| Background and Object:Acute decompensated heart failure(ADHF) is frequently complicated by renal deterioration due to acute kidney injury(AKI) and this is associated with poor outcomes. In current clinical practice, AKI is diagnosed by detecting increase in serum creatinine. But serum creatinine is not a 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 intervene AKI earlier, identification of new potential biomarker to predict AKI is of great clinical significance.Urine neutrophil gelatinase-associated lipocalin (uNGAL) has been demonstrated as a biomarker for the early detection of acute kidney injury (AKI) in different clinical settings.Urine angiotensinogen (UAGT) 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 AKI in acute decompensate heart failure is still undetermined. Whether urine AGT associated with clinical outcomes in ADHF patients is also unknown.The object of this paper is to determine predictive value and prognostic significance of urine AGT in AKI patients admitted with acute decompensated heart failure.Methods and materialsWe prospectively studied a heterogeneous population of145patients admitted with acute decompensated heart failure. Serial urine and plasma samples were analysed by ELIS A for AGT and NGAL during hospital stay. Urine AGT and NGAL were corrected for dilution/concentration by calculating Urine AGT (NAGL)/urine creatinine ratios. The primary outcome was AKI, defined by KDIGO2012criteria(increase in Scr by≧0.3mg/dl within48h or to≧1.5times baseline within the prior7days). The secondary outcomes were1-year death rate,1-year rehospitalization rate and new onset of CKD one year after AKI.Results:50patients (34.5%) developed AKI, diagnosed by serum creatinine2-7days after admission. In the fist7days in hospital, urine AGT(UAGT) levels were significantly higher in patients who developed AKI than those who did not. The median UAGT levels were significantly higher on admission in patients who developed AKI as compared with those who did not. On multivariable analysis, UAGT level independently predicted development of AKI developed in hospital after adjustement for demographs, serum NT-pro-BNP, and albuminuria.On diagnostic performance testing of UAGT on admission for AKI prediction, UAGT area under curve,0.84; combined UAGT and UNGAL area under curve,0.85; clinical model area under curve,0.78; UAGT plus UNGAL and clinical model area under curve0.86; improvements for net reclassification index(0.23P=0.001). In subgroups of patients who used RASI or not before admission, UAGT both predicted AKI.UAGT on the initial day of AKI diagnosis predict AKI unrecovery, area under curve0.75(P<0.05). Higher level UAGT on admission(above ROC best cutoff value) associated with1-year death rate (HR20.0,95%CI8.3-48.0) and rehospitalization rate (HR3.3,95%CI1.8-6.5).UAGT levesl were significantly higher in patients who developed new onset CKD after AKI than those did not, both UAGT level on day7in hosptal and increased percentage during7days after admission predicted new onset CKD, area under curve,0.84and0.72.ConclusionOur results indicated UAGT was an early, predictive biomarker of AKI and associated with clinical outcomes and new onset CKD in patients admitted with acute decompensated heart failure. |
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