Low levels of adropin are associated with acute kidney injury after decongestion in patients with acutely decompensated heart failure

Abstract

Background: Patients with acutely decompensated heart failure (ADHF) demonstrated a high risk of acute kidney injury (AKI) and its transition to acute kidney disease after diuretic therapy to reach euvolemic status. The purpose of the study was to investigate whether circulating levels of adropin predict AKI in ADHF patients after decongestive therapy.

Material and methods: A total of 325 individuals fulfilling the inclusion criteria of ADHF were consecutively enrolled from October 2020 to October 2024. The study was designed as prospective cohort study. The congestion was assessed using Framingham criteria of congestion (Framingham heart failure score ≥ 2). Patients with AHDF were divided into 2 groups according to the presence of AKI (n = 113) and without AKI (n = 212). Circulating levels of N-terminal brain natriuretic pro-peptide (NT-proBNP), high-sensitivity C-reactive protein, high-sensitive troponin T, interleukin-6, tumor necrosis factor-alpha, soluble suppression of tumorigenicity-2, procalcitonin were measured. Predictors of AKI were identified using univariate and multivariate logistic regression analysis.

Results: We found that the presence of atrial fibrillation, urinary albumin/creatinine ratio (UACR) ≥16.5 mg/g Cr, serum levels of adropin<2.1 ng/mL and NT-proBNP ≥19,540 pmol/mL were independent predictors for AKI in patients with ADHF. UACR and atrial fibrillation revealed a strict similarity in prediction of AKI, whereas discriminative ability of adropin<2.1 ng/mL were higher to NT-proBNP ≥19,540 pmol/mL. The combined predictive model (low levels of adropin + higher levels of NT-proBNP) showed significantly better discriminatory power compared to other models.

Conclusion: Low levels of adropin<2.1 ng/mL on hospital admission in patients with ADHF can predict AKI and that its predictive ability was significantly higher compared with the conventionally used urinary albumin/creatinine ratio and NT-proBNP. Adropin may add predictive information to NT-proBNP for AKI in individuals with ADHF.

Keywords: Acute kidney injury; Acutely decompensated heart failure; Adropin; Biomarkers; Decongestion; Prognosis.

Graphical abstract

Fig. 1

Flow chart and study design. Abbreviations: ADHF, acutely decompensated heart failure; AHF, acute heart failure; AKI, acute kidney injury; CRP, C-reactive protein; HOMA-IR, Homeostatic Assessment Model of Insulin Resistance; HbA1c, glycosylated haemoglobin; GFR, glomerular filtration rate; IL, interleukin; NT-proBNP, N-terminal brain natriuretic pro-peptide; SCAI, Society for Cardiovascular Angiography and Interventions; sST2, soluble suppression of tumorigenicity-2; TIA, transient ischemic attack; TnT, troponin T; TNF, tumor necrosis factor.

Fig. 2

Standard curve in which the average absorbance for each standard is plotted on the Y (vertical) axis against the known standard concentrations on the X (horizontal) axis.

Fig. 3

Heat map with Spearmen correlations between each pair of variables. Abbreviations: AF, atrial fibrillation; BMI, body mass index; CKD, chronic kidney disease; hs-CRP, high-sensitivity C-reactive protein; HOMA-IR, Homeostatic Assessment Model of Insulin Resistance; HDL-C, high-density lipoprotein cholesterol; HFrEF, heart with reduced ejection fraction; LAVI, left atrial volume index; LVEF, left ventricular ejection fraction; LDL-C, low-density lipoprotein cholesterol; NT-proBNP, N-terminal brain natriuretic pro-peptide; TG, triglycerides; TNF-alpha, tumor necrosis factor-alpha; UACR, urinary albumin/creatinine ratio.

Fig. 4

The percentage of patients with the levels of adropin higher and less cut-off point in individuals with and without AKI (A) in comparison with probability distributions of adropin concentration in eligible patients (B).