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.     

Concurrent follicular dysplasia and interface dermatitis in Boxer dogs

Recurrent or persistent follicular dysplasia and interface dermatitis are described in nine Boxers. Data on age, sex, seasonality of alopecia and histopathological features of the follicular dysplasia in these nine Boxers are comparable with those described in previous reports. The interface dermatitis was characterized by multifocal annular crusted lesions confined to the areas of follicular dysplasia. The inflammatory lesions were neither pruritic nor painful and affected dogs were otherwise healthy. Histopathologically the clinically inflammatory lesions were characterized as an interface dermatitis. Immunohistochemical studies failed to demonstrate immunoglobulins or complement at the basement membrane zone or within blood vessel walls. In dogs with recurrent or persistent disease, the follicular dysplasia and interface dermatitis ran identical, concurrent courses of spontaneous remission and recurrence, or persistence, respectively. One dog with persistent disease was treated successfully with tetracycline and niacinamide for the interface dermatitis, and melatonin for the follicular dysplasia. Although the aetiopathogenesis of this newly described condition and the relationship between the two histological reaction patterns are not known, photoperiod and genetic predisposition appear to play a role.     

Sodium Dodecyl Sulfate Polyacrylamide Gel Electrophoresis of Canine Urinary Proteins for the Analysis and Differentiation of Tubular and Glomerular Diseases

A preliminary investigation was performed to evaluate the use of a new, noninvasive technique for the localization of canine renal lesions by electrophoresis of urinary proteins. Urine specimens from six clinically healthy, nonproteinuric dogs and 12 dogs with persistent proteinuria were examined by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS PAGE). Urine electrophoretic patterns of proteinuric dogs were classified as glomerular (n=4), tubular (n=2), or mixed (glomerular and tubular) (n=6), based on the number and molecular weight of the silver-stained protein bands. Renal tissues from biopsies or necropsies were obtained from eight of the dogs with proteinuric disease. Interpretation of seven of eight electrophoretograms agreed with the histologic interpretation of renal lesions. We concluded SDS PAGE is a potentially valuable technique for detection and localization of renal lesions in dogs with proteinuric disease.     

Experimental Pyelonephritis in Dogs

Both E. coli and S. aureus were simultaneously injected into the left renal arteries of 55 female dogs. The arteries were occluded for 10 minutes prior to the injection and 10 minutes after. The renal veins were occluded during the injection and for 10 minutes after.

Ten animals did not survive longer than 24 hours. Ten of 45 developed neither renal lesions nor bacteriuria; of the remaining 35 which did, five were killed on each of the second, seventh and fourteenth days, and their renal lesions were assessed. Eighteen of the remaining 2 which developed bacteriuria were killed 3 to 12 weeks following surgery when bacteria could no longer be recovered from the urine. Only two dogs had persistent bacteriuria 12 weeks after surgery. All animals which developed bacteriuria had gross lesions in the left kidney but not the right.

Naturally occurring renal lesions were found in 17 of 78 random-source dogs at laparotomy. E. coli was cultured from the urine of five of these dogs but not from the kidneys. These lesions were morphologically similar to experimental ones.

It is concluded that with this method renal lesions similar to spontaneous ones can be produced, but care must be taken to exclude the relatively large percentage of random-source dogs with naturally occurring lesions from any study.

Various forms of infectious nephritis have been reported to be among the commonest diseases of dogs (1, 2). The successful production of chronic pyelonephritis in dogs depends on a variety of factors in addition to injecting bacteria into either the renal artery or ureter. Thus, ureteral obstruction, renal anoxia and reduced pulse pressure increased the susceptibility to renal infection (3, 4, 6, 7, 8).

Our laboratory has been concerned with the production of experimental pyelonephritis in dogs so that the efficacy of various treatments could be studied. The present work was undertaken to standardize methods of producing the disease and to compare experimental renal lesions with naturally occurring ones.

     

Sodium dodecyl sulfate polyacrylamide gel electrophoresis of canine urinary proteins for the analysis and differentiation of tubular and glomerular diseases

A preliminary investigation was performed to evaluate the use of a new, noninvasive technique for the localization of canine renal lesions by electrophoresis of urinary proteins. Urine specimens from six clinically healthy, nonproteinuric dogs and 12 dogs with persistent proteinuria were examined by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS PAGE). Urine electrophoretic patterns of proteinuric dogs were classified as glomerular (n = 4), tubular (n = 2), or mixed (glomerular and tubular) (n = 6), based on the number and molecular weight of the silver-stained protein bands. Renal tissues from biopsies or necropsies were obtained from eight of the dogs with proteinuric disease. Interpretation of seven of eight electrophoretograms agreed with the histologic interpretation of renal lesions. We concluded SDS PAGE is a potentially valuable technique for detection and localization of renal lesions in dogs with proteinuric disease.     

Canine elbow dysplasia and primary lesions in German shepherd dogs in France

Five hundred and twenty German shepherd dogs were screened for elbow dysplasia. The following primary lesions were analysed: joint incongruity (JI), fragmented medial coronoid process (FCP), osteochondrosis or osteochondritis of the medial humeral condyle and ununited anconeal process (UAP). Three radiographic views were used for each joint to achieve a definitive diagnosis. The prevalence of elbow dysplasia was 19.4 per cent. The most frequent lesion was JI (16.3 per cent), followed by FCP (11.3 per cent). UAP was diagnosed rarely (1.1 per cent). Combinations of lesions were very frequent (42.2 per cent of the dysplastic elbows). Although these results may be biased due to prescreening of dogs with UAP, it should be highlighted that JI and FCP occur frequently in German shepherd dogs and are probably the most common primary lesions of elbow dysplasia, although they have been under-reported until now.     

Inheritance of associated ocular and skeletal dysplasia in Labrador retrievers

A breeding colony was established to investigate the inheritance of associated ocular and skeletal dysplasia in Labrador Retrievers; 124 pups were produced. These pups were evaluated for the presence of ocular lesions, including cataracts, vitreous strands, persistent hyaloid remnants, retinal folds, retinal dysplasia, peripapillary hyperreflectivity, and rhegmatogenous retinal detachments, and skeletal abnormality, which was recognized by shorter than normal forelimbs and an abnormal morphologic appearance of the radius and ulna. Analysis of the distribution of lesions in pups indicated that the syndrome is caused by one abnormal gene, which has recessive effects on the skeleton and incompletely dominant effects on the eye. This would suggest that suspect carrier dogs could be identified by test matings with a known homozygote.     

Progressive nephropathy due to renal dysplasia in shih tzu dogs in Sweden: A clinical pathological and genetic study

The clinical and pathological findings in 45 shih tzu dogs with progressive nephropathy due to renal dysplasia are described. There was no sex dependence and the age at death/euthanasia varied from seven weeks to nine years, with a mean age of two years. The most common clinical signs were depression, polydipsia and vomiting. All dogs showed elevated blood urea levels and most passed dilute urine. Proteinuria and anaemia were the most common findings. At necropsy all dogs had small, lobulated, pale kidneys with capsular adhesion. Multiple cysts in the cortex and in the intermediary zone were found in most cases. The morphological changes were three different types based on microscopic examination:

• 1 Primary dysplastic lesions; where fetal glomeruli were the most consistent finding.
• 2 Compensatory changes; where hypertrophy and hyperplasia of the glomerular tufts and tubules were most frequently observed.
• 3 3 Inflammatory lesions and fibrosis were found in all cases.
• 4 A genetic study of 37 dogs suggests a simple recessive mode of inheritance. Based on this information a control scheme against renal dysplasia has been instigated.

     

Inherited retinal dysplasia and persistent hyperplastic primary vitreous in Miniature Schnauzer dogs

The objectives of this study were to define the clinical syndrome of retinal dysplasia and persistent primary vitreous in Miniature Schnauzer dogs and determine the etiology. We examined 106 Miniature Schnauzers using a biomicroscope and indirect ophthalmoscope. The anterior and posterior segments of affected dogs were photographed. Four enucleated eyes were examined using routine light microscopy and scanning electron microscopy. A pedigree was constructed and related dogs were test-bred to define the mode of inheritance of this syndrome. Congenital retinal dysplasia was confirmed in 24 of 106 related Miniature Schnauzer dogs. Physical and postmortem examinations revealed that congenital abnormalities were limited to the eyes. Biomicroscopic, indirect ophthalmoscopic, and neuro-ophthalmic examinations confirmed that some of these dogs were blind secondary to bilateral retinal dysplasia and detachment (nonattachment) (n = 13), and the remainder had generalized retinal dysplasia (n = 11). Fifteen of these dogs were also diagnosed with unilateral (n = 9) or bilateral (n = 6) persistent hyperplastic primary vitreous. Nutritional, infectious, or toxic etiologies were not evident on physical, postmortem, light microscopic, or transmitting and scanning electron microscopic examination of four affected Miniature Schnauzers. We examined the pedigree and determined that an autosomal recessive mode of inheritance was most likely. Three test-bred litters including those from affected parents, carrier and affected parents, and carrier parents confirmed this mode of inheritance. This study confirms that retinal dysplasia and persistent hyperplastic primary vitreous is a congenital abnormality that is inherited as an autosomal recessive condition in Miniature Schnauzers.     

Congenital and inherited renal disease of small animals.

Congenital renal diseases are present at birth and may be determined genetically; familial renal disorders occur in related animals with a higher frequency than would be expected by chance, and frequently are inherited. The most common familial disorders in cats and dogs include renal amyloidosis, renal dysplasia, polycystic kidneys, basement membrane disorders, and tubular dysfunction (Fanconi's syndrome). This article alerts the veterinarian to commonly observed congenital and hereditary conditions of the kidneys in small animals.     

Comparison of radiography and ultrasonography in the evaluation of renal lesions in the dog

Survey abdominal radiographs, excretory urograms, and nephrosonograms were obtained from 14 dogs with renal lesions. Renal enlargement was suspected on survey radiographs and confirmed by excretory urography in 13 dogs. Radiographic differentiation between a solid and cystic renal lesion was not possible in 9 dogs. Ultrasonography determined the presence of solid masses in 12 dogs, established the presence of a renal cyst in the opposite kidney in 1 dog, and revealed hydronephrosis in 2 dogs. Ultrasonography appeared to be more sensitive than radiography in differentiating the internal characteristics of renal lesions.     

Familial protein-losing enteropathy and protein-losing nephropathy in Soft Coated Wheaten Terriers: 222 cases (1983-1997)

Records and pedigrees of Soft Coated Wheaten Terriers (SCWT) with protein-losing enteropathy (PLE) or protein-losing nephropathy (PLN) were studied retrospectively. Criteria for inclusion were defined based on analysis of blood (panhypoproteinemia for PLE, hypoalbuminemia for PLN) and urine (proteinuria for PLN) and histopathologic examination of tissue. Two hundred twenty-two affected dogs (female:male ratio = 1.6, P < .001) were clinically identified. Dogs were diagnosed with PLE earlier (P < .005; mean +/- SD age: 4.7+/-2.6 years, n = 76) than with PLN (6.3+/-2.0 years, n = 84) or with both diseases (5.9+/-2.2 years, n = 62). Clinical signs included vomiting, diarrhea, weight loss, pleural and peritoneal effusions, and less commonly thromboembolic disease. Dogs with PLE generally had panhypoproteinemia and hypocholesterolemia; intestinal lesions included inflammatory bowel disease, dilated lymphatics, and lipogranulomatous lymphangitis. Dogs with PLN generally had hypoalbuminemia, proteinuria, hypercholesterolemia, and azotemia; renal lesions typically showed chronic glomerulonephritis/glomerulosclerosis, and less commonly endstage renal disease. Dogs with combined PLE/PLN had intermediate mean values (P < .001) for serum total protein, albumin, globulin, and cholesterol but had a higher mean urine protein:creatinine ratio than did PLN dogs (P < .05); intestinal and renal lesions in these dogs were similar to those in the other groups. Two dogs had incidental mild renal dysplasia. Pedigree analysis from 188 dogs demonstrated a common male ancestor, although the mode of inheritance is unknown. Both PLE and PLN are common diseases in this small breed population. The prognosis is poor. Compared with previously reported intestinal and renal diseases in dogs, a new, distinctive familial predisposition for both PLE and PLN has been recognized in the SCWT breed.     

Renal pathology in working dogs in the South African National Defence Force

Urine analysis, serum biochemical profile and a cortical wedge biopsy for histopathological examination was performed on 42 South African National Defence Force (SANDF) dogs from around the country. The only significant finding on urine analysis and serum biochemistry was a relatively large number (16/42) of dogs with elevated serum inorganic phosphate levels. Histopathology revealed that only 9 of the animals had normal kidneys reflected in the wedge biopsy material, with over 50% of them showing signs of glomerular pathology (primarily mesangioproliferative glomerulonephritis). Other conditions detected histopathologically were haemosiderosis (47% of animals), focal nephrosis (2.4%), membranoproliferative glomerulonephritis (2.4%), focal interstitial nephritis (4.7%) and acute tubular nephrosis (4.7%). The lesions observed were of limited distribution and extent; this histopathological finding may account for the absence of significant abnormalities on urine analysis or serum biochemistry profiles. It appears from these results that a large percentage of the SANDF population would be expected to have mild renal lesions, but that these lesions are not severe enough to lead to clinical signs. The findings of this study are similar to those of randomly selected populations of non-military dogs performed in other areas of the world, which also demonstrated an unexpectedly high incidence of histopathological renal pathology in dogs considered healthy. These lesions may well, however, play a role in later life, and it is recommended that military veterinarians maintain an index of suspicion for renal disease, particularly glomerular disease. The aetiology of the histopathological lesions is unknown.     

Progressive myelopathy and neuropathy in New Zealand Huntaway dogs

AIM: To investigate the nature and cause of a progressive ataxia in three 20-month-old Huntaway dogs that were litter mates. METHODS: Affected dogs were examined before they were humanely killed and submitted to necropsy. Selected formalin-fixed tissues were examined by light and electron microscopy. RESULTS: The lesions were those of axon and myelin degeneration within sensory, proprioceptive and motor tracts of the spinal cord and to a lesser degree some peripheral nerves. CONCLUSION: A progressive myelopathy and neuropathy, tentatively described as a central-peripheral distal axonopathy, was present in all 3 dogs. The cause was not determined but was likely to be either genetic or nutritional. CLINICAL RELEVANCE: In the early stages of this disease, careful examination may be necessary to distinguish the signs of ataxia from orthopaedic disease such as hip dysplasia. Affected animals are unlikely to be of use as working dogs.     

Additional kinematic variables to describe differences in the trot between clinically normal dogs and dogs with hip dysplasia

OBJECTIVE: To describe the abnormal gait of dogs with hip dysplasia by use of kinematic gait analysis. ANIMALS: 19 large-breed dogs with moderate to severe clinical and radiographic evidence of hip dysplasia and 10 clinically normal dogs (controls). PROCEDURE: Kinematic and force plate data were collected, and degree of coxofemoral joint abduction-adduction, mediolateral foot movement, distance between hind feet, maximum hind foot elevation, mediolateral pelvic movement, and coxofemoral joint angular acceleration were calculated. Essential Fourier coefficients were determined and used to reconstruct mean angular acceleration curves. Fourier coefficients and foot and pelvic movement data were compared between groups. RESULTS: Dogs with hip dysplasia had a greater degree of coxofemoral joint adduction and range of abduction-adduction and greater lateral pelvic movement, compared with controls. Foot movement variables did not differ significantly between groups. Coxofemoral joint angular acceleration was greater in the middle to end of the stance phase, whereas deceleration was greater in the late stance to early swing phase and middle to end of the swing phase in dogs with hip dysplasia, compared with controls. CONCLUSIONS AND CLINICAL RELEVANCE: Differences in degree of coxofemoral joint abduction-adduction, amount of mediolateral pelvic movement, and coxofemoral joint angular acceleration between clinically normal dogs and dogs with hip dysplasia may indicate a compensation in gait of affected dogs as a result of discomfort or biomechanical effects attributable to hip dysplasia and degenerative joint disease. Information gained from kinematic and kinetic gait analyses may be useful in evaluating treatments for hip dysplasia in dogs.     

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.     

COMPUTED TOMOGRAPHY OF CANINE ELBOW JOINTS AFFECTED BY PRIMARY AND CONCOMITANT FLEXOR ENTHESOPATHY

Flexor enthesopathy is an important differential diagnosis for elbow lameness in dogs. The disorder can be a primary cause of elbow lameness or concomitant with other elbow pathology. Since treatment differs for primary and concomitant forms of flexor enthesopathy, a noninvasive method for distinguishing between them is needed. In the current prospective study, computed tomographic (CT) examination was performed before and after IV injection of contrast in 17 dogs with primary flexor enthesopathy, 24 dogs with concomitant flexor enthesopathy, 13 dogs with elbow dysplasia, and seven normal dogs. Dogs were assigned to groups based on results of clinical examination and at least three other imaging modalities. Computed tomographic lesions consistent with flexor enthesopathy were found in all clinically affected joints with primary flexor enthesopathy and in 29 of the 30 clinically affected joints with concomitant flexor enthesopathy. Those lesions were not found in sound elbows or joints affected by elbow dysplasia. Flexor lesions detected in dogs with primary flexor enthesopathy were not significantly different from those detected in dogs with the concomitant form. Findings indicated that CT can be applied to detect flexor enthesopathy, but a distinction between the primary and concomitant forms was not always possible. Authors recommend the use of multiple diagnostic techniques for treatment planning in affected dogs.     

Glomerular lesions in dogs infected with Leishmania organisms

OBJECTIVE: To histologically identify glomerular lesions in dogs infected with Leishmania organisms. ANIMALS: 41 dogs (17 sexually intact males and 14 sexually intact and 10 ovariohysterectomized females) that had positive results when tested for leishmaniosis as determined by use of serologic evaluation (indirect fluorescent antibody test, titers of 1:80 to 1:640) and direct microscopic identification of the protozoal organisms. PROCEDURE: Urine samples were collected by use of cystocentesis and examined by qualitative SDS-agarose gel electrophoresis (AGE). All dogs had non-selective (glomerular) or mixed (glomerular and tubular) proteinemia. Specimens were obtained from each dog during ultrasound-assisted renal biopsy and used for histologic examination. Each specimen was stained with H&E, periodic acid-Schiff, Goldner's trichrome, methenamine silver, and Congo Red stains. Specimens were adequate for evaluation when they contained at least 5 glomeruli/section, except for specimens stained with Congo Red in which 1 glomerulus/section was adequate. RESULTS: Examination of renal biopsy specimens revealed various glomerular lesions in all dogs and interstitial or tubular (or both) lesions in 23 of 41 (55%) dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Glomerular lesions that develop in dogs during infection with Leishmania organisms can be classified histologically as mesangial glomerulonephritis, membranous glomerulonephritis, membranoproliferative glomerulonephritis, and focal segmental glomerulonephritis. Tubulointerstitial histopathologic conditions were not observed as the primary lesion, despite being evident in 23 of 41 (55%) dogs. Use of SDS-AGE for qualitative evaluation of proteinuria and successive collection of specimens during renal biopsies following diagnosis of nonselective glomerular proteinuria provides the possibility for early identification of renal lesions.     

ULTRASONOGRAPHIC FINDINGS IN CAIRN TERRIERS WITH PRECLINICAL RENAL DYSPLASIA

Renal dysplasia is a hereditary disease characterized by abnormal differentiation of renal tissue. The ultrasonographic appearance of dysplastic canine kidneys has been reported in the late stage of the disease where inflammatory and degenerative changes are already present and the dogs are in chronic renal failure. In this study, we describe the ultrasonographic appearance of the kidneys of five related Cairn Terriers affected with renal dysplasia before the onset of clinical or laboratory evidence of renal failure. Common findings included poor corticomedullary definition and multifocal hyperechoic speckles in the renal medulla, or a diffusely hyperechoic medulla. Severity of ultrasonographic changes was related to the severity of histopathologic findings. The ability to detect dysplastic changes before clinical signs develop makes ultrasound a potentially useful screening method for canine renal dysplasia.