Naoto Okada1, Masayuki Chuma2, Momoyo Azuma3, Shingen Nakamura4, Hirokazu Miki5, Hirofumi Hamano6, Mitsuhiro Goda6, Kenshi Takechi2, Yoshito Zamami6,7, Masahiro Abe4, Keisuke Ishizawa6,7. 1. Department of Pharmacy, Tokushima University Hospital, 2-50-1 Kuramoto, Tokushima, 770-8503, Japan. naoto-o@tokushima-u.ac.jp. 2. Clinical Trial Center for Developmental Therapeutics, Tokushima University Hospital, 2-50-1 Kuramoto, Tokushima, 770-8503, Japan. 3. Department of Infection Control and Prevention, Tokushima University Hospital, 2-50-1 Kuramoto, Tokushima, 770-8503, Japan. 4. Department of Hematology, Endocrinology and Metabolism, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-8-15 Kuramoto, Tokushima, 770-8503, Japan. 5. Division of Transfusion Medicine and Cell Therapy, Tokushima University Hospital, 2-50-1 Kuramoto, Tokushima, 770-8503, Japan. 6. Department of Pharmacy, Tokushima University Hospital, 2-50-1 Kuramoto, Tokushima, 770-8503, Japan. 7. Department of Clinical Pharmacology and Therapeutics, Tokushima University Graduate School of Biomedical Sciences, 3-8-15 Kuramoto, Tokushima, 770-8503, Japan.
Abstract
PURPOSE: Appropriate use of vancomycin (VCM) is important in preventing acute kidney injury (AKI). Because of the high frequency of VCM use for febrile neutropenia and concomitant use of other nephrotoxic drugs, haematologic patients have a different nephrotoxic background compared with patients with other diseases. Therefore, it is unclear whether the risk factors of VCM-induced AKI identified in other patient groups are also applicable to haematologic patients. Herein, we performed a single-centre retrospective analysis to identify the factors associated with VCM-induced AKI in haematologic patients. METHODS: We retrospectively analysed 150 haematologic patients to whom VCM was administered between April 2010 and March 2018 at Tokushima University Hospital. VCM-induced AKI was defined according to Kidney Disease Improving Global Outcomes (KDIGO) criteria. Multivariate logistic regression analyses were performed to identify risk factors for VCM-induced AKI. RESULTS: Seventeen patients had VCM-induced AKI. Multivariate analysis revealed that the risk factors of VCM-induced AKI were an initial VCM trough concentration of > 15 mg/L and concomitant use of tazobactam/piperacillin (TAZ/PIPC) and liposomal amphotericin B (L-AMB). Patients with an initial VCM trough concentration of < 10 mg/L showed significantly lower efficacy in febrile neutropenia. Interestingly, concomitant L-AMB use increased the incidence of VCM-induced AKI in a VCM concentration-dependent manner, whereas concomitant TAZ/PIPC increased the incidence in a VCM concentration-independent manner. CONCLUSIONS: The optimal initial VCM trough concentration was 10-15 mg/L in haematologic patients, considering safety and effectiveness. There were differences in the effect of VCM-induced AKI between nephrotoxic drugs.
PURPOSE: Appropriate use of vancomycin (VCM) is important in preventing acute kidney injury (AKI). Because of the high frequency of VCM use for febrile neutropenia and concomitant use of other nephrotoxic drugs, haematologic patients have a different nephrotoxic background compared with patients with other diseases. Therefore, it is unclear whether the risk factors of VCM-induced AKI identified in other patient groups are also applicable to haematologic patients. Herein, we performed a single-centre retrospective analysis to identify the factors associated with VCM-induced AKI in haematologic patients. METHODS: We retrospectively analysed 150 haematologic patients to whom VCM was administered between April 2010 and March 2018 at Tokushima University Hospital. VCM-induced AKI was defined according to Kidney Disease Improving Global Outcomes (KDIGO) criteria. Multivariate logistic regression analyses were performed to identify risk factors for VCM-induced AKI. RESULTS: Seventeen patients had VCM-induced AKI. Multivariate analysis revealed that the risk factors of VCM-induced AKI were an initial VCM trough concentration of > 15 mg/L and concomitant use of tazobactam/piperacillin (TAZ/PIPC) and liposomal amphotericin B (L-AMB). Patients with an initial VCM trough concentration of < 10 mg/L showed significantly lower efficacy in febrile neutropenia. Interestingly, concomitant L-AMB use increased the incidence of VCM-induced AKI in a VCM concentration-dependent manner, whereas concomitant TAZ/PIPC increased the incidence in a VCM concentration-independent manner. CONCLUSIONS: The optimal initial VCM trough concentration was 10-15 mg/L in haematologic patients, considering safety and effectiveness. There were differences in the effect of VCM-induced AKI between nephrotoxic drugs.
Authors: Marta Stanzani; Nicola Vianelli; Michele Cavo; Alessandro Maritati; Marta Morotti; Russell E Lewis Journal: Antimicrob Agents Chemother Date: 2017-08-24 Impact factor: 5.191
Authors: Branimir Jaksic; Giovanni Martinelli; Jaime Perez-Oteyza; Charlotte S Hartman; Linda B Leonard; Kenneth J Tack Journal: Clin Infect Dis Date: 2006-01-25 Impact factor: 9.079