Yorkshire terriers anecdotally have a higher incidence of increased BUN as compared with other breeds. However, this abnormality is often associated with normal creatinine levels and adequately concentrated urine, suggesting a prerenal cause. Differential diagnoses for prerenal causes of increased BUN in dogs include dehydration, GI bleeding, consumption of a high-protein diet, and increased protein catabolism (eg, due to strenuous exercise or corticosteroids), but in a large percentage of Yorkshire terriers, these causes are excluded.5
Yorkshire terriers are predisposed to GI disease, including protein-losing enteropathies (eg, lymphangiectasia).6 Thus, it has been postulated that the increased BUN may result from subclinical GI bleeding, although these patients do not appear to develop signs of iron-deficiency anemia and anecdotally have no response to GI-protectant therapy. In addition, a recent study in Yorkshire terriers with protein-losing enteropathy identified low BUN among the clinical pathologic findings.6 To further confound the issue, this breed has an increased incidence of congenital liver disease and corresponding decreased BUN synthesis.7
However, a renal origin cannot be completely excluded, as some Yorkshire terriers have concurrent proteinuria and in one study, Yorkies accounted for 5.8% of biopsy-confirmed cases of immune mediated glomerulonephritis,8 perhaps supporting glomerulotubular imbalance (anecdotal). Consequently, a cause for the increase remains unclear and more research (eg, evaluating SDMA) is needed. In the interim, high-protein diets, GI bleeding, and renal dysfunction should be eliminated as potential causes of increased BUN. Anecdotally, the biochemical abnormality does not appear to have much impact clinically in Yorkshire terriers.