Evidence map›Paper›PMID 28208659›Full record

ReviewInternational journal of molecular sciences2017

Developmental Origins of Chronic Kidney Disease: Should We Focus on Early Life?

You-Lin Tain, Chien-Ning Hsu

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
13.0field-weighted citation impact, top 1% of its field
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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Effect of Perinatal and Maternal Factors on Blood Pressure and Adiposity at Age 3.Journal of clinical hypertension (Greenwich, Conn.) · 2026
    Observational
  3. Review
  4. Review
  5. Review
  6. Pediatric and adult point of view on the gut-kidney axis in CKD.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Detect early, protect kidney health: World Kidney Day 2025.Pediatric nephrology (Berlin, Germany) · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Sex-specific epigenetic programming in renal fibrosis and inflammation.American journal of physiology. Renal physiology · 2023
    Review
  16. Article
  17. The NOS/NO System in Renal Programming and Reprogramming.Antioxidants (Basel, Switzerland) · 2023
    Review
  18. Hyperuricemia: the third key player for nephrosclerosis with ischemia.Hypertension research : official journal of the Japanese Society of Hypertension · 2023
    Article
  19. Article
  20. Review

1 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

2 authors at 2 institutions in 1 country.

You-Lin TainDepartment of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan. tainyl@hotmail.com.
Chien-Ning HsuDepartment of Pharmacy, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan. chien_ning_hsu@hotmail.com.
Chang Gung University · TWKaohsiung Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is becoming a global burden, despite recent advances in management. CKD can begin in early life by so-called "developmental programming" or "developmental origins of health and disease" (DOHaD). Early-life insults cause structural and functional changes in the developing kidney, which is called renal programming. Epidemiological and experimental evidence supports the proposition that early-life adverse events lead to renal programming and make subjects vulnerable to developing CKD and its comorbidities in later life. In addition to low nephron endowment, several mechanisms have been proposed for renal programming. The DOHaD concept opens a new window to offset the programming process in early life to prevent the development of adult kidney disease, namely reprogramming. Here, we review the key themes on the developmental origins of CKD. We have particularly focused on the following areas: evidence from human studies support fetal programming of kidney disease; insight from animal models of renal programming; hypothetical mechanisms of renal programming; alterations of renal transcriptome in response to early-life insults; and the application of reprogramming interventions to prevent the programming of kidney disease.

Indexed as

AnimalsDisease Models, AnimalDisease SusceptibilityEpigenesis, GeneticGene Expression RegulationGlucocorticoidsHumansOxidative StressRenal Insufficiency, ChronicRenin-Angiotensin SystemSex FactorsSodium ChannelsSympathetic Nervous SystemTranscriptomeGlucocorticoidsSodium Channelschronic kidney diseasecongenital anomalies of the kidney and urinary tract (CAKUT)developmental origins of health and disease (DOHaD)Epigenetic regulationnephron endowmentoxidative stressrenin-angiotensin systemsex differencessodium transportertranscriptome

Identifiers

PMID28208659
PMCPMC5343916
OpenAlexW2587776923

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.