Acute kidney injury recovery status predicts mortality and cardiorenal outcomes in patients admitted with acute decompensated heart failure.

BACKGROUND: Acute kidney injury (AKI) in the context of acute decompensated heart failure (ADHF) encompasses a broad spectrum of phenotypes with associated disparate outcomes. We evaluate the impact of 'ongoing AKI' on prognosis and cardiorenal outcomes and describe predictors of 'ongoing AKI'. METHODS: A prospective multicentre observational study of patients admitted with ADHF requiring intravenous furosemide was completed, with urinary angiotensinogen (uAGT) measured at baseline. AKI was defined using Kidney Disease Improving Global Outcomes (KDIGO) AKI criteria. AKI recovery status was defined as 'no AKI', 'recovered AKI' or 'ongoing AKI' based on renal function at hospital discharge. Event-free survival analysis was performed to predict death and cardiorenal outcomes at hospital discharge and 6-month follow-up. Multinomial logistic regression was performed to identify predictors of ongoing AKI. Multiclass receiver operator curve analysis was performed to evaluate the relationship between renin-angiotensin system (RAS) blockers and uAGT in predicting ongoing AKI. RESULTS: Among 271 enrolled patients, 121 (44.6%) patients developed AKI, of whom 62 patients had ongoing AKI. Ongoing AKI was associated with increased risk of death (HR 6.89, p<0.001), in-hospital end-stage kidney disease (HR 44.39, p<0.001), 6-month composite of death, transplant, left ventricular assist device and heart failure hospitalisation (HR 3.09, p<0.001), and 6-month composite major adverse kidney events (HR 5.71, p<0.001). Elevated baseline uAGT levels, chronic beta-blocker and thiazide diuretic therapy, and lack of RAS blocker prescription at recruitment were associated with ongoing AKI. While uAGT levels were lower with RAS blocker prescription, in patients with ongoing AKI, uAGT levels were elevated regardless of RAS blocker status. CONCLUSION: Patients experiencing ongoing AKI during ADHF admission were at increased risk of death and other adverse cardiorenal outcomes. Differential uAGT response in patients receiving RAS blockers with ongoing AKI suggests biomarkers may be helpful in predicting treatment responses and cardiorenal outcomes.