Familial renal disease in dogs

Juvenile renal disease in dogs has been encountered in over 20 breeds but in only nine of these (cocker spaniel, Norwegian elkhound, lhasa apso, shih tzu, samoyed, dobermann, standard poodle, soft-coated wheaten terrier and bull terrier) have familial nephropathies been reported, and in only two (samoyed and cocker spaniel) has the exact mode of inheritance been elucidated. Reasons for this unsatisfactory state of affairs are: 1 Renal failure in young dogs may not be due to a familial nephropathy, and while helpful diagnostic information may be gained from blood and urine analysis, accurate diagnosis of the specific type of renal disease requires examination of renal biopsy or post mortem material by an experienced pathologist. 2 Not all affected animals show clinical signs at the same age, making collection of data, often from widely dispersed animals, both difficult and slow. 3 The disease process in one breed may be very different from that in another, so that each breed has to be investigated separately. 4 There has to be a willing determination to face the problem by individual breed clubs, with the commitment of a large number of breeders, owners and veterinary surgeons. Resistance or inertia at any level will prevent or delay successful investigation and possible prevention of the disease.     

Familial insulin-dependent diabetes mellitus in Samoyed dogs

Five adult Samoyed dogs from two unrelated litters were diagnosed with diabetes mellitus. Two full-sibling male dogs (Family A) were raised in the same household. The other three dogs, two female and one male, were also full siblings (Family B) raised in different households. All five dogs developed polyuria and polydipsia and demonstrated fasting hyperglycemia and glucosuria. Diabetes mellitus was diagnosed in all five dogs and responded to appropriate therapy with insulin. The occurrence of insulin-dependent diabetes mellitus in multiple, closely related Samoyed dogs suggests a familial predisposition in this breed.     

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.     

Proximal aortic dissection (dissecting aortic aneurysm) in a mature ostrich

The gross and histopathologic lesions observed in a case of spontaneous proximal aortic dissection (dissecting aortic aneurysm) in a mature ostrich are reported. At necropsy, a dissecting intramural hematoma was seen in the proximal aorta, extended about 12 cm distally from the aortic valves. Histopathologic changes in aortic dissection included fragmentation and disruption of elastic laminae, presence of cystic extracellular spaces, and pooling of ground substance in the tunica media. Hepatic copper levels were measured, and the low concentration found suggested that a copper deficiency together with other risk factors such as the elevation of blood pressure may have been implicated in the development of the aortic dissection seen in this ostrich.     

Familial dilated cardiomyopathy of young Portuguese water dogs

A novel dilated cardiomyopathy (DCM) in 12 related Portuguese Water Dogs was identified by retrospective analysis of postmortem and biopsy case records. Male and female puppies born to clinically healthy parents typically died at 13 (+/- 7.3) weeks of age (range, 2-32 weeks) because of congestive heart failure. Puppies died suddenly without previous signs or with mild depression followed by clinical signs of congestive heart failure 1-5 days before death. There was no sex predilection. The hearts were enlarged and rounded, with marked left ventricular and atrial dilation. No other significant structural cardiac defects were noted. The histologic changes in the myocardium were diffuse and characterized by myofibers of irregular sizes separated by an edematous interstitium. The myofibers had multifocal swollen, cleared segments often involving perinuclear areas that contained granular, phosphotungstic-acid-hematoxylin-positive material consistent with mitochondria. There was loss of the cross-striation pattern, and intercalated discs were difficult to identify. There was no evidence of concurrent myocardial fibrosis; rare chronic inflammatory infiltrates were noted in one dog. Noncardiac skeletal muscles were not affected. The underlying cause is unknown. From the pedigree analysis, an autosomal recessive pattern of inheritance is suspected. Based on the histologic findings, this DCM is most likely due to an underlying molecular (biochemical or structural) defect. The early onset and rapid progression of the disease makes this a clinically distinctive form of canine DCM.     

Familial motor neuron disease in Rottweiler dogs: neuropathologic studies

Two 6-week-old female Rottweiler littermates were evaluated for regurgitation, diminished growth, progressive ataxia, and pelvic limb weakness. Clinical examination indicated a progressive, diffuse, lower motor neuron disorder and megaesophagus. The pups were killed at 6 and 8 weeks of age. Lesions included central chromatolysis and swelling of the perikarya in many large motor neurons in the ventral gray matter of the spinal cord. Some involvement of red, oculomotor, trigeminal motor, and ambiguus nuclei of the brainstem was noted. Ultrastructurally, chromatolytic neurons had excess neurofilaments, and an increase in and enlargement of Golgi complexes. Wallerian-like degeneration was prominent in neuropil of spinal cord and in peripheral nerve. Clinical, histological, and ultrastructural findings were consistent with a progressive motor neuron disease.     

Computed tomography findings in portal vein aneurysm of dogs

In this retrospective study, the appearances of extrahepatic and intrahepatic portal vein aneurysms (PVAs) in dogs were evaluated using multidetector computed tomography (CT). Data from 3060 dogs that underwent abdominal CT were reviewed for focal portal vein dilatation. PVAs were detected in 15/3060 (0.49%) dogs. The bodyweights of dogs with PVAs were significantly higher than the bodyweights of dogs without aneurysms (P=0.0001). Male sex was also significantly associated with PVAs (OR=6.23). Boxers were predisposed to the development of PVA (OR=11.88). Extrahepatic PVAs were always located in the portal vein at the level of the gastroduodenal vein insertion and were saccular in 10/15 dogs and fusiform in 5/15 dogs. One dog had an additional intrahepatic aneurysm of the umbilical part of the left intrahepatic portal branch. No dogs had clinical signs related to the PVA(s), although one dog developed a portal vein thrombosis in the site of the aneurysm.     

Spontaneous aortic dissecting hematoma in two dogs.

This report describes 2 cases of spontaneous aortic dissecting hematoma in young Border Collie and Border Collie crossbred dogs. Histology was performed in one of the cases involving an unusual splitting of the elastin present within the wall of the aorta, consistent with elastin dysplasia as described in Marfan syndrome in humans. The first case involved a young purebred Border Collie that died suddenly and the second case involved a Border Collie crossbred dog that died after a 1-month history of seizures. Gross lesions included pericardial tamponade with dissection of the ascending aorta in the former case and thoracic cavity hemorrhage, mediastinal hematoma, and aortic dissection in the latter. Histologic lesions in the case of the Border Collie crossbred dog included a dissecting hematoma of the ascending aorta with elastin dysplasia and right axillary arterial intimal proliferation.     

Aortopulmonary fistula in a Warmblood mare associated with an aortic aneurysm and supravalvular aortic stenosis

This case report describes the clinical presentation, the necropsy findings, and genetic results of a 13-year-old Warmblood mare presented with colic and a bilaterally loud, holosystolic murmur. Echocardiographic examination revealed the presence of a thoracic aortic aneurysm, an aortic pseudoaneurysm, a periaortic hematoma (circumferential cuffing by perivascular hemorrhage), and aortopulmonary fistulation. A supravalvular aortic stenosis (SVAS) was visible during echocardiography. Necropsy confirmed that the thoracic aortic aneurysm had ruptured and connected to the pseudoaneurysm, which fistulated into the pulmonary artery. Histologically, the aneurysm wall revealed chronic lesions such as fibrosis, mucin depositions, mineralizations, and elastin fragmentation. The mid abdominal aorta showed lesions suggestive of a systemic elastin arteriopathy. Molecular analysis, however, could not attribute this disease to a variant in the elastin gene, the most common causative gene for SVAS. To the authors' knowledge, this case report describes a case of aortopulmonary fistulation in a Warmblood horse associated with the presence of SVAS and an aortic aneurysm.     

Clinical and neurological characteristics of aortic thromboembolism in dogs

OBJECTIVES: To characterise the clinical presentation and neurological abnormalities in dogs affected by aortic thromboembolism. METHODS: The medical records of 13 dogs diagnosed with aortic thromboembolism as the cause of the clinical signs, and where a complete neurological examination was performed, were reviewed retrospectively. RESULTS: The onset was acute in only four dogs, chronic in five dogs (with all of these presenting as exercise intolerance) or chronic with acute deterioration in four dogs. Dogs with an acute onset of clinical signs were more severely affected exhibiting neurological deficits, while dogs with a chronic onset of disease predominantly presented with the exercise intolerance and minimal deficits. The locomotor deficits included exercise intolerance with pelvic limb weakness (five of 13), pelvic limb ataxia (one of 13), monoparesis (two of 13), paraparesis (two of 13), non-ambulatory paraparesis (two of 13) and paraplegia (one of 13). There was an apparent male predisposition and the cavalier King charles spaniel was overrepresented. CLINICAL SIGNIFICANCE: The rate of onset of clinical signs appears to segregate dogs affected by aortic thromboembolism into two groups, with different clinical characteristics and outcomes. Dogs with an acute onset of the clinical signs tend to be more severely affected, while dogs with a chronic onset predominantly present with exercise intolerance. It is therefore important to consider aortic thromboembolism as a differential diagnosis in dogs with an acute onset of pelvic limb neurological deficits and in dogs with longer standing exercise intolerance.     

Familial subvalvular aortic stenosis in golden retrievers: inheritance and echocardiographic findings

Objectives : To describe the echocardiographic findings and pedigree analysis of golden retrievers with subvalvular aortic stenosis. Methods : Seventy‐three golden retrievers were evaluated by auscultation and echocardiography. A subcostal continuous‐wave Doppler aortic velocity ê2·5 m/s and presence of a left basilar systolic ejection murmur were required for diagnosis of subvalvular aortic stenosis. Three echocardiographic characteristics were recorded: evidence of aortic insufficiency, subvalvular ridge or left ventricular hypertrophy. A disease status score was calculated by totalling the number of echocardiographic ‐characteristics per subject. Results : Thirty‐two of 73 dogs were affected and their aortic velocities were as follows: range 2·5 to 6·8 m/s, median 3·4 m/s and standard deviation 1·2 m/s. Echocardiographic characteristics of 32 affected dogs were distributed as follows: left ventricular hypertrophy 12 of 32, aortic insufficiency 20 of 32 and subvalvular ridge 20 of 32. Disease status score ranged from 0 to 3 with a median of 2. There was a statistically significant correlation between aortic velocity and disease status score (r=0·644, P<0·0001). Subvalvular aortic stenosis was observed in multiple generations of several families and appears familial. Clinical Significance : Subvalvular aortic stenosis in the golden retriever is familial. Severity of stenosis correlates well with cumulative presence of echocardiographic characteristics (left ventricular hypertrophy, subvalvular ridge and aortic insufficiency).     

Rupture of an aortic sinus aneurysm in a 15-year-old broodmare

A 15-year-old, Standardbred broodmare with an aortic sinus aneurysm developed rupture of the aneurysm with subsequent rupture of a tricuspid valve chorda tendinae, tricuspid regurgitation, acute right-sided congestive heart failure, and pulmonary thromboembolism. Shunting of blood from the aorta through the ruptured aneurysm into the right ventricle resulted in decreased renal perfusion and acute renal failure. Initially, treatment of the mare with analgesics, fluids, and digoxin resulted in clinical improvement, but the mare's condition deteriorated after 8 days and the mare was euthanatized due to unrelenting pain and a poor prognosis. Echocardiography was useful in diagnosis of the cardiac disease in the broodmare.     

Contrast echocardiography in Boxer dogs with and without aortic stenosis

ObjectivesThe aim of this study was to investigate whether contrast echocardiography could enhance the subcostal Doppler signal for aortic flow measurements and achieve myocardial opacification, in Boxer dogs with and without AS.BackgroundIn evaluating dogs for aortic stenosis (AS) subcostal Doppler echocardiography was used for measurement of the aortic flow velocity, a measurement that can sometimes be difficult to perform in Boxer dogs.Animals, materials, and methodsCardiac auscultation, phonocardiographic and echocardiographic examinations, including a contrast study with Optison, were performed on 29 Boxer dogs selected based on previous examinations.ResultsThe initial subcostal Doppler signal was weak in 66% of the dogs and a marked improvement was seen in all dogs after contrast injection. The peak aortic flow velocity increased 5% from 2.58 ± 1.42 m/s before contrast to 2.71 ± 1.54 m/s after contrast (p = 0.003). This corresponds to a 2.8 mmHg increase in the pressure gradient from 26.6 mmHg before to 29.4 mmHg after contrast. A dose of 0.05–0.1 mL of Optison administered intravenously resulted in approximately 4 min of Doppler signal enhancement. With the present technique contrast echocardiography did not achieve myocardial opacification.ConclusionsSingle use of the contrast agent Optison can be recommended for enhancement of the subcostal Doppler signal in dogs, in which plain Doppler signals are difficult to obtain. Albeit statistically significant, the mild increase in peak aortic flow velocity after contrast was not considered biologically or clinically significant.