Tobias Breidthardt1, Zaid Sabti2, Ronny Ziller3, Frank Rassouli4, Raphael Twerenbold5, Nikola Kozhuharov2, Etienne Gayat6, Samyut Shrestha2, Sara Barata2, Patrick Badertscher2, Jasper Boeddinghaus7, Thomas Nestelberger7, Christian Mueller2. 1. Department of Internal Medicine, University of Basel, Switzerland; Cardiovascular Research Institute Basel (CRIB), University of Basel, Switzerland. Electronic address: tobias.breidthardt@usb.ch. 2. Cardiovascular Research Institute Basel (CRIB), University of Basel, Switzerland; Department of Cardiology all at the University Hospital Basel, University of Basel, Switzerland. 3. Cardiovascular Research Institute Basel (CRIB), University of Basel, Switzerland; Department of Geriatric Medicine, Spital Interlaken, Switzerland. 4. Medical University Clinic, Kantonsspital, Aarau, Switzerland. 5. Cardiovascular Research Institute Basel (CRIB), University of Basel, Switzerland; Department of Cardiology all at the University Hospital Basel, University of Basel, Switzerland; Department of General and Interventional Cardiology, Hamburg University Heart Center, Hamburg, Germany. 6. Hôpital Lariboisière APHP, University of Paris, France. 7. Department of Internal Medicine, University of Basel, Switzerland; Cardiovascular Research Institute Basel (CRIB), University of Basel, Switzerland; Department of Cardiology all at the University Hospital Basel, University of Basel, Switzerland.
Abstract
BACKGROUND: The accurate early diagnosis of acute kidney injury (AKI) in patients with acute heart failure (AHF) is an unmet clinical need. Cystatin C might improve the early detection of AKI. METHODS: 207 patients presenting to the emergency department with AHF were enrolled. Cystatin C was measured in plasma in a blinded fashion at presentation and serially thereafter. The potential of Cystatin C levels to predict AKI was assessed as the primary endpoint. Long-term mortality was assessed as a secondary endpoint. RESULTS: At presentation, creatinine (140μmol/L [91-203] vs. 97μmol/L [76-132], p<0.01) and Cystatin C (2.00mg/L [1.30-3.08] vs. 1.45mg/L [1.00-1.90], p<0.01) levels were significantly higher in AKI compared to Non-AKI patients. The diagnostic accuracy for AKI quantified by the area under the receiver operating characteristic curve was mediocre and comparable for both markers (creatinine 0.68; 95%CI 0.58-78 vs. Cystatin C 0.67; 95%CI 0.58-0.76). Serial measurements of Cystatin C did not further increase the prognostic accuracy for AKI. Cystatin C levels were significantly higher in decedents than in survivors (1.90mg/L [1.30-2.70] vs. 1.30mg/L [1.0-1.6], p<0.001). The combination of Cystatin C and BNP levels significantly improved the prediction of mortality provided by either parameter alone. In multivariable regression analysis Cystatin C remained independently associated with mortality (HR 1.41; 95%CI 1.02-1.95). CONCLUSION: Plasma Cystatin C levels do not adequately predict AKI in patients with AHF. However, in multivariable regression analysis Cystatin C predicted mortality after the adjustment for baseline renal function, AKI, BNP levels and heart failure risk factors.
BACKGROUND: The accurate early diagnosis of acute kidney injury (AKI) in patients with acute heart failure (AHF) is an unmet clinical need. Cystatin C might improve the early detection of AKI. METHODS: 207 patients presenting to the emergency department with AHF were enrolled. Cystatin C was measured in plasma in a blinded fashion at presentation and serially thereafter. The potential of Cystatin C levels to predict AKI was assessed as the primary endpoint. Long-term mortality was assessed as a secondary endpoint. RESULTS: At presentation, creatinine (140μmol/L [91-203] vs. 97μmol/L [76-132], p<0.01) and Cystatin C (2.00mg/L [1.30-3.08] vs. 1.45mg/L [1.00-1.90], p<0.01) levels were significantly higher in AKI compared to Non-AKI patients. The diagnostic accuracy for AKI quantified by the area under the receiver operating characteristic curve was mediocre and comparable for both markers (creatinine 0.68; 95%CI 0.58-78 vs. Cystatin C 0.67; 95%CI 0.58-0.76). Serial measurements of Cystatin C did not further increase the prognostic accuracy for AKI. Cystatin C levels were significantly higher in decedents than in survivors (1.90mg/L [1.30-2.70] vs. 1.30mg/L [1.0-1.6], p<0.001). The combination of Cystatin C and BNP levels significantly improved the prediction of mortality provided by either parameter alone. In multivariable regression analysis Cystatin C remained independently associated with mortality (HR 1.41; 95%CI 1.02-1.95). CONCLUSION: Plasma Cystatin C levels do not adequately predict AKI in patients with AHF. However, in multivariable regression analysis Cystatin C predicted mortality after the adjustment for baseline renal function, AKI, BNP levels and heart failure risk factors.