Abstract 13420: The Serum Heart-Type Fatty Acid-Binding Protein (HFABP) Level Can be Used to Detect Acute Kidney Injury on Admission and Predict an Adverse Outcome in Patients With Acute Heart Failure
Background: It was demonstrated the presence of renal tubular injury was the mechanism underlying the acute kidney injury (AKI), and this is determined based on the levels of urine biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL), liver fatty acid-binding protein (LFABP) and N acetyl-β-D glucosaminidase (NAG). However, different mechanisms of AKI may exist in acute heart failure (AHF) patients. This study evaluated biomarkers to detect AKI on admission and predict adverse outcomes for AHF.
Methods: Two hundred patients with AHF admitted to the intensive care unit were prospectively analyzed. The urine and serum biomarkers were measured within 30 minutes of admission. Patients were assigned to a no-AKI (n=146) or AKI group (Class R (n=34), Class I (n=13) or Class F (n=7)) using the RIFLE classifications on admission. We evaluated the relationships between the biomarkers and AKI, in-hospital mortality, all-cause death and HF events (HF re-admission or all-cause death) within one year.
Results: The urinary NGAL, LFABP, NAG excretion and serum heart-type FABP (s-HFABP) levels were significantly higher in the AKI group than in the no-AKI group. The only specific biomarker for AKI and Class I/F status was s-HFABP (OR: 5.398; 95% CI: 2.276-12.801 and OR: 16.504; 95% CI: 3.192-80.754) by the multivariate analysis. Furthermore, the specific biomarker for in-hospital mortality was also s-HFABP (OR: 3.794; 95% CI: 1.298-11.086). S-HFABP demonstrated an optimal balance between sensitivity and specificity (67.9% and 80.2%; AUC=0.789) at 20.5 ng/ml for AKI, at 32.5 ng/ml for Class I /F (80.0% and 87.2%; AUC=0.890) and at 20.5 ng/ml for in-hospital mortality (76.2% and 71.8%; AUC=0.728). The Kaplan-Meier survival curves showed that the prognosis, including all-cause death and HF events, was significantly poorer in the high serum HFABP group (≥ 20.5 ng/ml) than in the low serum HFABP group (< 20.5 ng/ml). Furthermore, the prognosis, including all-cause death, were significantly poorer in the high serum HFABP with AKI group than in the low serum HFABP with AKI group and the low serum HFABP without AKI group.
Conclusions: The serum HFABP level can indicate AKI on admission, and a high serum HFABP level is associated with poorer prognosis in AHF patients.
- © 2013 by American Heart Association, Inc.