• Journal of Veterinary Clinics
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• v.24 no.4
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• pp.647-652
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• 2007

In the present study, we address systemically a case of renal disease developed in a 1 year-old male cocker spaniel dog in terms of clinical signs, clinical pathology and pathological examinations. The animal has been suffered from renal dysfunction signs such as polyuria, anorexia, vomiting, diarrhea and weight loss. The dog was very weak and emaciated and had foamy contents with foul-smell in oral cavity. The animals showed notable decrease in the number of red blood cells and severe decreases of hemoglobin and hematocrit with or without changes of mean corpuscular volume and mean corpuscular hemoglobin concentration values, indicating microcytic or normocytic hypochromatic anemia. In serum chemistry, blood urea nitrogen, creatinine, phosphorous, Na and Cl, which are associated with renal function, were dramatically increased. In addition, alanine aminotransferase, aspartate transferase, alkaline phosphatase, cholesterol, lipase and amylase were also significantly elevated, while K concentration was notably decreased. Urinalysis indicated prominent proteinuria with increase of bilirubin. Despite of symptomatic treatments, the dog was getting worse in healthy condition and dead in the end. At necropsy, both kidneys were brownish, pale, slightly small, and have diffuse, firm and subcapsular pits. Histologically, the kidneys indicated prominent segmental or diffuse interstitial fibrosis in cortex and medulla as well as glomerulonephritis. The clinical signs, clinical pathology and histopathological abnormalities of the young dog presented were consistent with chronic glomerulonephropathy, which was suspected to be a case of familial renal disease in the juvenile cocker spaniel dog.

• Childhood Kidney Diseases
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• v.14 no.1
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• pp.32-41
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• 2010

Purpose : Glomerulonephropathy (GN) often manifests as proteinuria and progresses to chronic renal failure without specific therapy. Mesenchymal stem cell (MSC) has been tried as a therapeutic agent in experimental GN, and previous studies showed that administration of MSC concomitantly to the insult inducing GN or via intra-renal administration ameliorated proteinuria. The purpose of this study was to test the therapeutic potential of MSC administered via intravenous route at the time of clinically evident proteinuria. Methods : MSCs were administered intravenously via tail vain into the mice with adriamycin (ADR) induced nephropathy (ADR-GN), two weeks after ADR injection when massive proteinuria was evident. To test the capacity of MSC modulate the cytokine production in the inflammatory milieu, the concentrations of IFN-$\gamma$ and IL-10 were measured in the supernatant of in vitro mixed lymphocyte culture (MLC) with or without additional MSC. Results : MSCs administered intravenously into the proteinuric mice with ADR-GN accelerated the recovery of this experimental GN with disappearance of proteinuria in two weeks when the saline treated (control) mice still showed significant proteinuria. The mice treated with MSC also had a tendency of better survival. Addition of MSC decreased IFN-$\gamma$ and increased IL-10 in the supernatant of MLC. Conclusion : This study showed that MSC had a therapeutic potential even when administered in a more clinically relevant setting into a proteinuric glomerulonephropathy model. Further study to verify the mechanism and long-term safety of this phenomenon is required.