ArticleJournal of translational medicine2016
The magnitude of nephron number reduction mediates intrauterine growth-restriction-induced long term chronic renal disease in the rat. A comparative study in two experimental models.
Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Fetal growth restriction leads to prolonged nephrogenesis and gene dysregulation in the adult kidney.Life science alliance · 2026Article
- Renal proteomics of male offspring exposed to maternal protein restriction: molecular, epigenetic, and nephron-specific signatures of metabolic programming.Journal of physiology and biochemistry · 2026Article
- Guidelines for in vivo models of developmental programming of cardiovascular disease risk.American journal of physiology. Heart and circulatory physiology · 2024Review
- Use of novel structural features to identify urinary biomarkers during acute kidney injury that predict progression to chronic kidney disease.BMC nephrology · 2023Article
- The impact of intrauterine growth restriction and prematurity on nephron endowment.Nature reviews. Nephrology · 2023Review
- Antenatal Programming of Hypertension: Paradigms, Paradoxes, and How We Move Forward.Current hypertension reports · 2022Review
- Development of the Diabetic Kidney Disease Mouse Model Culturing Embryos in α-Minimum Essential MediumFrontiers in endocrinology · 2021Article
- Ouabain Protects Nephrogenesis in Rats Experiencing Intrauterine Growth Restriction and Partially Restores Renal Function in Adulthood.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Fetal Growth Restriction and Hypertension in the Offspring: Mechanistic Links and Therapeutic Directions.The Journal of pediatrics · 2020Review
- Prenatal hypoxia increases susceptibility to kidney injury.PloS one · 2020Article
- Effect of sex on glomerular filtration rate in programmed rats by prenatal dexamethasone.Physiological reports · 2019Article
- Low Birth Weight, Blood Pressure and Renal Susceptibility.Current hypertension reports · 2019Review
- Renal injury after uninephrectomy in male and female intrauterine growth-restricted aged rats.PloS one · 2019Article
- Developmental origins of nonalcoholic fatty liver disease as a risk factor for exaggerated metabolic and cardiovascular-renal disease.American journal of physiology. Endocrinology and metabolism · 2018Review
- Preterm Birth: Long Term Cardiovascular and Renal Consequences.Current pediatric reviews · 2018Review
- Elevated renal tissue oxygenation in premature fetal growth restricted neonates: An observational study.PloS one · 2018Observational
- Developmental Programming of Renal Function and Re-Programming Approaches.Frontiers in pediatrics · 2018Review
- Complications during pregnancy and fetal development: implications for the occurrence of chronic kidney disease.Expert review of cardiovascular therapy · 2017Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntrauterine growth restriction (IUGR) is a risk factor for hypertension (HT) and chronic renal disease (CRD). A reduction in the nephron number is proposed to be the underlying mechanism; however, the mechanism is debated. The aim of this study was to demonstrate that IUGR-induced HT and CRD are linked to the magnitude of nephron number reduction, independently on its cause.
methodsSystolic blood pressure (SBP), glomerular filtration rate (GFR), proteinuria, nephron number, and glomerular sclerosis were compared between IUGR offspring prenatally exposed to a maternal low-protein diet (9% casein; LPD offspring) or maternal administration of betamethasone (from E17 to E19; BET offspring) and offspring with a normal birth weight (NBW offspring).
resultsBoth prenatal interventions led to IUGR and a similar reduction in birth weight. In comparison to NBW offspring, BET offspring had a severe nephron deficit (-50% in males and -40% in females, p < 0.01), an impaired GFR (-33%, p < 0.05), and HT (SBP+ 17 mmHg, p < 0.05). Glomerular sclerosis was more than twofold higher in BET offspring than in NBW offspring (p < 0.05). Long-term SBP, GFR, and glomerular sclerosis were unchanged in LPD offspring while the nephron number was moderately reduced only in males (-28% vs. NBW offspring, p < 0.05).
conclusionIn this study, the magnitude of nephron number reduction influences long term renal disease in IUGR offspring: a moderate nephron number is an insufficient factor. Extremely long-term follow-up of adults prenatally exposed to glucocorticoids are required.
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