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Autumn Vetter

Autumn Vetter

2017 Morris Animal Foundation Veterinary Student Scholar
The University of Georgia
College of Veterinary Medicine
Class of 2019

Research Interests

Assessment of renal angiotensin II immunoreactivity in an ischemic model of feline chronic kidney disease

Autumn Vetter, Amanda Coleman, Bianca Lourenco, Cathy Brown, Dan Rissi, James Stanton, Chad Schmiedt, Elizabeth Howerth, Jaime Tarigo

Department of Pathology (Vetter, Brown, Rissi, Stanton, Howerth, Tarigo) and Department of Small Animal Medicine and Surgery (Coleman, Lourenco, Schmiedt), College of Veterinary Medicine, University of Georgia, Athens, GA

Over one third of all domestic cats will be affected by chronic kidney disease (CKD) in their lifetimes. Unfortunately, a full understanding of the pathways involved in feline CKD is limited, hindering our ability to prevent its occurrence and progression. Hallmark histologic lesions of feline CKD include chronic tubulointerstitial nephritis and fibrosis. In human CKD and in rodent models of CKD, the renin-angiotensin system (RAS) appears to be a major mediator of renal fibrosis, with angiotensin II (Ang II) acting as the major effector protein of this pathway. Predictably, clinical outcomes in human CKD have been improved by use of medications that block the RAS, and it is reasonable to suspect that these drugs may provide a viable therapeutic option in feline CKD as well. To date, little work has been done to characterize the intra-renal RAS in cats. Our group has recently described an ischemic model of feline renal fibrosis which induces chronic histological and biochemical changes that mimic those observed in naturally occurring CKD. Using archived renal tissue from healthy cats (n=8) and cats having previously undergone ischemic injury as a model of CKD (n=6), immunohistochemistry was performed in order to localize and semi-quantitate intra-renal Ang II. Compared to normal control tissues, those from cats having undergone ischemic injury displayed increased Ang II immunoreactivity. These results suggest that the RAS may be activated in cats with naturally occurring CKD and will provide the basis for future studies of cats with spontaneous disease. Understanding the role of RAS in feline CKD will help us better evaluate our current approach to medical management of this disease.

Research Grant: Grants on the Edge, University of Georgia, College of Veterinary Medicine and the Office of Research, FY 2017

Student Support: Morris Animal Foundation, Veterinary Medical Experiment Station, UGA College of Vet Med

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