Cardiac and Stress Biomarkers and Chronic Kidney Disease Progression: The CRIC Study.


Journal

Clinical chemistry
ISSN: 1530-8561
Titre abrégé: Clin Chem
Pays: England
ID NLM: 9421549

Informations de publication

Date de publication:
11 2019
Historique:
received: 12 04 2019
accepted: 27 08 2019
pubmed: 4 10 2019
medline: 27 5 2020
entrez: 4 10 2019
Statut: ppublish

Résumé

Increases in cardiac and stress biomarkers may be associated with loss of kidney function through shared mechanisms involving cardiac and kidney injury. We evaluated the associations of cardiac and stress biomarkers [N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity troponin T (hsTnT), growth differentiation factor 15 (GDF-15), soluble ST-2 (sST-2)] with progression of chronic kidney disease (CKD). We included 3664 participants with CKD from the Chronic Renal Insufficiency Cohort study. All biomarkers were measured at entry. The primary outcome was CKD progression, defined as progression to end-stage renal disease (ESRD) or 50% decline in estimated glomerular filtration rate (eGFR). Cox models tested the association of each biomarker with CKD progression, adjusting for demographics, site, diabetes, cardiovascular disease, eGFR, urine proteinuria, blood pressure, body mass index, cholesterol, medication use, and mineral metabolism. There were 1221 participants who had CKD progression over a median (interquartile range) follow-up of 5.8 (2.4-8.6) years. GDF-15, but not sST2, was significantly associated with an increased risk of CKD progression [hazard ratios (HRs) are per SD increase in log-transformed biomarker]: GDF-15 (HR, 1.50; 95% CI, 1.35-1.67) and sST2 (HR, 1.07; 95% CI, 0.99-1.14). NT-proBNP and hsTnT were also associated with increased risk of CKD progression, but weaker than GDF-15: NT-proBNP (HR, 1.24; 95% CI, 1.13-1.36) and hsTnT (HR, 1.11; 95% CI, 1.01-1.22). Increases in GDF-15, NT-proBNP, and hsTnT are associated with greater risk for CKD progression. These biomarkers may inform mechanisms underlying kidney injury.

Sections du résumé

BACKGROUND
Increases in cardiac and stress biomarkers may be associated with loss of kidney function through shared mechanisms involving cardiac and kidney injury. We evaluated the associations of cardiac and stress biomarkers [N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity troponin T (hsTnT), growth differentiation factor 15 (GDF-15), soluble ST-2 (sST-2)] with progression of chronic kidney disease (CKD).
METHODS
We included 3664 participants with CKD from the Chronic Renal Insufficiency Cohort study. All biomarkers were measured at entry. The primary outcome was CKD progression, defined as progression to end-stage renal disease (ESRD) or 50% decline in estimated glomerular filtration rate (eGFR). Cox models tested the association of each biomarker with CKD progression, adjusting for demographics, site, diabetes, cardiovascular disease, eGFR, urine proteinuria, blood pressure, body mass index, cholesterol, medication use, and mineral metabolism.
RESULTS
There were 1221 participants who had CKD progression over a median (interquartile range) follow-up of 5.8 (2.4-8.6) years. GDF-15, but not sST2, was significantly associated with an increased risk of CKD progression [hazard ratios (HRs) are per SD increase in log-transformed biomarker]: GDF-15 (HR, 1.50; 95% CI, 1.35-1.67) and sST2 (HR, 1.07; 95% CI, 0.99-1.14). NT-proBNP and hsTnT were also associated with increased risk of CKD progression, but weaker than GDF-15: NT-proBNP (HR, 1.24; 95% CI, 1.13-1.36) and hsTnT (HR, 1.11; 95% CI, 1.01-1.22).
CONCLUSIONS
Increases in GDF-15, NT-proBNP, and hsTnT are associated with greater risk for CKD progression. These biomarkers may inform mechanisms underlying kidney injury.

Identifiants

pubmed: 31578216
pii: clinchem.2019.305797
doi: 10.1373/clinchem.2019.305797
pmc: PMC6927328
mid: NIHMS1062207
doi:

Substances chimiques

Biomarkers 0
GDF15 protein, human 0
Growth Differentiation Factor 15 0
IL1RL1 protein, human 0
Interleukin-1 Receptor-Like 1 Protein 0
Peptide Fragments 0
Troponin T 0
pro-brain natriuretic peptide (1-76) 0
Natriuretic Peptide, Brain 114471-18-0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1448-1457

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK072231
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002548
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK060963
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR024131
Pays : United States
Organisme : NCRR NIH HHS
ID : M01 RR013987
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000003
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000439
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK060990
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR029879
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061028
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000433
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK060984
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061021
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK060990
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK060980
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK061022
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK103612
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000424
Pays : United States
Organisme : NCRR NIH HHS
ID : M01 RR016500
Pays : United States
Organisme : NIGMS NIH HHS
ID : P20 GM109036
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK060902
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002003
Pays : United States

Informations de copyright

© 2019 American Association for Clinical Chemistry.

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Auteurs

Nisha Bansal (N)

Department of Medicine, University of Washington, Seattle, WA; nbansal@nephrology.washington.edu.

Leila Zelnick (L)

Department of Medicine, University of Washington, Seattle, WA.

Michael G Shlipak (MG)

Department of Medicine, University of California, San Francisco, CA.

Amanda Anderson (A)

Department of Epidemiology, Tulane University, New Orleans, LA.

Robert Christenson (R)

Department of Laboratory Science, University of Maryland, Baltimore, MD.

Rajat Deo (R)

Department of Medicine, University of Pennsylvania, Philadelphia, PA.

Christopher deFilippi (C)

Department of Medicine, Inova Health System, Baltimore, MD.

Harold Feldman (H)

Department of Medicine, University of Pennsylvania, Philadelphia, PA.

James Lash (J)

Department of Medicine, University of Illinois, Chicago, IL.

Jiang He (J)

Department of Epidemiology, Tulane University, New Orleans, LA.

John Kusek (J)

Department of Medicine, University of Pennsylvania, Philadelphia, PA.

Bonnie Ky (B)

Department of Medicine, University of Pennsylvania, Philadelphia, PA.

Stephen Seliger (S)

Department of Laboratory Science, University of Maryland, Baltimore, MD.

Elsayed Z Soliman (EZ)

Department of Medicine, Wake Forest University, Winston-Salem, NC.

Alan S Go (AS)

Division of Research, Kaiser Permanente Northern California Division of Research, Oakland, CA.

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Classifications MeSH