An inherited renal disease that causes juvenile-onset renal failure has been recognized in Cocker Spaniels (known in North America as English Cocker Spaniels) worldwide for more than 50 years. During the last decade, research has demonstrated that the disease is caused by certain molecular abnormalities of the collagen content of the walls of the glomerular capillaries through which blood filtration occurs in the kidneys. This renal disease is analogous to a condition called Alport syndrome that occurs in people.
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English Cocker spaniels with FN develop chronic renal failure, usually while they are between 6 months and 2 years of age. The clinical signs associated with chronic renal failure caused by FN are the same as those associated with chronic renal failure due to any other cause. Clinical signs that are often observed include excessive water consumption (polydipsia), excessive urine volume (polyuria), reduced growth rate or weight loss, poor quality hair coat, reduced appetite, and vomiting. Such signs can develop insidiously and escape recognition until the degree of renal failure is so severe that overt uremia supervenes. At this late stage of the disease, physical examination findings may include thin body condition, dehydration, pallor of mucous membranes, uremic breath odor, and oral ulcerations. Alternatively, especially at earlier stages of the disease, physical exam findings may be normal.
English Cocker spaniels Laboratory features
When English Cocker spaniels dog with FN develop renal failure, serum chemistry test results will be abnormal in proportion to the severity of renal failure. Expected abnormalities include azotemia (increased BUN and creatinine concentrations), hyperphosphatemia, and metabolic acidosis. Hematology test results usually show some degree of anemia. Urinalysis findings for dogs in renal failure invariably include evidence of impaired urine concentrating ability (inappropriately low urine specific gravity). All of the laboratory test abnormalities mentioned so far might be associated with chronic renal failure due to any cause; they do not help to differentiate FN from any other potential cause of renal failure.
English Cocker spaniels |
Because FN is a glomerular disease, affected dogs invariably exhibit proteinuria by the time that any clinical illness that can be attributed to FN first develops. Indeed, as renal disease evolves in dogs that have FN, proteinuria always is the first abnormality that can be detected by non-invasive testing. Of course, proteinuria can be associated with a variety of different urinary tract disorders (e.g., bacterial urinary tract infection, urolithiasis, etc.), so an appropriate clinical investigation must be conducted to exclude such other conditions. Nonetheless, persistent renal proteinuria that is not otherwise explained in a young (3- to 12-month-old) Cocker Spaniel most often proves to be due to FN. If discovered very early in the course of disease, the magnitude of proteinuria may be mild, but it typically becomes marked within a month or two. Urine protein-to-creatinine (UPC) ratios commonly are in the 5-10 range, and occasionally are greater than 10.
If detected early, proteinuria may be observed while urine concentrating ability is well preserved (i.e., urine specific gravity is still high) and serum creatinine concentrations are still within the normal reference range. However, with continued monitoring, English Cocker spaniels with FN will have persistent proteinuria, will subsequently loose their urine concentrating ability, and will gradually develop increasing serum creatinine concentrations. If FN has progressed to renal failure by the time that laboratory tests are performed, the findings will include marked proteinuria and isosthenuria, as well as the hematologic and serum chemistry abnormalities expected with the severity of renal failure that then exists.
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English Cocker spaniels Treatment
The renal disease caused by FN invariably is progressive and ultimately fatal; however, the rate of disease progression observed in affected dogs is more rapid in some individuals than in others. Additionally, certain treatments (feeding a diet formulated for dogs with renal failure and administering an angiotensin converting-enzyme inhibitor such as enalapril or benazepril) may slow the rate of renal disease progression somewhat. Even if they are effective, however, such therapeutic efforts generally forestall the development of terminal renal failure by several weeks or a few months at best. Moreover, the rate of renal disease progression usually is fairly rapid during the late stages of the disorder. Once an affected dog develops moderate azotemia, the disease typically progresses to the terminal stage of renal failure within 3 to 6 more weeks.
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