentrated urine spontaneously throughout the day in a pattern similar to what has been observed in healthy pet dogs. This finding can be regarded as diagnostic and precludes the need for a water deprivation test. During water deprivation testing, all 4 dogs produced highly concentrated urine in the face of low basal plasma VP concentrations. The observed abnormal VP release in response to hypertonic stimulation may be interpreted as a primary disturbance in the regulation of VP secretion, although it might also be the result of overhydration caused by a primary abnormality in drinking behavior.     

Renal dysplasia in boxers and Finnish harriers

Puppies from two litters of dogs were found to have severe polyuria and polydipsia. Four of the dogs were investigated by means of clinical examination, haematological and biochemical analysis, and urinalysis. A modified water deprivation response test was also performed in two of the dogs. Renal changes on postmortem examination in three of the dogs were found to be consistent with renal dysplasia. A possible explanation for the finding of hyposthenuria and the extreme polyuria and polydipsia in association with renal dysplasia may be lack of response to antidiuretic hormone owing to anomalous maturation of the renal tubules. Six other puppies from the two litters of dogs did not show any clinical signs of polyuria and polydipsia, although postmortem examination in one of them also revealed renal dysplasia. The clinical features of renal dysplasia may therefore vary greatly between individuals.     

Severe polyuria and polydipsia as major clinical signs in a horse with unilateral renal adenocarcinoma

A 14‐year‐old Swiss Warmblood gelding was presented with chronic severe polyuria, polydipsia and weight loss. At the time of admission, water intake was 240 l/day. On rectal examination, a large mass was identified in the left dorsal abdominal quadrant, which was shown to originate from the left kidney by transabdominal ultrasonographic examination. Unilateral nephrectomy via flank incision was performed under general anaesthesia. Histopathological examination of the tumour revealed a papillary renal adenocarcinoma. Successful outcome and survival was documented 13 months after surgery. Severe polyuria and polydipsia should be considered as major clinical signs for renal carcinoma in horses, which can be successfully treated with unilateral nephrectomy if no signs of metastatic spread are evident.     

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.     

Urologic disorders of the geriatric dog

Disorders of the urinary system are common in geriatric dogs. Common urinary disorders that are seen in older dogs include chronic renal failure, urinary incontinence, bladder tumors, and prostate problems. Therapy for chronic renal failure is aimed at both slowing the progression of the disease and ameliorating the signs of uremia. Therapeutic recommendations for the conservative medical management of chronic renal failure include reducing dietary protein, moderately reducing salt intake, maintaining normal serum phosphorus levels, providing free access to water, avoiding stress, supplementing water soluble vitamins, using anabolic steroids to treat the anemia of chronic renal failure, treating acidosis, and controlling hypocalcemia. Urinary incontinence can often be controlled or eliminated. The appropriate approach to management of this disorder is to identify and remove specific causes. Common causes of urinary incontinence are urethral incompetence, urinary tract infection, and polyuria and polydypsia. Bladder tumors are, fortunately, not a common tumor of dogs, but are more common in geriatric dogs than in the young. The most common bladder tumor is the transitional cell carcinoma. Therapy for this tumor is usually palliative because of its malignant nature and because it is usually located in the neck of the bladder. Its location in the bladder often makes it impossible to resect the tumor completely without removing the entire bladder and diverting the ureters. New chemotherapeutic modalities are being evaluated that may increase life expectancy after diagnosis and, therefore, improve prognosis. Prostate disease is also seen in older dogs. Types of prostate abnormalities seen in dogs include prostatic hyperplasia, cysts, abscesses, acute and chronic infection, and neoplasia. The institution of proper therapy requires an accurate diagnosis; neutering is often recommended as a part of therapy regardless of the type of prostatic disease present.     

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.     

Hypercalcaemia in the dog: a study of 40 cases

Forty dogs referred to the University Department of Clinical Veterinary Medicine, Cambridge for medical and oncological conditions between 1985 and 1990 were found to be hypercalcaemia In 18 cases the primary or underlying condition was diagnosed as lymphoproliferative disease with multicentric lymphoma occurring most commonly. Ten dogs were suffering from hypoadrenocorticism (Addison's disease) and two had adenocarcinomas of the apocrine glands of the anal sac. In three dogs a clinical diagnosis of renal dysplasia was made, this diagnosis being confirmed at post mortem examination in one dog. In the remaining cases hypercalcaemia was associated with a primary lung tumour, a thymoma, an osteosarcoma with widespread skeletal metastases, primary hyperparathyroidism due to a parathyroid adenoma, chronic panniculitis, iatrogenic hypoadrenocorticism following mito-tane therapy (one case each] and, in a further case, no diagnosis was reached. The most common clinical signs were inappetence, polyuria/ polydipsia, weakness, vomiting, lethargy and depression. As a group, the dogs with lymphoproliferative disease had a significantly higher mean plasma calcium concentration (4-3 ± 0–7 vs 3–5 ± 0–4 mmol/litre), a significantly lower mean plasma inorganic phosphate concentration (1–5 ± 0–5 vs 2–4 ± 09 mmol/litre) and were significantly older (5-5 ± 2–4 vs 3-3 + 1–8 years) than the dogs with hypoadrenocorticism.     

Familial progressive nephropathy in young Bull Terriers

The clinical, clinicopathological and pathological findings are described in three Bull Terrier bitches with advanced renal disease. The bitches were less than four years old and showed variable presenting signs but anorexia, lethargy and polydipsia were the most frequent. All three dogs were azotaemic and isosthenuric. Urinary protein was measured in two of the three cases. Both were proteinuric. At necropsy all dogs had shrunken kidneys. Histological examination revealed nephron loss, atrophy of glomerular tufts, interstitial fibrosis, and mineralisation of basement membranes.

The progressive renal disease in these dogs was similar to the condition reported in Bull Terriers in Australia, and is probably familial and inherited.     

Clinical evaluation of sodium sulfanilate clearance for the diagnosis of renal disease in dogs

Sodium sulfanilate (ss) clearance time was measured in 13 clinically normal dogs and in 24 dogs with suspected renal disease. The results were compared with those from more routine tests of renal function to assess whether measurement of ss clearance provided additional information about the degree of renal dysfunction. It was concluded that ss clearance is a more sensitive measure of renal dysfunction than is serum creatinine or blood urea nitrogen. Sodium sulfanilate half-life was increased before the complete loss of ability to concentrate urine; however, urine concentrating ability was impaired in some dogs with normal ss clearance. In dogs with glomerular disease, proteinuria developed before increased ss clearances. However, ss clearance was a more reliable method of monitoring the degree of renal dysfunction than was protein concentration in single urine samples.     

Familial progressive nephropathy in young Bull Terriers

The clinical, clinicopathological and pathological findings are described in three Bull Terrier bitches with advanced renal disease. The bitches were less than four years old and showed variable presenting signs but anorexia, lethargy and polydipsia were the most frequent. All three dogs were azotaemic and isosthenuric. Urinary protein was measured in two of the three cases. Both were proteinuric. At necropsy all dogs had shrunken kidneys. Histological examination revealed nephron loss, atrophy of glomerular tufts, interstitial fibrosis, and mineralisation of basement membranes. The progressive renal disease in these dogs was similar to the condition reported in Bull Terriers in Australia, and is probably familial and inherited.     

Prevalence of gastrointestinal tract lesions in 73 brachycephalic dogs with upper respiratory syndrome

OBJECTIVES: To determine the prevalence of gastrointestinal tract lesions in brachycephalic dogs with upper respiratory tract disease. METHODS: The gastrointestinal tract and respiratory disorders of 73 brachycephalic dogs presented with upper respiratory signs were evaluated. Clinical signs and endoscopic and histological anomalies of the upper digestive tract were analysed. RESULTS: A very high prevalence of gastrointestinal tract problems in brachycephalic dogs presented with upper respiratory problems was observed clinically, endoscopically and histologically. Endoscopic anomalies of the upper digestive tract were present even in dogs without digestive clinical signs. Furthermore, histological evaluation of the digestive tract sometimes showed inflammatory lesions not macroscopically visible at endoscopy. Statistical analysis showed a relationship between the severity of the respiratory and digestive signs. This was significant in French bulldogs, males and heavy brachycephalic dogs. CLINICAL SIGNIFICANCE: These observations show a correlation between upper respiratory and gastrointestinal tract problems in brachycephalic breeds with upper respiratory disease. Surgical treatment of respiratory disease could improve the digestive clinical signs, and/or gastro-oesophageal medical treatment could improve the outcome for surgically treated brachycephalic dogs.     

Ibuprofen Ingestion in Ferrets: 43 Cases January 1995–March 2000)

Objective: To summarize typical clinical signs, characterize the anticipated course of action, and give treatment recommendations for ibuprofen ingestion in ferrets.
Design: Retrospective study
Patients: Records of 43 cases of ibuprofen ingestion in ferrets that were reported between January 1996-March 2000, to the ASPCA Animal Poison Control Center (APCC).
Measurements and Main Results: Twenty-seven (93.1%) ferrets that had ingested ibuprofen developed neurologic signs, such as depression, coma, ataxia, recumbency, tremors, and weakness. In addition, 16 cases (55.2%) had one or more GI effects including anorexia, vomiting, retching or gagging, diarrhea, and melena. Polydipsia, polyuria, dysuria, renal failure, weight loss, shallow breathing, metabolic acidosis, dehydration, and hypothermia were also reported. Death was reported in 4 cases. The lowest dose associated with death was 220 mg/kg.
Conclusion: Data in this study indicate that clinical signs of ibuprofen toxicosis in ferrets are more severe than those expected at similar dosages in dogs. The reason for this difference is poorly understood since the pathophysiology of ibuprofen is relatively unknown in ferrets. The onset of clinical signs appeared to occurr soon after ingestion and the toxic effects in ferrets typically involve the CNS, GI and renal systems. Treatment for ibuprofen toxicosis in the ferret includes stabilization, gastrointestinal decontamination, fluid diuresis, GI protection, and supportive care.(J Vet Emerg Crit Care 2001; 11(1):53–59)     

Familial Glomerulonephritis in Doberman Pinscher Dogs

Progressive renal disease in 13 related Doberman pinscher dogs had the histological criteria of membranoproliferative glomerulonephritis. Polyuria, polydipsia and weight loss were the usual initial abnormalities and were observed at one year of age or less in seven of 11 dogs diagnosed antemortem as having renal disease. There was no sex predilection. All dogs were traced to a common male dog no more than four generations previously.     

Chronic active hepatitis in 26 Doberman pinschers

Chronic active hepatitis with increased hepatic copper concentration was diagnosed in 25 female and 1 male Doberman Pinscher dogs. Common clinical signs included polyuria/polydipsia, weight loss, anorexia, icterus, and ascites. Increased liver enzyme activities and abnormal liver function test results were the most consistent clinicopathologic changes. The dogs were assigned to 3 groups on the basis of clinical course of the disease. Group 1 dogs (n = 12) had clinical signs of advanced liver failure and died within one week. Group 2 dogs (n = 7) had less severe clinical signs of liver disease and died within one month. Group 3 dogs (n = 5) did not have clinical signs of illness or had mild clinical signs of liver disease and died 1 to 42 months after initial evaluation. One dog could not be reevaluated and another dog was alive 3 months after initial examination. Treatments consisted of supportive care for dogs in group 1, and dietary manipulations and corticosteroids for dogs in groups 2 and 3. The association of increased liver copper concentration and chronic active hepatitis is not known.     

The relationship between water intake and the production of "wet" droppings in the domestic fowl

Production of “wet” droppings by laying hens was associated with polydipsia. Restriction of “wet droppers” to a “normal” water intake did not lead to dehydration, loss of body weight, decline in water balance or changes in electrolyte excretion and retention. It is concluded that “wet” droppings were the direct result of a primary polydipsia rather than an obligatory loss of body water followed by an increased water intake.     

Splenic Infarction in 16 Dogs: A Retrospective Study

Sixteen dogs with splenic infarction due to causes other than splenic torsion were identified. Dogs with splenic infarction often had multiple concurrent diseases, and surgical management of splenic infarction was associated with high mortality. Splenic infarction occurred in dogs with hypercoagulable conditions associated with liver disease, renal disease, and hyperadrenocorticism, or as a consequence of uniform splenomegaly, neoplasia, or thrombosis associated with cardiovascular disease. Clinical signs and common laboratory findings generally reflected the underlying disease process. A variety of splenic abnormalities were detected by abdominal ultrasound in 15 dogs, with the ventral extremity of the spleen being most often abnormal. Four dogs were euthanized or died because of the presence of severe systemic disease, whereas 12 dogs underwent laparotomy. Complete splenectomy was performed in 9 dogs and partial splenectomy was performed in 2 dogs. Seven dogs died in the immediate postoperative period, 3 required chronic veterinary care, and 2 had uncomplicated long-term recoveries. Splenic infarction should be regarded as a sign of altered blood flow and coagulation, rather than as a primary disease, and surgical management should be reserved for patients with life-threatening complications such as hemoabdomen or sepsis.     

Familial glomerulonephropathy in a litter of beagles

Membranoproliferative glomerulonephropathy was diagnosed in 5 of 7 adult Beagles from the same litter. Dogs were raised in more than 1 area of the United States. One died without evidence of renal disease when it was 3 years old. At 8 years of age, 2 dogs developed signs of uremia, including polyuria, polydipsia, and infrequent episodes of anorexia and vomiting. Serum biochemical variables and urine specific gravity values were consistent with renal azotemia. Both dogs had proteinuria. Although healthy, 3 of the 4 remaining Beagles had proteinuria. Of these 3, only 1 was azotemic. Membranoproliferative glomerulonephritis was diagnosed on the basis of results of histologic examination of renal biopsy specimens from 4 of the dogs. Electron microscopy performed on 3 of the renal biopsy specimens revealed identical lesions, consisting of an extremely thickened glomerular basement membrane with multilaminar splitting. Immunoglobulin or amyloid deposits were not detected. On the basis of similar clinicopathologic abnormalities, common genetic background, and identical histopathologic and electron microscopic findings, familial renal disease was diagnosed. Additional studies involving other related Beagles are needed to identify the hereditary nature of membranoproliferative glomerulonephropathy in Beagles.     

Familial renal amyloidosis in Chinese Shar Pei dogs

Renal amyloidosis was diagnosed in 14 young Chinese Shar Pei dogs, all of which were related. Clinical signs were those of renal failure and included vomiting, anorexia, lethargy, polydipsia, polyuria, weight loss, and dehydration. Some dogs had a history of intermittent fever and joint swelling. Laboratory findings also were compatible with renal failure and included azotemia, hyperphosphatemia, low total CO2 content in serum, isosthenuria, proteinuria, and hypercholesterolemia. All dogs had medullary deposition of amyloid, and 9 of 14 (64%) had glomerular involvement. The remaining renal lesions were typical of end-stage renal disease. In some dogs, amyloid deposits were found in other tissues (eg, liver, spleen, stomach, small intestine, myocardium, lymph node, prostate gland, thyroid gland, and pancreas). Amyloid deposits were sensitive to potassium permanganate oxidation, suggesting the presence of amyloid protein AA.