Fibroblast Growth Factor 23 and Outcomes in Acute Heart Failure

Q: What is the clinical evidence from this study?

Study design: Cohort. Population: Acute Worsening Heart Failure (n=635). Intervention: Fibroblast growth factor 23 (FGF23) levels vs. Lower FGF23 levels. Primary outcome: All-cause mortality (per doubling of FGF23) (HR 1.17, 95% CI 1.05-1.31, p=0.004).

Q: What does this research mean for the field?

In patients presenting with acute worsening heart failure, each doubling of circulating FGF23 levels independently increases the risk of long-term all-cause mortality by 17%. Novelty: ClaimNovelty.CONFIRMATORY. Consensus alignment: ConsensusAlignment.NEUTRAL.

Arancha Martí-Martínez; Julio E. Núñez; Herminio López‐Escribano; Rafael de la Espriella; Enrique Santas; Enrique Rodríguez Borja; Òscar Miró; Pere Llorens; Aitor Alquézar‐Arbé; Pablo Herrero

doi:10.3390/biom16091362

September 18, 2026BiomoleculesOpen Access

Fibroblast Growth Factor 23 and Outcomes in Acute Heart Failure

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Key result

Doubling of FGF23 linked to ~17% higher all-cause mortality in acute heart failure.

HR 1.17
95% CI 1.05-1.31
P=0.004
n=635

Figures

Why the study?

Fibroblast growth factor 23 (FGF23) is an emerging proxy of fibrosis and may influence long-term outcomes in worsening heart failure (WHF) patients, but its prognostic value is not well established.

Does elevated circulating FGF23 predict long-term adverse clinical outcomes in patients presenting to the emergency department with acute worsening heart failure?

Study Design

Type

Cohort (n=635)

Multicenter

Yes

Structured PICO

Does elevated circulating FGF23 predict long-term adverse clinical outcomes in patients presenting to the emergency department with acute worsening heart failure?

P

Population

635 older patients (mean age 82.4, 53% female) with acute heart failure evaluated in the emergency department, followed for a median of 380 days.

E

Exposure

Higher circulating Fibroblast Growth Factor 23 (FGF23) levels (evaluated as a continuous variable per doubling, or categorized by median/quartiles)

C

Comparator

Lower FGF23 levels

O

Outcome

All-cause mortality, composite of all-cause death or WHF ED reconsultation, and composite of all-cause death or HF hospitalizationhard clinical

Main Result

Hazard Ratio: 1.17 (95% CI 1.05–1.31)

p-value: p=0.004

FGF23 provides independent, incremental prognostic information for long-term mortality and decompensation events in elderly patients presenting with acute heart failure.

Limitations

Potential residual confounding related to renal and mineral metabolism
Lack of echocardiographic parameters other than LVEF
Requires independent external validation to establish clinical utility
No established biological or clinical decision threshold for FGF23
Older Spanish cohort may limit generalizability to other populations
Residual confounding cannot be excluded
Lack of additional echocardiographic parameters beyond LVEF
Cohort-derived median concentration does not represent an established clinical threshold
Lack of external validation
Older Spanish cohort may limit generalizability

Implication

May refine acute HF risk stratification; hypothesis-generating and should not yet change practice.

Abstract

Worsening heart failure (WHF) is a complex clinical syndrome associated with a high risk of mortality and further decompensations, characterized by fluid overload and upregulated inflammatory and fibrotic processes linked to organ dysfunction. Fibroblast growth factor 23 (FGF23) is an emerging proxy of fibrosis and may interact to influence long-term outcomes in WHF patients. This study evaluated the association between FGF23 levels and long-term outcomes in patients with WHF evaluated in the emergency department (ED). A total of 635 patients from the EAHFE registry, enrolled during 2007, 2009, and 2011, were prospectively included. FGF23 was measured in the first blood sample obtained at ED presentation. During a median follow-up of 380 days (interquartile range: 126 to 456), all-cause mortality occurred in 216 patients (34.0%), while 351 patients (55.3%) experienced the composite endpoint of death/WHF ED reconsultation and 295 (46.5%) experienced death/HF hospitalization. Event rates increased progressively across FGF23 levels. Patients with FGF23 above the median (48.4 pg/mL) displayed higher rates (per 100 patient-years) of all-cause mortality (49 vs. 31, p = 0.003), death/WHF ED reconsultation (93 vs. 65, p = 0.003), and death/HF hospitalization (77 vs. 56, p = 0.043). In continuous analyses, each doubling of FGF23 remained significantly associated with an increased risk of all three outcomes after multivariable adjustment. These associations were consistent across clinically relevant subgroups, including those defined by age, sex, and kidney function, supporting the potential prognostic value of FGF23 within this cohort, although external validation is warranted.

Discussion

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Cite This Study

Martí-Martínez et al. (2026) conducted a cohort in Acute Worsening Heart Failure (n=635). Fibroblast growth factor 23 (FGF23) levels vs. Lower FGF23 levels was evaluated on All-cause mortality (per doubling of FGF23) (HR 1.17, 95% CI 1.05-1.31, p=0.004). Each doubling of FGF23 levels at emergency department presentation independently increased the risk of all-cause mortality by 17% (HR 1.17, 95% CI 1.05-1.31, p=0.004) in patients with acute heart failure.

synapsesocial.com/papers/6ad0fd403afa093ea9ad02d3 https://doi.org/10.3390/biom16091362

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Fibroblast Growth Factor 23 and Outcomes in Acute Heart Failure

Figures

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

Fibroblast Growth Factor 23 and Outcomes in Acute Heart Failure

Figures

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

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