Compensatory glomerulopathy in 3H1 Brachyrrhine mice with genetic renal hypoplasia is exacerbated by salt treatment

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2008
Authors
Kim, Jin Seon
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The Brachyrrhine (Br/+) mice displays a mutation that directly affects the six2 gene, and this results in premature development of the kidneys and nephrons. These mice exhibit renal hypoplasia which is characterized by a reduced kidney volume with a fewer number of nephrons. The purpose of this study is to compare the morphological differences between the 3H1 wild-type (Wt) and Br/+ mice subjected to salt loading. The specific aim of this project is to determine whether salt loading results in glomerulopathy in mice with heritable renal hypoplasia A total of 24 3Hl mice, ranging in age from 12 to 20 weeks, were divided into four groups of 6 mice each: (1) Wt, no salt, (2) Wt, salt-treated, (3) Br/+, no salt and (4) Br/+, salt-treated. The salt-treated groups were given 2% NaCl solution as a sole source of their fluid intake for 5 days while the control animals were given distilled water. After the mice were perfusion-fixed at the end of the 5th day, the kidneys were removed and embedded in paraffin in preparation for histological sectioning. The sections were stained using H&E, and relevant sections were photographed using an Olympus BX41light microscope. The sections were analyzed for the various stereological parameters and analyzed statistically. The fina1 results showed significant differences between the Wt and the Br/+ in kidney volume, glomerular density/number, and glomerular surface area The Wt mice were significantly larger in kidney volume, glomerular density, and glomerular number, while the salt-treated Br/+ were significantly larger in glomerular surface area Results indicate that salt treatment worsens glomerulopathy in the Br/+ mice as a result of compensatory hyperfiltration.
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Thesis (M.S.)--University of Hawaii at Manoa, 2008.
Includes bibliographical references (leaves 39-44).
vi, 44 leaves, bound ill. 29 cm
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Theses for the degree of Master of Science (University of Hawaii at Manoa). Biomedical Sciences (Physiology); no. 4318
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