Evidence map›Paper›PMID 30137494›Full record

ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2020

Elevated lipoxygenase and cytochrome P450 products predict progression of chronic kidney disease.

Farsad Afshinnia, Lixia Zeng, Jaeman Byun, Stefanie Wernisch, Rajat Deo, Jing Chen, Lee Hamm, Edgar R Miller, Eugene P Rhee, Michael J Fischer and 5 more

Open access · greenAbstract read
In one paragraph

Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Alleles ofPeerJ · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

15 authors at 8 institutions in 1 country.

Farsad AfshinniaDepartment of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.
Lixia ZengDepartment of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.
Jaeman ByunDepartment of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.
Stefanie WernischDepartment of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.
Rajat DeoDivision of Cardiovascular Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Jing ChenDivision of Nephrology and Hypertension, Tulane University, New Orleans, LA, USA.
Lee HammDivision of Nephrology and Hypertension, Tulane University, New Orleans, LA, USA.
Edgar R MillerDepartment of Internal Medicine, Jones Hopkins University, Baltimore, MD, USA.
Eugene P RheeDepartment of Internal Medicine, Massachusetts General Hospital, Boston, MA, USA.
Michael J FischerDepartment of Medicine, University of Illinois, Center of Innovation for Complex Chronic Healthcare, Jesse Brown VAMC, Chicago, IL, USA.
Kumar SharmaDepartment of Internal Medicine-Nephrology, University of Texas Health San Antonio, San Antonio, TX, USA.
Harold I FeldmanCenter for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia, PA, USA.
George MichailidisDepartment of Statistics, University of Florida, Gainesville, FL, USA.
Subramaniam PennathurDepartment of Internal Medicine-Nephrology, University of Michigan, Ann Arbor, MI, USA.
CRIC Study Investigators
University of Michigan · USTulane University · USUniversity of Illinois Chicago · USUniversity of Pennsylvania · USJohns Hopkins University · USMassachusetts General Hospital · USThe University of Texas Health Science Center at San Antonio · USUniversity of Florida · US

Funding

UCSF CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTEUL1RR024131 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JOHNSTON, S. CLAIBORNE · 2006 to 2011
$111.2M
Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 2012 to 2026
$69.1M
Scientific and Data Coordinating Center(SDCC) for the P*U01DK060990 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI FELDMAN, HAROLD I · 2001 to 2017
$50.1M
Clinical and Translational Science Collaborative of ClevelandUL1TR000439 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI KONSTAN, MICHAEL W. · 2012 to 2016
$50.0M
Michigan Institute for Clinical and Health Research (MCHR)UL1TR000433 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MASHOUR, GEORGE ALEXANDER · 2012 to 2016
$49.9M
Institutional Clinical and Translational Science AwardUL1TR000003 · NCATS · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2012 to 2015
$38.9M
Clinical and Translational Science Collaborative of ClevelandUL1TR002548 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI MCCOMSEY, GRACE A · 2018 to 2022
$35.5M
Strengthening Stakeholder Engagement in Human Research Protections.UL1TR002003 · NCATS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI KARNIK, NIRANJAN SUBHASH, MERMELSTEIN, ROBIN J. · 2016 to 2024
$33.7M
Tulane COBRE in Cardiometabolic Diseases Clinical Research CoreP20GM109036 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI JING CHEN · 2016 to 2026
$25.3M
Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Continuation of the Coordinating Center for the Chronic Renal Insufficiency Cohort (CRIC) StudyU24DK060990 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Amanda Hyre Anderson, Laura M Dember · 2018 to 2026
$21.5M
Pilot and Feasibility (P and F) ProgramP30DK089503 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Joyce Lee · 2010 to 2026
$20.3M
NCATS NIH HHS UL1 TR000003NCATS NIH HHS UL1 TR000424NCATS NIH HHS UL1 TR000433NCATS NIH HHS UL1 TR000439NCATS NIH HHS UL1 TR002003NCATS NIH HHS UL1 TR002548NCRR NIH HHS M01 RR013987NCRR NIH HHS M01 RR016500NCRR NIH HHS UL1 RR024131NCRR NIH HHS UL1 RR029879NIDDK NIH HHS K08 DK106523NIDDK NIH HHS P30 DK020572NIDDK NIH HHS P30 DK081943NIDDK NIH HHS P30 DK089503NIDDK NIH HHS R01 DK072231NIDDK NIH HHS R01 DK139225NIDDK NIH HHS R24 DK082841NIDDK NIH HHS U01 DK060902NIDDK NIH HHS U01 DK060963NIDDK NIH HHS U01 DK060980NIDDK NIH HHS U01 DK060984NIDDK NIH HHS U01 DK060990NIDDK NIH HHS U01 DK061021NIDDK NIH HHS U01 DK061022NIDDK NIH HHS U01 DK061028NIDDK NIH HHS U01 DK114920NIDDK NIH HHS U24 DK060990NIDDK NIH HHS U24 DK097153NIGMS NIH HHS P20 GM109036NIGMS NIH HHS U54 GM104940
6 · The paper itself

Abstract

backgroundThe clinical relevance of arachidonic acid (AA) metabolites in chronic kidney disease (CKD) progression is poorly understood. We aimed to compare the concentrations of 85 enzymatic pathway products of AA metabolism in patients with CKD who progressed to end-stage kidney disease (ESKD) versus patients who did not in a subcohort of Chronic Renal Insufficiency Cohort (CRIC) and to estimate the risk of CKD progression and major cardiovascular events by levels of AA metabolites and their link to enzymatic metabolic pathways.

methodsA total 123 patients in the CRIC study who progressed to ESKD were frequency matched with 177 nonprogressors and serum eicosanoids were quantified by mass spectrometry. We applied serum collected at patients' Year 1 visit and outcome of progression to ESKD was ascertained over the next 10 years. We used logistic regression models for risk estimation.

resultsBaseline 15-hydroxyeicosatetraenoate (HETE) and 20-HETE levels were significantly elevated in progressors (false discovery rate Q ≤ 0.026). The median 20-HETE level was 7.6 pmol/mL [interquartile range (IQR) 4.2-14.5] in progressors and 5.4 pmol/mL (IQR 2.8-9.4) in nonprogressors (P < 0.001). In an adjusted model, only 20-HETE independently predicted CKD progression. Each 1 standard deviation increase in 20-HETE was independently associated with 1.45-fold higher odds of progression (95% confidence interval 1.07-1.95; P = 0.017). Principal components of lipoxygenase (LOX) and cytochrome P450 (CYP450) pathways were independently associated with CKD progression.

conclusionsWe found higher odds of CKD progression associated with higher 20-HETE, LOX and CYP450 metabolic pathways. These alterations precede CKD progression and may serve as targets for interventions aimed at halting progression.

Indexed as

Case-Control StudiesCohort StudiesCytochrome P-450 Enzyme SystemDisease ProgressionFemaleHumansHydroxyeicosatetraenoic AcidsKidney Failure, ChronicLipoxygenaseMaleMiddle AgedRenal Insufficiency, Chronic20-hydroxy-5,8,11,14-eicosatetraenoic acidCytochrome P-450 Enzyme SystemHydroxyeicosatetraenoic AcidsLipoxygenasecardiovascularCKDheart failureprogressionprostaglandins

Identifiers

PMID30137494
PMCPMC7391277
OpenAlexW2884885188

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.