| Background and ObjectiveAcute decompensated heart failure is frequently complicated by renal deterioration due to acute kidney injury(AKI),especialy acute-on-chronic kidney injury(ACKI), and this is associated with poor outcomes. In current clinical practice, ACKI is diagnosed by detecting increase of serum creatinine. But serum creatinine is not an early and sensitive indicator owing to that serum creatinine might not change until more than half of renal function has been lost. Therefore, in order to prevent and treat ACKI earlier, identification of potential biomarker to predict ACKI on admission is of great clinical significance.Urinary neutrophil gelatinase-associated lipocalin (uNGAL) has shown promise as a biomarker for the early detection of acute kidney injury (AKI) in fixed models of injury, but its ability to predict ACKI and provide prognostic information in patients with acute decompensate heart failure accompany by chronic kidney disease is unknown.Urinary angiotensinogen has been demonstrated as a marker of intrarenal RAS status and asscicated with deterioration and severity of chronic kidney disease. Its potential role as a biomarker of ACKI in acute decompensate heart failure accompany by chronic kidney disease still undetermined. Whether urinary AGT associated with clinical outcomes in those patients is unknown.The objective of this paper is to determine predictive value and prognostic significance of urinary AGT in ACKI patients admitted with acute decompensated heart failure accompany by chronic kidney disease.Methods and materialsWe prospectively studied a heterogeneous population of 83 patients admitted with acute decompensate heart failure accompany by chronic kidney disease. Serial urine and plasma samples were analysed by ELISA for AGT and NGAL in the first 7 days after admission. Urinary AGT and NGAL were corrected for dilution/concentration by calculating Urinary AGT (NAGL)/urine creatinine ratios. The primary outcome was ACKI, defined by 2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury.The secondary outcome were severe ACKI, 180-day mortality,180-day mortality or re-hospitalization,and 1-year re-hospitalization.Results:35 patients (42.2%) developed AKI, diagnosed by serum creatinine 2-7days after admission. In the first 7 days in hospital, urine AGT(uAGT) levels were significantly higher in patients who developed ACKI than those who did not.The median uAGT level was significantly higher on admission in patients who developed ACKI than those who did not.On multivariable analysis, uAGT level independently predicted development of ACKI in hospital after adjustment by demographs,serum NT-pro-BNP,and serum creatinine.On diagnostic performance testing for ACKI prediction, uAGT/cr dl area under curve was 0.87 (95%CI,0.79-0.95). uNGAL/cr d1 area under curve was 0.80 (95%CI,0.70-0.89).Combined uAGT/cr d1 and uNGAL/cr d1 area under curve was 0.88 (95%CI,0.81-0.96). Clinical model area under curve was 0.78 (95% CI,0.69-0.88). uNGAL plus clinical model area under curve was0.87 (95%CI,0.80-0.95rP=0.03). uAGT plus uNGAL and clinical model area under curve was 0.90 (95%CI,0.84-0.97),P=0.02. In the subgroups of patients who used RASI or not before admission, uAGT both predicted ACKI.On diagnostic performance testing for severe ACKI prediction, uAGT/cr dl area under curve was 0.879. uNGAL/cr dl area under curve was 0.882.Combined uAGT/cr dl and uNGAL/cr d1 area under curve was 0.932.Higher level UAGT on admission(by ROC best cutoff) associated with 180-day mortality,HR=9.4 (95%CI,3.7-23.8),P=0.000;the combinedend point of 180-day mortality or re-hospitalization,HR=6.6 (95%CI,2.3-19.0),P=0.000;and 1-year re-hospitalization, HR=4.6 (95%CI,1.3-16.6),P=0.000.ConclusionOur results indicate that uAGT was an early, predictive biomarkers of ACKI and associated with clinical outcomes in pre-existed chronic kidney disease patients admitted with acute decompensated heart failure. |
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