ArticleBMC nephrology2021
Renal biomarkers of acute kidney injury in response to increasing intermittent hypoxia episodes in the neonatal rat.
Article in BMC nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Neonatal kidney injury in the hyperoxia-induced bronchopulmonary dysplasia mouse models: effect on morphology and biomarkers.Pediatric research · 2026Article
- Neonatal hyperoxia exposure leads to developmental programming of cardiovascular and renal disease in adult rats.Scientific reports · 2024Article
- Caffeine and kidney function at two years in former extremely low gestational age neonates.Pediatric research · 2024Article
- Hypoxia-Induced Kidney Injury in Newborn Rats.Toxics · 2023Article
- Educational Review: The Impact of Perinatal Oxidative Stress on the Developing Kidney.Frontiers in pediatrics · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe tested the hypotheses that: 1) early exposure to increasing episodes of clinically relevant intermittent hypoxia (IH) is detrimental to the developing kidneys; and 2) there is a critical number of daily IH episodes which will result in irreparable renal damage that may involve angiotensin (Ang) II and endothelin (ET)-1.
methodsAt birth (P0), neonatal rat pups were exposed to brief IH episodes from the first day of life (P0) to P7 or from P0-P14. Pups were either euthanized immediately or placed in room air (RA) until P21. RA littermates served as controls. Kidneys were harvested at P7, P14, and P21 for histopathology; angiotensin converting enzyme (ACE), ACE-2, ET-1, big ET-1, and malondialdehyde (MDA) levels; immunoreactivity of ACE, ACE-2, ET-1, ET-2, ET receptors (ET
resultsHistopathology showed increased renal damage with 8-12 IH episodes/day, and was associated with Ang II, ACE, HIF
conclusionsChronic neonatal IH causes severe damage to the developing kidney with associated elevations in vasoconstrictors, suggesting hypertension, particularly with 8 neonatal IH episodes. ACE-2 is not activated in early postnatal life, and this may contribute to IH-induced vasoconstriction. Therapeutic targeting of ACE and ET-1 may help decrease the risk for kidney injury in the developing neonate to prevent and/or treat neonatal acute kidney injury and/or chronic kidney disease.
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Registered trials
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