Admission kidney tubule biomarkers do not predict acute kidney injury or in-hospital adverse events in acute heart failure

BACKGROUND AND HYPOTHESIS: Serum creatinine frequently increases during hospitalizations for acute heart failure (AHF) meeting criteria for acute kidney injury (AKI), but the significance of this increase is variable. We evaluated whether admission levels of kidney tubule and cardiac biomarkers are associated with increases in serum creatinine and adverse in-hospital events. METHODS: In a nested case-control, we identified 214 cases with at least stage 1 AKI defined by the 2012 Kidney Disease Improving Global Outcomes criteria within seven days of admission in the Acute Kidney Injury Neutrophil Gelatinase-Associated Lipocalin Evaluation of Symptomatic Heart Failure Study and matched with 214 controls who did not experience AKI. The primary outcome was the development of AKI within the first seven days; secondary outcomes were the development of severe AKI (stages 2 or 3) and a composite of adverse in-hospital events. Associations of 6 blood and 14 urine biomarkers were assessed with logistic regression and Receiver Operating Characteristic Area Under the Curve (ROC-AUC) curve analysis. RESULTS: Individuals were 71 ± 13 years; 64% were men; with median admission creatinine 1.3 [IQR 1.0-1.8] mg/dL. Among AKI cases, 181 (85%), 16 (8%), and 17 (8%) were stages 1, 2, and 3, respectively. Compared to the lowest tertile, only the highest tertiles of fractional excretion of sodium (FeNa ≥ 3.65; OR 1.7, 95% CI 1.0-2.9) and urinary MCP-1 (≥ 433 ng/g; OR 1.7, 95% CI 1.0-2.8) were associated with AKI risk, though discrimination was poor (ROC-AUC < 0.60). Neither was associated with severe AKI. Only elevated B-type natriuretic peptide (≥ 932 pg/mL) predicted the composite adverse in-hospital event (OR 2.3, 95% CI 1.2-4.2). CONCLUSION: Kidney tubule and cardiac biomarkers at admission for AHF are not associated with risk for increases in creatinine or adverse in-hospital events reaffirming that creatinine changes in AHF are largely functional in nature.