Evidence map›Paper›PMID 27974318›Full record

ReviewAmerican journal of physiology. Renal physiology2017

A perspective on chronic kidney disease progression.

Jianyong Zhong, Hai-Chun Yang, Agnes B Fogo

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 3 pooled it
5.5field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 3 syntheses or guidelines pooled it, 142 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Trial
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  7. Trial
  8. Associations of Pre-Pandemic CKD With Acute and Post-Acute COVID-19: The C4R Study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. Microbes and GFR in Health and CKD in Mice.Journal of the American Society of Nephrology : JASN · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Urinary Plasminogen as a Marker of Disease Progression in Human Glomerular Disease.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2024
    Article

10 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

3 authors at 1 institution in 1 country.

Jianyong ZhongDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.
Hai-Chun YangDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee.ORCID 0000-0003-4265-7492
Agnes B FogoDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee; agnes.fogo@vanderbilt.edu.
Vanderbilt University Medical Center · US

Funding

RESOLUTION OF GLOMERULOSCLEROSISR01DK056942 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI FOGO, AGNES B. · 2001 to 2021
$4.9M
NIDDK NIH HHS R01 DK056942
6 · The paper itself

Abstract

Chronic kidney disease (CKD) will progress to end stage without treatment, but the decline of renal function may not be linear. Compared with glomerular filtration rate and proteinuria, new surrogate markers, such as kidney injury molecule-1, neutrophil gelatinase-associated protein, apolipoprotein A-IV, and soluble urokinase receptor, may allow potential intervention and treatment in the earlier stages of CKD, which could be useful for clinical trials. New omic-based technologies reveal potential new genomic and epigenomic mechanisms that appear different from those causing the initial disease. Various clinical studies also suggest that acute kidney injury is a major risk for progressive CKD. To ameliorate the progression of CKD, the first step is optimizing renin-angiotensin-aldosterone system blockade. New drugs targeting endothelin, transforming growth factor-β, oxidative stress, and inflammatory- and cell-based regenerative therapy may have add-on benefit.

Indexed as

Acute Kidney InjuryAnimalsDisease ProgressionEpigenesis, GeneticGenetic MarkersGenetic Predisposition to DiseaseGlomerular Filtration RateHumansKidneyKidney Failure, ChronicPhenotypeProteinuriaRenal Insufficiency, ChronicRenin-Angiotensin SystemRisk FactorsUrological AgentsGenetic MarkersUrological Agentsacute kidney injurygenomicregenerative therapysurrogate marker

Identifiers

PMID27974318
PMCPMC5374308
OpenAlexW2562945016

What OpenQuestion holds

Textmetadata
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.