Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure

Ingrid A. Andersen, Brenda K. Huntley, Sharon S. Sandberg, Denise M. Heublein, John C Jr. Burnett

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Background Elevated plasma fibroblast growth factor 23 (FGF23) is a prognostic marker in chronic kidney disease. Recently, FGF23 was reported to also be a predictive factor in chronic congestive heart failure (HF). To date however, plasma levels in acute decompensated HF (ADHF) have not been reported and myocardial production and distribution of FGF23 in HF is poorly defined. We aimed to determine plasma levels and myocardial production of FGF23 in ADHF. Methods Plasma FGF23, N-terminal pro B-type natriuretic peptide (NT-proBNP) and estimated glomerular filtration rate (eGFR) were assessed in 21 ADHF patients and 19 controls. Myocardial gene expression and distribution of FGF23 was determined on left ventricular samples from HF patients and normal controls. Results Plasma FGF23 was markedly higher in ADHF patients compared with controls (1498 ± 1238 versus 66 ± 27 RU/mL, P <0.0001). There were no correlations between FGF23 and eGFR, NT-proBNP, ejection fraction or age. ADHF subjects with eGFR >60 mL/min/1.73 m2 had FGF23 levels of 1526 ± 1601 RU/mL versus 55 ± 20 RU/mL in controls (P = 0.007). Quantified myocardial FGF23 gene expression was similar between HF patients and controls. Myocardial FGF23 immunostaining was similar between HF patients and controls, with equal distribution throughout cardiomyocytes. Conclusion Patients with ADHF had markedly elevated plasma FGF23 levels. Myocardial FGF23 gene expression was present in HF at a similar level as normal controls, and immunohistochemistry showed similar cellular distribution of FGF23 in HF and controls, suggesting that the myocardium does not contribute to the elevated circulating FGF23 in HF.

Original languageEnglish (US)
Pages (from-to)767-772
Number of pages6
JournalNephrology Dialysis Transplantation
Volume31
Issue number5
DOIs
StatePublished - May 1 2016

Fingerprint

Heart Failure
fibroblast growth factor 23
Gene Expression
Brain Natriuretic Peptide
Glomerular Filtration Rate
Chronic Renal Insufficiency
Cardiac Myocytes
Myocardium
Immunohistochemistry

Keywords

  • biomarkers FGF23gene expression
  • GFR
  • heart failure
  • myocardium

ASJC Scopus subject areas

  • Nephrology
  • Transplantation

Cite this

Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure. / Andersen, Ingrid A.; Huntley, Brenda K.; Sandberg, Sharon S.; Heublein, Denise M.; Burnett, John C Jr.

In: Nephrology Dialysis Transplantation, Vol. 31, No. 5, 01.05.2016, p. 767-772.

Research output: Contribution to journalArticle

Andersen, Ingrid A. ; Huntley, Brenda K. ; Sandberg, Sharon S. ; Heublein, Denise M. ; Burnett, John C Jr. / Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure. In: Nephrology Dialysis Transplantation. 2016 ; Vol. 31, No. 5. pp. 767-772.
@article{20db8f65a4404002bdc9851c6d94e556,
title = "Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure",
abstract = "Background Elevated plasma fibroblast growth factor 23 (FGF23) is a prognostic marker in chronic kidney disease. Recently, FGF23 was reported to also be a predictive factor in chronic congestive heart failure (HF). To date however, plasma levels in acute decompensated HF (ADHF) have not been reported and myocardial production and distribution of FGF23 in HF is poorly defined. We aimed to determine plasma levels and myocardial production of FGF23 in ADHF. Methods Plasma FGF23, N-terminal pro B-type natriuretic peptide (NT-proBNP) and estimated glomerular filtration rate (eGFR) were assessed in 21 ADHF patients and 19 controls. Myocardial gene expression and distribution of FGF23 was determined on left ventricular samples from HF patients and normal controls. Results Plasma FGF23 was markedly higher in ADHF patients compared with controls (1498 ± 1238 versus 66 ± 27 RU/mL, P <0.0001). There were no correlations between FGF23 and eGFR, NT-proBNP, ejection fraction or age. ADHF subjects with eGFR >60 mL/min/1.73 m2 had FGF23 levels of 1526 ± 1601 RU/mL versus 55 ± 20 RU/mL in controls (P = 0.007). Quantified myocardial FGF23 gene expression was similar between HF patients and controls. Myocardial FGF23 immunostaining was similar between HF patients and controls, with equal distribution throughout cardiomyocytes. Conclusion Patients with ADHF had markedly elevated plasma FGF23 levels. Myocardial FGF23 gene expression was present in HF at a similar level as normal controls, and immunohistochemistry showed similar cellular distribution of FGF23 in HF and controls, suggesting that the myocardium does not contribute to the elevated circulating FGF23 in HF.",
keywords = "biomarkers FGF23gene expression, GFR, heart failure, myocardium",
author = "Andersen, {Ingrid A.} and Huntley, {Brenda K.} and Sandberg, {Sharon S.} and Heublein, {Denise M.} and Burnett, {John C Jr.}",
year = "2016",
month = "5",
day = "1",
doi = "10.1093/ndt/gfv398",
language = "English (US)",
volume = "31",
pages = "767--772",
journal = "Nephrology Dialysis Transplantation",
issn = "0931-0509",
publisher = "Oxford University Press",
number = "5",

}

TY - JOUR

T1 - Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure

AU - Andersen, Ingrid A.

AU - Huntley, Brenda K.

AU - Sandberg, Sharon S.

AU - Heublein, Denise M.

AU - Burnett, John C Jr.

PY - 2016/5/1

Y1 - 2016/5/1

N2 - Background Elevated plasma fibroblast growth factor 23 (FGF23) is a prognostic marker in chronic kidney disease. Recently, FGF23 was reported to also be a predictive factor in chronic congestive heart failure (HF). To date however, plasma levels in acute decompensated HF (ADHF) have not been reported and myocardial production and distribution of FGF23 in HF is poorly defined. We aimed to determine plasma levels and myocardial production of FGF23 in ADHF. Methods Plasma FGF23, N-terminal pro B-type natriuretic peptide (NT-proBNP) and estimated glomerular filtration rate (eGFR) were assessed in 21 ADHF patients and 19 controls. Myocardial gene expression and distribution of FGF23 was determined on left ventricular samples from HF patients and normal controls. Results Plasma FGF23 was markedly higher in ADHF patients compared with controls (1498 ± 1238 versus 66 ± 27 RU/mL, P <0.0001). There were no correlations between FGF23 and eGFR, NT-proBNP, ejection fraction or age. ADHF subjects with eGFR >60 mL/min/1.73 m2 had FGF23 levels of 1526 ± 1601 RU/mL versus 55 ± 20 RU/mL in controls (P = 0.007). Quantified myocardial FGF23 gene expression was similar between HF patients and controls. Myocardial FGF23 immunostaining was similar between HF patients and controls, with equal distribution throughout cardiomyocytes. Conclusion Patients with ADHF had markedly elevated plasma FGF23 levels. Myocardial FGF23 gene expression was present in HF at a similar level as normal controls, and immunohistochemistry showed similar cellular distribution of FGF23 in HF and controls, suggesting that the myocardium does not contribute to the elevated circulating FGF23 in HF.

AB - Background Elevated plasma fibroblast growth factor 23 (FGF23) is a prognostic marker in chronic kidney disease. Recently, FGF23 was reported to also be a predictive factor in chronic congestive heart failure (HF). To date however, plasma levels in acute decompensated HF (ADHF) have not been reported and myocardial production and distribution of FGF23 in HF is poorly defined. We aimed to determine plasma levels and myocardial production of FGF23 in ADHF. Methods Plasma FGF23, N-terminal pro B-type natriuretic peptide (NT-proBNP) and estimated glomerular filtration rate (eGFR) were assessed in 21 ADHF patients and 19 controls. Myocardial gene expression and distribution of FGF23 was determined on left ventricular samples from HF patients and normal controls. Results Plasma FGF23 was markedly higher in ADHF patients compared with controls (1498 ± 1238 versus 66 ± 27 RU/mL, P <0.0001). There were no correlations between FGF23 and eGFR, NT-proBNP, ejection fraction or age. ADHF subjects with eGFR >60 mL/min/1.73 m2 had FGF23 levels of 1526 ± 1601 RU/mL versus 55 ± 20 RU/mL in controls (P = 0.007). Quantified myocardial FGF23 gene expression was similar between HF patients and controls. Myocardial FGF23 immunostaining was similar between HF patients and controls, with equal distribution throughout cardiomyocytes. Conclusion Patients with ADHF had markedly elevated plasma FGF23 levels. Myocardial FGF23 gene expression was present in HF at a similar level as normal controls, and immunohistochemistry showed similar cellular distribution of FGF23 in HF and controls, suggesting that the myocardium does not contribute to the elevated circulating FGF23 in HF.

KW - biomarkers FGF23gene expression

KW - GFR

KW - heart failure

KW - myocardium

UR - http://www.scopus.com/inward/record.url?scp=84965145976&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84965145976&partnerID=8YFLogxK

U2 - 10.1093/ndt/gfv398

DO - 10.1093/ndt/gfv398

M3 - Article

C2 - 26666498

AN - SCOPUS:84965145976

VL - 31

SP - 767

EP - 772

JO - Nephrology Dialysis Transplantation

JF - Nephrology Dialysis Transplantation

SN - 0931-0509

IS - 5

ER -