Evidence map›Paper›PMID 25906781›Full record

ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2015

The role of renin-angiotensin-aldosterone system genes in the progression of chronic kidney disease: findings from the Chronic Renal Insufficiency Cohort (CRIC) study.

Tanika N Kelly, Dominic Raj, Mahboob Rahman, Matthias Kretzler, Radhakrishna R Kallem, Ana C Ricardo, Sylvia E Rosas, Kaixiang Tao, Dawei Xie, Lotuce Lee Hamm and 2 more

Abstract read
In one paragraph

Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Role of noncoding RNAs in cardiac ageing.Frontiers in cardiovascular medicine · 2023
    Review
  9. Article
  10. An update on ACE2 amplification and its therapeutic potential.Acta physiologica (Oxford, England) · 2021
    Review
  11. Genetics and ESKD Disparities in African Americans.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2019
    Review
  12. 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

12 authors.

Tanika N KellySchool of Public Health and Tropical Medicine, Tulane University, New Orleans, LA 70112, USA.
Dominic RajMedical Faculty Associates, George Washington University, Washington, DC 20037, USA.
Mahboob RahmanUniversity Hospitals Case Medical Center, Case Western Reserve University, Louis Stokes Cleveland VA Medical Center, Cleveland, OH 44106, USA.
Matthias KretzlerUniversity of Michigan, Ann Arbor, MI 48109, USA.
Radhakrishna R KallemUniversity of Pennsylvania, Translational Research Center, Philadelphia, PA 19104, USA.
Ana C RicardoUniversity of Illinois at Chicago, Chicago, IL 60612, USA.
Sylvia E RosasJoslin Diabetes Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Kaixiang TaoThe Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Dawei XieThe Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Lotuce Lee HammTulane University School of Medicine, New Orleans, LA 70112, USA.
Jiang HeSchool of Public Health and Tropical Medicine, Tulane University, New Orleans, LA 70112, USA Tulane University School of Medicine, New Orleans, LA 70112, USA.
CRIC Study Investigators

Funding

UCSF CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTEUL1RR024131 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JOHNSTON, S. CLAIBORNE · 2006 to 2011
$111.2M
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
Zonulin Antibodies in Intestinal Permeabilitiy in IDDMM01RR016500 · NCRR · UNIVERSITY OF MARYLAND BALTIMORE · PI OSWALD, LYNN M · 2002 to 2009
$20.2M
Study of the Care and Outcomes of REnal InsufficiencyU01DK060902 · NIDDK · KAISER FOUNDATION RESEARCH INSTITUTE · PI GO, ALAN S · 2001 to 2025
$19.5M
Limited Competition for the Continuation of the Chronic Renal Insufficiency CohorU01DK061021 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI RAHMAN, MAHBOOB · 2001 to 2025
$17.3M
Prospective Renal Insufficiency Cohort Evaluation:PRICEU01DK060984 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI COHEN, DEBBIE L · 2001 to 2025
$17.0M
Prospective Cohort Study of Chronic Renal InsufficiencyU01DK061028 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RAO, PANDURANGA S · 2001 to 2025
$16.9M
Limited Competition for the Continuation of the Chronic Renal Insufficiency Cohort (CRIC) Hopkins Clinical CenterU01DK061022 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI APPEL, LAWRENCE JOHN · 2001 to 2025
$15.7M
Proposal for a Chicago-CRIC Clinical CenterU01DK060980 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LASH, JAMES P. · 2001 to 2025
$15.4M
NCATS NIH HHS UL1 TR000003NCATS NIH HHS UL1TR000003NCATS NIH HHS UL1 TR-000424NCATS NIH HHS UL1 TR000424NCATS NIH HHS UL1 TR000433NCATS NIH HHS UL1TR000433NCATS NIH HHS UL1 TR000439NCATS NIH HHS UL1TR000439NCRR NIH HHS M01 RR016500NCRR NIH HHS M01 RR-16500NCRR NIH HHS UL1 RR-024131NCRR NIH HHS UL1 RR024131NCRR NIH HHS UL1 RR029879NCRR NIH HHS UL1RR029879NIDDK NIH HHS R01 DK073665NIDDK NIH HHS R01 DK073665-01A1NIDDK NIH HHS U01 DK060902NIDDK NIH HHS U01DK060902NIDDK NIH HHS U01 DK060963NIDDK NIH HHS U01DK060963NIDDK NIH HHS U01 DK060980NIDDK NIH HHS U01DK060980NIDDK NIH HHS U01 DK060984NIDDK NIH HHS U01DK060984NIDDK NIH HHS U01 DK060990NIDDK NIH HHS U01DK060990NIDDK NIH HHS U01 DK061021NIDDK NIH HHS U01DK061021NIDDK NIH HHS U01 DK061022NIDDK NIH HHS U01DK061022NIDDK NIH HHS U01 DK061028NIDDK NIH HHS U01DK061028NIGMS NIH HHS P30 GM103337NIGMS NIH HHS P30GM103337
6 · The paper itself

Abstract

backgroundWe conducted single-marker, gene- and pathway-based analyses to examine the association between renin-angiotensin-aldosterone system (RAAS) variants and chronic kidney disease (CKD) progression among Chronic Renal Insufficiency Cohort study participants.

methodsA total of 1523 white and 1490 black subjects were genotyped for 490 single nucleotide polymorphisms (SNPs) in 12 RAAS genes as part of the ITMAT-Broad-CARe array. CKD progression phenotypes included decline in estimated glomerular filtration rate (eGFR) over time and the occurrence of a renal disease event, defined as incident end-stage renal disease or halving of eGFR from baseline. Mixed-effects models were used to examine SNP associations with eGFR decline, while Cox proportional hazards models tested SNP associations with renal events. Gene- and pathway-based analyses were conducted using the truncated product method. All analyses were stratified by race, and a Bonferroni correction was applied to adjust for multiple testing.

resultsAmong white and black participants, eGFR declined an average of 1.2 and 2.3 mL/min/1.73 m(2)/year, respectively, while renal events occurred in a respective 11.5 and 24.9% of participants. We identified strong gene- and pathway-based associations with CKD progression. The AGT and RENBP genes were consistently associated with risk of renal events in separate analyses of white and black participants (both P < 1.00 × 10(-6)). Driven by the significant gene-based findings, the entire RAAS pathway was also associated with renal events in both groups (both P < 1.00 × 10(-6)). No single-marker associations with CKD progression were observed.

conclusionsThe current study provides strong evidence for a role of the RAAS in CKD progression.

Indexed as

AdultAgedBiomarkersCohort StudiesDisease ProgressionFemaleGenotypeGlomerular Filtration RateHumansKidney Failure, ChronicMaleMiddle AgedPolymorphism, Single NucleotideProportional Hazards ModelsRenin-Angiotensin SystemYoung AdultBiomarkerschronic kidney diseasegeneticsrenin–angiotensin–aldosterone system

Identifiers

PMID25906781
PMCPMC4838004

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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.