ArticleTranslational research : the journal of laboratory and clinical medicine2012
Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.
Article in Translational research : the journal of laboratory and clinical medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 54 papers, 3 of them syntheses that pooled it.
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Who cites it
54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 89 citations in OpenAlex.
- Association between early exposure to famine and risk of renal impairment in adulthood: a systematic review and meta-analysis.Nutrition & diabetes · 2024Pooled it
- A best-practice position statement on pregnancy after kidney transplantation: focusing on the unsolved questions. The Kidney and Pregnancy Study Group of the Italian Society of Nephrology.Journal of nephrology · 2018Guideline
- Type 1 diabetes, diabetic nephropathy, and pregnancy: a systematic review and meta-study.The review of diabetic studies : RDS · 2013Pooled it
- Epigenetic regulation of nephrogenesis: from Waddington's landscape to adult disease.American journal of physiology. Renal physiology · 2026Review
- Article
- Preterm Birth Increases Susceptibility to Hyperglycemia-Induced Kidney Injury With Sex-Specific Differences in Structural and Molecular Responses.Endocrinology, diabetes & metabolism · 2026Article
- Protecting Kidney Health in the First 1000 Days: The Pediatrician's Role in Safeguarding the Weakest.Diseases (Basel, Switzerland) · 2026Review
- Slight acceleration in podocyte mRNA loss in preterm-born children aged 3-5 years.Pediatric nephrology (Berlin, Germany) · 2026Article
- Placental epigenetic age and adolescent blood pressure: the Extremely Low Gestational Age Newborn cohort.Pediatric research · 2025Article
- Restricted mating windows and thrombospondin 2 gene deletion improve the precision of parturition timing in mice†.Biology of reproduction · 2025Article
- Preterm birth increases susceptibility to hyperglycemia induced glomerular alterations in male mice.Scientific reports · 2025Article
- Birthweight and risk of chronic kidney disease after a type 2 diabetes diagnosis in the DD2 cohort.Diabetologia · 2025Article
- Caspase 9-induced apoptosis enables efficient fetal cell ablation and disease modeling.Nature communications · 2025Article
- Podocyte involvement in the pathogenesis of preterm-related long-term chronic kidney disease.Histology and histopathology · 2024Review
- Associations of MRI-derived kidney volume, kidney function, body composition and physical performance in ≈38 000 UK Biobank participants: a population-based observational study.Clinical kidney journal · 2024Article
- Attenuation of acute kidney injury in a murine model of neonatalFrontiers in cellular and infection microbiology · 2024Article
- Exposure to Chinese famine and the risk of hyperuricemia in later life: a population-based cross-sectional study.Frontiers in nutrition · 2024Article
- The impact of intrauterine growth restriction and prematurity on nephron endowment.Nature reviews. Nephrology · 2023Review
- Low nephron endowment increases susceptibility to renal stress and chronic kidney disease.JCI insight · 2023Article
- Preterm birth leads to a decreased number of differentiated podocytes and accelerated podocyte differentiation.Frontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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.
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