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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
2006-9-1
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pubmed:abstractText |
Mineralocorticoids stimulate renal tubular Na(+) reabsorption, enhance salt appetite, increase blood pressure, and favor the development of renal fibrosis. The effects of mineralocorticoids on renal tubular Na(+) reabsorption and salt appetite involve the serum- and glucocorticoid-inducible kinase 1 (SGK1). The kinase is highly expressed in fibrosing tissue. The present experiments thus explored the involvement of SGK1 in renal fibrosis. To this end, SGK1-knockout mice (sgk1 (-/-)) and their wild-type littermates (sgk1 (+/+)) were implanted with desoxycorticosterone acetate (DOCA)-release pellets and offered 1% saline as drinking water for 12 weeks. The treatment led to significant increases in fluid and Na(+) intake and urinary output of fluid and Na(+) in sgk1 (+/+) mice, effects blunted in sgk1 (-/-) mice. Blood pressure increased within the first 7 weeks to a similar extent in both genotypes, but within the next 5 weeks, it increased further only in sgk1 (+/+) mice. Creatinine clearance did not change significantly but albuminuria increased dramatically in sgk1 (+/+) mice, an effect significantly blunted in sgk1 (-/-) mice. Histology after 12 weeks treatment revealed marked glomerular sclerosis and tubulointerstitial damage with interstitial fibrosis and inflammation in kidneys from sgk1 (+/+) mice, but not from sgk1 (-/-) mice. In conclusion, a lack of SGK1 protects against DOCA/high-salt-induced albuminuria and renal fibrosis.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0946-2716
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pubmed:author |
pubmed-author:AmannKerstinK,
pubmed-author:ArtuncFerruhF,
pubmed-author:FriedrichBjörnB,
pubmed-author:JahovicNerminaN,
pubmed-author:KuhlDietmarD,
pubmed-author:LangFlorianF,
pubmed-author:NasirOmaimaO,
pubmed-author:RislerTeutT,
pubmed-author:SandulacheDianaD,
pubmed-author:VallonVolkerV,
pubmed-author:WulffPeerP
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pubmed:issnType |
Print
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pubmed:volume |
84
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
737-46
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pubmed:dateRevised |
2011-11-2
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pubmed:meshHeading |
pubmed-meshheading:16924469-Albuminuria,
pubmed-meshheading:16924469-Animals,
pubmed-meshheading:16924469-Blood Pressure,
pubmed-meshheading:16924469-Body Weight,
pubmed-meshheading:16924469-Calcium,
pubmed-meshheading:16924469-Creatinine,
pubmed-meshheading:16924469-Desoxycorticosterone,
pubmed-meshheading:16924469-Feeding Behavior,
pubmed-meshheading:16924469-Gene Targeting,
pubmed-meshheading:16924469-Hematocrit,
pubmed-meshheading:16924469-Immediate-Early Proteins,
pubmed-meshheading:16924469-Kidney Glomerulus,
pubmed-meshheading:16924469-Kidney Tubules,
pubmed-meshheading:16924469-Mice,
pubmed-meshheading:16924469-Nephritis, Interstitial,
pubmed-meshheading:16924469-Organ Size,
pubmed-meshheading:16924469-Potassium,
pubmed-meshheading:16924469-Protein-Serine-Threonine Kinases,
pubmed-meshheading:16924469-Sodium,
pubmed-meshheading:16924469-Sodium Chloride, Dietary
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pubmed:year |
2006
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pubmed:articleTitle |
Blunted DOCA/high salt induced albuminuria and renal tubulointerstitial damage in gene-targeted mice lacking SGK1.
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pubmed:affiliation |
Department of Physiology, University of Tübingen, Gmelinstr. 5, 72076, Tübingen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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