| Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria. | |
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MedLine Citation:
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PMID: 22243792 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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The nephron number at birth is a quantitative trait that correlates inversely with the risk of hypertension and chronic kidney disease later in life. During kidney development, the nephron number is controlled by multiple factors including genetic, epigenetic, and environmental modifiers. Premature birth, which represents more than 12% of annual live births in the United States, has been linked to low nephron number and the development of hypertension later in life. In this report, we describe the development of a mouse model of prematurity-induced reduction of nephron number. Premature mice, delivered 1 and 2 days early, have 17.4 ± 2.3% (n = 6) and 23.6 ± 2% (n = 10) fewer nephrons, respectively, when compared with full-term animals (12,252 ± 571 nephrons/kidney, n = 10). After 5 weeks of age, the mice delivered 2 days premature show lower real-time glomerular filtration rate (GFR, 283 ± 13 vs 389 ± 26 μL/min). The premature mice also develop hypertension (mean arterial pressure [MAP], 134 ± 18 vs 120 ± 14 mm Hg) and albuminuria (286 ± 83 vs 176 ± 59 μg albumin/mg creatinine). This mouse model provides a proof of concept that prematurity leads to reduced nephron number and hypertension, and this model will be useful in studying the pathophysiology of prematurity-induced nephron number reductions and hypertension. |
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Authors:
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Cary Stelloh; Kenneth P Allen; David L Mattson; Alexandra Lerch-Gaggl; Sreenivas Reddy; Asraf El-Meanawy |
Publication Detail:
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Type: Journal Article Date: 2011-11-08 |
Journal Detail:
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Title: Translational research : the journal of laboratory and clinical medicine Volume: 159 ISSN: 1878-1810 ISO Abbreviation: Transl Res Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-01-16 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101280339 Medline TA: Transl Res Country: United States |
Other Details:
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Languages: eng Pagination: 80-9 Citation Subset: AIM; IM |
Copyright Information:
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Published by Mosby, Inc. |
Affiliation:
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Department of Medicine, Medical College of Wisconsin, Milwaukee, Wis. |
Export Citation:
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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