ArticleScientific reports2018
Neonatal nephron loss during active nephrogenesis - detrimental impact with long-term renal consequences.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Cystatin C as a Renal Biomarker in Infants with Congenital Anomalies of the Kidney and Urinary Tract (CAKUT): A Systematic Review.Diagnostics (Basel, Switzerland) · 2026Review
- Preceding risks and mortality outcomes of different neonatal acute kidney injury in preterm infants.Pediatric research · 2023Article
- Sex differences in long-term kidney fibrosis following neonatal nephron loss during ongoing nephrogenesis.Molecular and cellular pediatrics · 2023Article
- Elevation of Arginase-II in Podocytes Contributes to Age-Associated Albuminuria in Male Mice.International journal of molecular sciences · 2023Article
- Low nephron endowment increases susceptibility to renal stress and chronic kidney disease.JCI insight · 2023Article
- No benefit of HIF prolyl hydroxylase inhibition for hypertensive renal damage in renovascular hypertensive rats.Frontiers in physiology · 2023Article
- Regulation of nephron progenitor cell lifespan and nephron endowment.Nature reviews. Nephrology · 2022Review
- Structural and functional changes in the kidney caused by adverse fetal and neonatal environments.Molecular biology reports · 2022Review
- Neonatal acute kidney injury: a case-based approach.Pediatric nephrology (Berlin, Germany) · 2021Review
- Prematurity, perinatal inflammatory stress, and the predisposition to develop chronic kidney disease beyond oligonephropathy.Pediatric nephrology (Berlin, Germany) · 2021Review
- Nephron number and its determinants: a 2020 update.Pediatric nephrology (Berlin, Germany) · 2021Article
- Expression of Retinoid Acid Receptor-Responsive Genes in Rodent Models of Placental Pathology.International journal of molecular sciences · 2019Article
- Effect of cocoa powder on hypertension and antioxidant status in uninephrectomized hypertensive rats.Veterinary world · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neonatal nephron loss may follow hypoxic-ischemic events or nephrotoxic medications. Its long-term effects on the kidney are still unclear. Unlike term infants, preterm neonates less than 36 weeks gestational age show ongoing nephrogenesis. We hypothesized that nephron loss during nephrogenesis leads to more severe renal sequelae than nephron loss shortly after the completion of nephrogenesis. Rats show nephrogenesis until day 10 of life resembling the situation of preterm infants. Animals were uninephrectomized at day 1 (UNX d1) resulting in nephron reduction during nephrogenesis and at day 14 of life (UNX d14) inducing nephron loss after the completion of nephrogenesis. 28 days after uninephrectomy the compensatory renal growth was higher in UNX d1 compared to UNX d14. Nephrin was reduced and collagen deposition increased in UNX d1. At 1 year of age, glomerulosclerosis and markers of tubulointerstitial damage were most prevalent in UNX d1. Moreover, the number of desmin-positive podocytes was higher and nephrin was reduced in UNX d1 indicating podocyte damage. Infiltration of inflammatory cells was heightened after UNX d1. Uninephrectomized animals showed no arterial hypertension. We conclude that neonatal nephron loss during active nephrogenesis leads to more severe glomerular and tubulointerstitial damage, which is not a consequence of compensatory arterial hypertension.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.