Literature DB >> 34689571

FGF-23 (Fibroblast Growth Factor-23) and Cardiorenal Interactions.

Juan B Ivey-Miranda1,2, Brendan Stewart1, Zachary L Cox3, Wendy McCallum4, Christopher Maulion1, Olyvia Gleason1, Grace Meegan1, Jonathan G Amatruda5, Julieta Moreno-Villagomez1,6, Devin Mahoney1, Jeffrey M Turner7, F Perry Wilson8, Michelle M Estrella5, Michael G Shlipak5, Veena S Rao1, Jeffrey M Testani1.   

Abstract

BACKGROUND: Animal models implicate FGF-23 (fibroblast growth factor-23) as a direct contributor to adverse cardiorenal interactions such as sodium avidity, diuretic resistance, and neurohormonal activation, but this has not been conclusively demonstrated in humans. Therefore, we aimed to evaluate whether FGF-23 is associated with parameters of cardiorenal dysfunction in humans with heart failure, independent of confounding factors.
METHODS: One hundred ninety-nine outpatients with heart failure undergoing diuretic treatment at the Yale Transitional Care Center were enrolled and underwent blood collection, and urine sampling before and after diuretics.
RESULTS: FGF-23 was associated with several metrics of disease severity such as higher home loop diuretic dose and NT-proBNP (N-terminal pro-B-type natriuretic peptide), and lower estimated glomerular filtration rate, serum chloride, and serum albumin. Multivariable analysis demonstrated no statistically significant association between FGF-23 and sodium avidity measured by fractional excretion of sodium, or proximal or distal tubular sodium reabsorption, either before diuretic administration or at peak diuresis (P≥0.11 for all). Likewise, FGF-23 was not independently associated with parameters of diuretic resistance (diuretic excretion, cumulative urine and sodium output, and loop diuretic efficiency [P≥0.33 for all]) or neurohormonal activation (plasma or urine renin [P≥0.36 for all]). Moreover, the upper boundary of the 95% CI of all the partial correlations were ≤0.30, supporting the lack of meaningful correlations. FGF-23 was not associated with mortality in multivariable analysis (P=0.44).
CONCLUSIONS: FGF-23 was not meaningfully associated with any cardiorenal parameter in patients with heart failure. While our methods cannot rule out a small effect, FGF-23 is unlikely to be a primary driver of cardiorenal interactions.

Entities:  

Keywords:  chloride; diuretic; heart failure; models, animal; outpatient

Mesh:

Substances:

Year:  2021        PMID: 34689571      PMCID: PMC8782627          DOI: 10.1161/CIRCHEARTFAILURE.121.008385

Source DB:  PubMed          Journal:  Circ Heart Fail        ISSN: 1941-3289            Impact factor:   8.790


  34 in total

1.  Fibroblast growth factor 23 is related to profiles indicating volume overload, poor therapy optimization and prognosis in patients with new-onset and worsening heart failure.

Authors:  Jozine M Ter Maaten; Adriaan A Voors; Kevin Damman; Peter van der Meer; Stefan D Anker; John G Cleland; Kenneth Dickstein; Gerasimos Filippatos; Pim van der Harst; Hans L Hillege; Chim C Lang; Marco Metra; Gerjan Navis; Leong Ng; Wouter Ouwerkerk; Piotr Ponikowski; Nilesh J Samani; Dirk J van Veldhuisen; Faiez Zannad; Aeilko H Zwinderman; Martin H de Borst
Journal:  Int J Cardiol       Date:  2018-02-15       Impact factor: 4.164

2.  Limited role for fibroblast growth factor 23 in assessing prognosis in heart failure patients: data from the TIME-CHF trial.

Authors:  Robert Stöhr; Vincent M Brandenburg; Gunnar H Heine; Micha T Maeder; Gregor Leibundgut; Alexander Schuh; Urs Jeker; Matthias Pfisterer; Sandra Sanders-van Wijk; Hans-Peter Brunner-la Rocca
Journal:  Eur J Heart Fail       Date:  2020-02-05       Impact factor: 15.534

3.  Cross talk between the renin-angiotensin-aldosterone system and vitamin D-FGF-23-klotho in chronic kidney disease.

Authors:  Martin H de Borst; Marc G Vervloet; Piet M ter Wee; Gerjan Navis
Journal:  J Am Soc Nephrol       Date:  2011-08-18       Impact factor: 10.121

Review 4.  Renal sodium avidity in heart failure: from pathophysiology to treatment strategies.

Authors:  Wilfried Mullens; Frederik Hendrik Verbrugge; Petra Nijst; Wai Hong Wilson Tang
Journal:  Eur Heart J       Date:  2017-06-21       Impact factor: 29.983

5.  FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1.

Authors:  Jyothsna Gattineni; Carlton Bates; Katherine Twombley; Vangipuram Dwarakanath; Michael L Robinson; Regina Goetz; Moosa Mohammadi; Michel Baum
Journal:  Am J Physiol Renal Physiol       Date:  2009-06-10

6.  C-terminal FGF23 is a strong predictor of survival in systolic heart failure.

Authors:  Damien Gruson; Thibault Lepoutre; Jean-Marie Ketelslegers; Jean Cumps; Sylvie A Ahn; Michel F Rousseau
Journal:  Peptides       Date:  2012-08-10       Impact factor: 3.750

7.  Prognostic Role of Serum Chloride Levels in Acute Decompensated Heart Failure.

Authors:  Justin L Grodin; Jennifer Simon; Rory Hachamovitch; Yuping Wu; Gregory Jackson; Meghana Halkar; Randall C Starling; Jeffrey M Testani; W H Wilson Tang
Journal:  J Am Coll Cardiol       Date:  2015-08-11       Impact factor: 24.094

Review 8.  The role of fibroblast growth factor-23 in cardiorenal syndrome.

Authors:  Csaba P Kovesdy; L Darryl Quarles
Journal:  Nephron Clin Pract       Date:  2013-08-06

Review 9.  Bumetanide. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic use.

Authors:  A Ward; R C Heel
Journal:  Drugs       Date:  1984-11       Impact factor: 9.546

10.  A comparative transcriptome analysis identifying FGF23 regulated genes in the kidney of a mouse CKD model.

Authors:  Bing Dai; Valentin David; Aline Martin; Jinsong Huang; Hua Li; Yan Jiao; Weikuan Gu; L Darryl Quarles
Journal:  PLoS One       Date:  2012-09-06       Impact factor: 3.240

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  1 in total

Review 1.  Novel Biomarkers of Kidney Disease in Advanced Heart Failure: Beyond GFR and Proteinuria.

Authors:  Bethany Roehm; Meredith McAdams; S Susan Hedayati
Journal:  Curr Heart Fail Rep       Date:  2022-05-28
  1 in total

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