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The subject of this study was to determine urine specific gravity (USg) and urinary creatinine (UCrn) in dogs with different diseases but with normal renal function. Sick dogs with different diseases were divided into nine groups. Dogs suffering from polyuria/polydipsia, vomits, diarrhoea and females in oestrus or pregnant were excluded from the studies. The healthy dogs served as a control group. Over a three-year period, a total of 267 dogs were examined clinically as well as using imaging and laboratory diagnostics methods. In sick dogs, USg and UCrn were found to be essentially decreased (except animals with neurological and uterine diseases, and neurological diseases, respectively), as compared with normal dogs. In clinically healthy animals of the control group, UCrn and USg did not significantly differ between the females and males. As for the control group, no correlation between UCrn/USg and the body weight/age was found, either.
The hypothesis that acute pancreatitis in dogs could be diagnosed based on the ratio of urinary α-amylase activity to creatinine concentration (U-A/C) was tested. The study was performed on 292 dogs. Based on clinical, laboratory , and imaging findings, the dogs were divided into the following groups: 34 healthy patients serving as the control, 48 sick dogs with U-A/C>2.9, and 210 sick dogs with U/A-C<2.9. The sick dogs were subsequently divided into subgroups according to their diseases. The results of blood and urine analyses of sick dogs were compared to those of healthy dogs. The subgroups of dogs with U-A/C>2.9 differed from the control group in the same way: their serum and urine α-amylase activity and total urinary protein levels were significantly higher (P>0.001 ), and their urine specific gravity and urinary creatinine concentration were significantly lower (P<0.001). Acute or chronic pancreatitis was confirmed in many of the sick dogs with U-A/C>2.9 that were tested by ultrasonography (48%, 10/21) and histopathology (100%, 7/7). The findings might suggest that U-A/C ratio higher than 2.9 could serve as a cut-off value for diagnosing pancreatitis in dogs (excluding advanced chronic pancreatitis), regardless of concurrent diseases.
A dog (male, dachshund, aged 16.5 years) was euthanised due to hypoglycaemia, which had lasted for about eight years. Macroscopic examinations revealed bilateral tumours of the following sizes 7 cm x 5 cm x 4 cm (right) and 6 cm x 5 cm x 3.5 cm (left) in the sublumbar area. The presence of these tumours was found with an ultrasound examination performed on the dog at the age of 8 years. At that time, the tumours were only half the size. Histopathologically, the tumours were classified as phaeochromocytoma. The morphology of the liver, extensive necrotic foci and hyperplasia of connective tissue in particular, contributed to the dog's hypoglycaemia. The lesions could have developed as a result of damage to acinar cells of the pancreas and became advanced due to long-term glycocorticotherapy. In turn, originally, hypoglycaemia might have developed in the dog as a result of adrenal medulla failure induced by phaeochromocytoma.
A female dog of the Shar Pei breed, aged 28 months, was euthanised due to familial shar pei fever with amyloidosis. Microscopic and ultrastructural analyses demonstrated the dog to be affected by acute pancreatitis as an outcome of renal amyloidosis and morphological lesions occurring in the liver. The presented case report depicts the microscopic and ultrastructural pattern of the dog pancreas under the condition of acute inflammation and is a contribution to the knowledge on lesions in the kidneys and liver that induces disorders in the pancreas as well as on concomitant changes occurring in the spleen.
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