Association of Urine Galectin-3 With Cardiorenal Outcomes in Patients With Heart Failure.


Journal

Journal of cardiac failure
ISSN: 1532-8414
Titre abrégé: J Card Fail
Pays: United States
ID NLM: 9442138

Informations de publication

Date de publication:
Feb 2024
Historique:
received: 13 11 2022
revised: 10 05 2023
accepted: 11 05 2023
pmc-release: 01 02 2025
medline: 19 2 2024
pubmed: 11 6 2023
entrez: 10 6 2023
Statut: ppublish

Résumé

Approaches to distinguishing pathological cardiorenal dysfunction in heart failure (HF) from functional/hemodynamically mediated changes in serum creatinine are needed. We investigated urine galectin-3 as a candidate biomarker of renal fibrosis and a prognostic indicator of cardiorenal dysfunction phenotypes. We measured urine galectin-3 in 2 contemporary HF cohorts: the Yale Transitional Care Clinic (YTCC) cohort (n = 132) and the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist (TOPCAT) trial (n = 434). We assessed the association of urine galectin-3 with all-cause mortality in both cohorts and the association with an established marker of renal tissue fibrosis, urinary amino-terminal propeptide of type III procollagen (PIIINP) in TOPCAT. In the YTCC cohort, there was significant effect modification between higher urine galectin-3 and lower estimated glomerular filtration rates (eGFRs) (P Urine galectin-3 levels correlated with an established biomarker of renal fibrosis in 2 cohorts and was able to differentiate high- vs low-risk phenotypes of chronic kidney disease in HF. These proof-of-concept results indicate that additional biomarker research to differentiate cardiorenal phenotypes is warranted.

Sections du résumé

BACKGROUND AND OBJECTIVES OBJECTIVE
Approaches to distinguishing pathological cardiorenal dysfunction in heart failure (HF) from functional/hemodynamically mediated changes in serum creatinine are needed. We investigated urine galectin-3 as a candidate biomarker of renal fibrosis and a prognostic indicator of cardiorenal dysfunction phenotypes.
METHODS METHODS
We measured urine galectin-3 in 2 contemporary HF cohorts: the Yale Transitional Care Clinic (YTCC) cohort (n = 132) and the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist (TOPCAT) trial (n = 434). We assessed the association of urine galectin-3 with all-cause mortality in both cohorts and the association with an established marker of renal tissue fibrosis, urinary amino-terminal propeptide of type III procollagen (PIIINP) in TOPCAT.
RESULTS RESULTS
In the YTCC cohort, there was significant effect modification between higher urine galectin-3 and lower estimated glomerular filtration rates (eGFRs) (P
CONCLUSIONS CONCLUSIONS
Urine galectin-3 levels correlated with an established biomarker of renal fibrosis in 2 cohorts and was able to differentiate high- vs low-risk phenotypes of chronic kidney disease in HF. These proof-of-concept results indicate that additional biomarker research to differentiate cardiorenal phenotypes is warranted.

Identifiants

pubmed: 37301248
pii: S1071-9164(23)00194-X
doi: 10.1016/j.cardfail.2023.05.018
pmc: PMC10947725
mid: NIHMS1907582
pii:
doi:

Substances chimiques

Galectin 3 0
Biomarkers 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

340-346

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL128973
Pays : United States
Organisme : NHLBI NIH HHS
ID : R21 HL143092
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL139629
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL148354
Pays : United States
Organisme : NHLBI NIH HHS
ID : L30 HL115790
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL114868
Pays : United States

Informations de copyright

Copyright © 2023 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Disclosures JMT reports grants and/or personal fees from 3ive labs, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Astra Zeneca, Novartis, Cardionomic, MagentaMed, Reprieve, FIRE1,W.L. Gore, Sanofi, Sequana Medical, Otsuka, Abbott, Merck, Windtree Therapeutics, Lexicon Pharmaceuticals, Precardia, Relypsa, Regeneron, BD, Edwards Life Sciences, and Lilly; he has a patent for treatment of diuretic resistance issued to Yale and Corvidia Therapeutics, a patent for methods of measuring renalase issued to Yale, and a patent for treatment of diuretic resistance pending with Reprieve. VSR has a patent for treatment of diuretic resistance, US20200079846A1, issued to Yale and Corvidia Therapeutics, with royalties paid to Yale University, VSR and JMT and a patent for measuring renalase WO2019133665A2 issued to Yale. VSR reports personal fees from Translational Catalyst. ZLC reports grants from AstraZeneca. JBIM reports personal fees from Astra-Zeneca, Boehringer Inglheim, Novartis, Merck, Moksha8, and Translational Catalyst. All other authors report no disclosures relevant to the content of this article.

Références

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Auteurs

Veena S Rao (VS)

Division of Internal Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, CT, USA.

Juan B Ivey-Miranda (JB)

Division of Internal Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, CT, USA; Heart Failure and Heart Transplant Clinic, Hospital de Cardiologia, Instituto Mexicano del Seguro Social, Mexico City, Mexico.

Zachary L Cox (ZL)

Department of Pharmacy Practice, Lipscomb University College of Pharmacy, Nashville, TN, USA; Department of Pharmacy, Vanderbilt University Medical Center, Nashville, TN, USA.

Julieta Moreno-Villagomez (J)

Division of Internal Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, CT, USA.

Jeffrey M Testani (JM)

Division of Internal Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, CT, USA. Electronic address: jeffrey.testani@yale.edu.

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Classifications MeSH