Evidence map›Paper›PMID 24877124›Full record

ReviewBioMed research international2014

The role of uric acid in kidney fibrosis: experimental evidences for the causal relationship.

Il Young Kim, Dong Won Lee, Soo Bong Lee, Ihm Soo Kwak

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 78 citations in OpenAlex.

  1. Pooled it
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  16. Redox regulation in diabetic kidney disease.American journal of physiology. Renal physiology · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Serum Uric Acid Levels and Cardiometabolic Profile in Middle-Aged, Treatment-Naïve Hypertensive Patients.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2022
    Article
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

4 authors at 2 institutions in 1 country.

Il Young KimDivision of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of Korea ; Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan 626-770, Republic of Korea.
Dong Won LeeDivision of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of Korea ; Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan 626-770, Republic of Korea.
Soo Bong LeeDivision of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of Korea ; Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan 626-770, Republic of Korea.ORCID 0000-0002-3388-7993
Ihm Soo KwakDivision of Nephrology, Department of Internal Medicine, Pusan National University School of Medicine, Yangsan 626-770, Republic of Korea ; Medical Research Institute, Pusan National University Hospital, Busan 602-739, Republic of Korea.
Pusan National University Yangsan Hospital · KRPusan National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperuricemia is a common finding in chronic kidney disease due to decreased uric acid clearance. The role of uric acid as a risk factor for chronic kidney disease has been largely debated, and recent studies suggested a role of uric acid in the causation and progression of kidney fibrosis, a final common pathway in chronic kidney disease. Uric acid and xanthine oxidase may contribute to kidney fibrosis mainly by inducing inflammation, endothelial dysfunction, oxidative stress, and activation of the renin-angiotensin system. Besides, hyperuricemia induces alterations in renal hemodynamics via afferent arteriolopathy and contributes to the onset and progression of kidney fibrosis. Xanthine oxidase inhibitors may prevent kidney damage via lowering uric acid and/or inhibiting xanthine oxidase. However, there is still no sufficient evidence from interventional clinical researches supporting the causal relationship between uric acid and kidney fibrosis. The effect and role of xanthine oxidase inhibitors in preventing kidney fibrosis and chronic kidney disease progression must be further explored by performing future large scale clinical trials.

Indexed as

AnimalsDisease Models, AnimalFibrosisHumansInflammationRenal Insufficiency, ChronicUric AcidXanthine OxidaseUric AcidXanthine Oxidase

Identifiers

PMID24877124
PMCPMC4026934
OpenAlexW2171046290

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.