Highlights
- •Galectin-3 was associated with renal dysfunction, renal tubular damage and myocardial injury in acute heart failure.
- •Higher Galctin-3 levels predicted in-hospital adverse events and higher 1-year mortality rates.
- •Galectin-3 may help to identify patients at higher risk for cardiorenal adverse events and worse prognoses.
ABSTRACT
Background
Galectin-3, a biomarker of inflammation and fibrosis, can be associated with renal
and myocardial damage and dysfunction in patients with acute heart failure (AHF).
Methods and Results
We retrospectively analyzed 790 patients with AHF who were enrolled in the AKINESIS
study. During hospitalization, patients with galectin-3 elevation (> 25.9 ng/mL) on
admission more commonly had acute kidney injury (assessed by KDIGO criteria), renal
tubular damage (peak urine neutrophil gelatinase-associated lipocalin [uNGAL] > 150
ng/dL) and myocardial injury (≥ 20% increase in the peak high-sensitivity cardiac
troponin I [hs-cTnI] values compared to admission). They less commonly had ≥ 30% reduction
in B-type natriuretic peptide from admission to last measured value. In multivariable
linear regression analysis, galectin-3 was negatively associated with estimated glomerular
filtration rate and positively associated with uNGAL and hs-cTnI. Higher galectin-3
was associated with renal replacement therapy, inotrope use and mortality during hospitalization.
In univariable Cox regression analysis, higher galectin-3 was associated with increased
risk for the composite of death or rehospitalization due to HF and death alone at
1 year. After multivariable adjustment, higher galectin-3 levels were associated only
with death.
Conclusions
In patients with AHF, higher galectin-3 values were associated with renal dysfunction,
renal tubular damage and myocardial injury, and they predicted worse outcomes.
Key Words
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Article info
Publication history
Published online: October 31, 2022
Accepted:
September 28,
2022
Received in revised form:
September 28,
2022
Received:
May 28,
2022
Identification
Copyright
© 2022 Elsevier Inc. All rights reserved.
