Abstract
Simple SummaryThis study describes clinical findings in Boxer dogs with renal maldevelopment and proposes a possible mode of inheritance. Medical records of 9 female Boxer dogs, older than 5 months and with a clinical diagnosis of proteinuric chronic kidney disease prior to one year of age, showed the presence of polyuria and polydipsia, decreased appetite, weight loss, lethargy and weakness in all affected dogs. Common laboratory findings were proteinuria and diluted urine, non-regenerative anemia, azotemia, hyperphosphatemia, hypoalbuminemia and hypercholesterolemia. Histopathology of the kidneys identified the presence of immature glomeruli in all dogs. In 7 out of 9 related dogs, the pedigree analysis showed that a simple autosomal recessive trait may be a possible mode of inheritance. Renal glomerular immaturity should be suspected in Boxer dogs with a history of polyuria, polydipsia, decreased appetite, weight loss, lethargy, weakness and proteinuria. A prompt diagnosis of renal maldevelopment, potentially hereditary, may help to evaluate if relatives of the affected dogs might be at risk, thus assisting clinicians in reaching an early diagnosis. A routine clinical renal screening evaluation in this breed, especially when this disease is suspected, should be strongly recommended.Renal maldevelopment (RM) has been proposed to replace the old and sometimes misused term “renal dysplasia” in dogs. Although renal dysplasia has been described in Boxers, hereditary transmission has only been hypothesized. This study reports clinical and renal histological findings in Boxer dogs with RM, proposing a possible mode of inheritance. Medical records of 9 female Boxer dogs, older than 5 months and with a clinical diagnosis of chronic kidney disease prior to one year of age, were retrospectively reviewed. Polyuria and polydipsia (PU/PD), decreased appetite, weight loss, lethargy and weakness were described in all affected dogs. Common laboratory findings were proteinuria, diluted urine, non-regenerative anemia, azotemia, hyperphosphatemia, hypoalbuminemia and hypercholesterolemia. Histopathology of the kidneys revealed the presence of immature glomeruli in all dogs, which is consistent with RM. In 7 related dogs, the pedigree analysis showed that a simple autosomal recessive trait may be a possible mode of inheritance. Renal maldevelopment should be suspected in young Boxer dogs with a history of PU/PD, decreased appetite, weight loss, lethargy, weakness and proteinuria. Due to its possible inheritance, an early diagnosis of RM may allow clinicians to promptly identify other potentially affected dogs among the relatives of the diagnosed case.
Highlights
Renal dysplasia is a frequently described congenital disease in veterinary medicine [1], defined as a disorganized development of the renal parenchyma due to an abnormal differentiation [2,3,4]
The term “renal maldevelopment” (RM) has been proposed to replace the old and sometimes misused term “renal dysplasia” in order to describe a type of juvenileonset chronic kidney disease (JOCKD) [5]
In dogs affected by familial glomerulopathies, clinical signs can be observed at different ages ranging from a few weeks to several years, the most common being lethargy, anorexia, vomiting, weight loss, and polyuria and polydipsia (PU/PD) [5]
Summary
Renal dysplasia is a frequently described congenital disease in veterinary medicine [1], defined as a disorganized development of the renal parenchyma due to an abnormal differentiation [2,3,4]. In severe forms (i.e., more than 25% of glomeruli affected in total), most of the affected dogs die of renal insufficiency at between 3 and 6 months of age; alongside anemia, azotemia and PU/PD, failure to grow is a prominent feature. Dogs affected by moderate forms (i.e., 10–25% of glomeruli affected in total) usually live for 1–3 years, during which time they develop progressive chronic kidney disease (CKD); excessive water intake, azotemia and stunted growth are frequent findings. In the presence of mild forms (i.e., less than 10% of glomeruli affected in total), dogs may develop renal failure in adulthood or else remain clinically normal; excessive water intake represents the hallmark of the clinical history [3]. Proteinuria of different degrees is identified regardless of the form in the majority of cases, whereas laboratory findings such as non-regenerative anemia, azotemia, hyperphosphatemia, hypoalbuminemia, hypercholesterolemia and diluted urine are less frequent [4,6]
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