Evidence map›Paper›PMID 28101838›Full record

ReviewMolecular and cellular pediatrics2017

Renal consequences of preterm birth.

Amelie Stritzke, Sumesh Thomas, Harish Amin, Christoph Fusch, Abhay Lodha

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular and cellular pediatrics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 4 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  6. Postnatal maximal weight loss, fluid administration, and outcomes in extremely preterm newborns.Journal of perinatology : official journal of the California Perinatal Association · 2022
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12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Amelie StritzkeDepartment of Pediatrics, Section of Neonatology, University of Calgary, Cumming School of Medicine, 780-1403 29th St NW, Calgary, AB, T2N 2T9, Canada. Amelie.Stritzke@albertahealthservices.ca.ORCID http://orcid.org/0000-0003-4809-0765
Sumesh ThomasDepartment of Pediatrics, Section of Neonatology, University of Calgary, Cumming School of Medicine, C536-1403 29St Nw, Calgary, AB, T2N2T9, Canada.
Harish AminDepartment of Pediatrics, University of Calgary, C4-615 2888 Shaganappi Trail NW, Calgary, AB, T3B 6A8, Canada.
Christoph FuschDivision of Neonatology, Department of Pediatrics, McMaster University, Room 4F5, 1280, Main Street West, Hamilton, Ontario, L8S4K1, Canada.
Abhay LodhaDepartment of Pediatrics and Community Health Sciences, Alberta Children's Hospital Research Institute, University of Calgary, C211C 1403 29St NW, Calgary, AB, T2N 2T9, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe developmental origin of health and disease concept identifies the brain, cardiovascular, liver, and kidney systems as targets of fetal adverse programming with adult consequences. As the limits of viability in premature infants have been pushed to lower gestational ages, the long-term impact of prematurity on kidneys still remains a significant burden during hospital stay and beyond.

objectivesThe purpose of this study is to summarize available evidence, mechanisms, and short- and long-term renal consequences of prematurity and identify nephroprotective strategies and areas of uncertainty.

resultsKidney size and nephron number are known to be reduced in surviving premature infants due to disruption of organogenesis at a crucial developmental time point. Inflammation, hyperoxia, and antiangiogenic factors play a role in epigenetic conditioning with potential life-long consequences. Additional kidney injury from hypoperfusion and nephrotoxicity results in structural and functional changes over time which are often unnoticed. Nephropathy of prematurity and acute kidney injury confound glomerular and tubular maturation of preterm kidneys. Kidney protective strategies may ameliorate growth failure and suboptimal neurodevelopmental outcomes in the short term. In later life, subclinical chronic renal disease may progress, even in asymptomatic survivors.

conclusionAwareness of renal implications of therapeutic interventions and renal conservation efforts may lead to a variety of short and long-term benefits. Adequate monitoring and supplementation of microelement losses, gathering improved data on renal handling, and exploration of new avenues such as reliable markers of injury and new therapeutic strategies in contemporary populations, as well as long-term follow-up of renal function, is warranted.

Indexed as

Acute kidney injuryDevelopmental origin of health and diseaseFetal origin of adult diseaseKidney diseaseNephrotoxicityPrematurityRenal developmentTubulopathy of prematurity

Identifiers

PMID28101838
PMCPMC5243236

What OpenQuestion holds

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Registered trials

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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.