J Sanchez-Serna1, M Martinez-Villanueva2, Á Hernández-Vicente3, M C Asensio-Lopez4, J A Noguera2, D A Pascual-Figal5. 1. Servicio de Cardiología, Hospital Universitario Virgen de la Arrixaca, Murcia, España. Electronic address: juans87@gmail.com. 2. Servicio de Bioquímica, Hospital Universitario Virgen de la Arrixaca, Murcia, España. 3. Servicio de Cardiología, Hospital Universitario Virgen de la Arrixaca, Murcia, España. 4. Departamento de Medicina, Facultad Medicina, Universidad de Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, España. 5. Servicio de Cardiología, Hospital Universitario Virgen de la Arrixaca, Murcia, España; Departamento de Medicina, Facultad Medicina, Universidad de Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, España; CIBER cardiovascular, Madrid, España.
Abstract
INTRODUCTION: In decompensated heart failure (HF), both acute kidney injury (AKI) and high Galectina-3 (Gal-3) levels have been associated with poorer outcomes. Plasma Gal-3 levels are affected by renal function; however, the potential role of Gal-3 as a predictor of AKI has not been established. METHODS: We measured Gal-3 concentrations at admission for 175 patients hospitalised for HF and recorded the onset of AKI according to the Risk, Injury, Failure, Loss and End-stage kidney disease (RIFLE) analytical criteria. RESULTS: During hospitalisation, 44 patients (25.1%) developed AKI, although only 14 (8%) corresponded to more advanced stages. These 14 patients had significantly higher Gal-3 levels at admission, which remained a predictor of AKI after the multivariate adjustment by other predictors and by baseline renal function. CONCLUSIONS: High Gal-3 levels at admission are associated with a higher risk of AKI during hospitalisation for decompensated HF.
INTRODUCTION: In decompensated heart failure (HF), both acute kidney injury (AKI) and high Galectina-3 (Gal-3) levels have been associated with poorer outcomes. Plasma Gal-3 levels are affected by renal function; however, the potential role of Gal-3 as a predictor of AKI has not been established. METHODS: We measured Gal-3 concentrations at admission for 175 patients hospitalised for HF and recorded the onset of AKI according to the Risk, Injury, Failure, Loss and End-stage kidney disease (RIFLE) analytical criteria. RESULTS: During hospitalisation, 44 patients (25.1%) developed AKI, although only 14 (8%) corresponded to more advanced stages. These 14 patients had significantly higher Gal-3 levels at admission, which remained a predictor of AKI after the multivariate adjustment by other predictors and by baseline renal function. CONCLUSIONS: High Gal-3 levels at admission are associated with a higher risk of AKI during hospitalisation for decompensated HF.