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Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria. Transl Res 2012 Feb;159(2):80-9

Date

01/17/2012

Pubmed ID

22243792

Pubmed Central ID

PMC3896045

DOI

10.1016/j.trsl.2011.10.004

Scopus ID

2-s2.0-84855827231 (requires institutional sign-in at Scopus site)   66 Citations

Abstract

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.

Author List

Stelloh C, Allen KP, Mattson DL, Lerch-Gaggl A, Reddy S, El-Meanawy A

Authors

Kenneth Paul Allen DVM Associate Professor in the Research Office department at Medical College of Wisconsin
Ashraf El-Meanawy MD, PhD Professor in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Animals, Newborn
Cesarean Section
Disease Models, Animal
Female
Gestational Age
Glomerulonephritis
Humans
Hypertension, Renal
Infant, Newborn
Infant, Premature
Kidney Failure, Chronic
Mice
Nephrons
Pregnancy
Proteinuria