{"title":"[利用医学信息数据库探究抗生素引发急性肾损伤及其转为慢性肾病的风险因素]。","authors":"Masaya Ieda, Yuka Kuroda, Takahiro Matsumoto, Ayaka Yamashita, Takashi Watanabe, Katsuhito Hori, Michio Kimura, Junichi Kawakami, Masahiro Tohkin","doi":"10.1248/yakushi.23-00198","DOIUrl":null,"url":null,"abstract":"<p><p>Drug-induced acute kidney injury (AKI) is a serious adverse drug reaction, which results in a significant decline in renal function and is known to progress to chronic kidney disease (CKD). Therefore, appropriate drug therapy is important to avoid the risk of drug-induced AKI and CKD, which are serious concerns in clinical practice. In this study, using the medical information database of Hamamatsu University Hospital, we investigated the risk factors that accelerate the onset of drug-induced AKI or its progression to CKD in patients who received aminoglycoside antibiotics (AGs) or glycopeptide antibiotics (GPs), which are strongly associated with drug-induced AKI and CKD. We performed logistic regression analysis using patients' background, laboratory test results, and concomitant drug use, among other such factors as explanatory variables and drug-induced AKI or CKD onset as objective variables to explore the risk factors for drug-induced AKI and CKD. Our results showed that co-administration of amphotericin B, piperacillin-tazobactam and other AGs and GPs, increased serum creatinine (Scr) and chloride concentrations, serum lactate dehydrogenase activity, and decreased serum albumin concentration were risk factors for drug-induced AKI onset. Moreover, a reduced blood urea nitrogen : Scr ratio at drug-induced AKI onset served as a risk factor for CKD. These results suggest that careful monitoring of the aforementioned factors is important to ensure appropriate usage of these drugs in patients treated with AGs and GPs.</p>","PeriodicalId":23810,"journal":{"name":"Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan","volume":" ","pages":"447-462"},"PeriodicalIF":0.3000,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Exploration of Risk Factors of the Onset of Antibiotics-induced Acute Kidney Injury and Its Transfer to Chronic Kidney Disease Using the Medical Information Database].\",\"authors\":\"Masaya Ieda, Yuka Kuroda, Takahiro Matsumoto, Ayaka Yamashita, Takashi Watanabe, Katsuhito Hori, Michio Kimura, Junichi Kawakami, Masahiro Tohkin\",\"doi\":\"10.1248/yakushi.23-00198\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Drug-induced acute kidney injury (AKI) is a serious adverse drug reaction, which results in a significant decline in renal function and is known to progress to chronic kidney disease (CKD). Therefore, appropriate drug therapy is important to avoid the risk of drug-induced AKI and CKD, which are serious concerns in clinical practice. In this study, using the medical information database of Hamamatsu University Hospital, we investigated the risk factors that accelerate the onset of drug-induced AKI or its progression to CKD in patients who received aminoglycoside antibiotics (AGs) or glycopeptide antibiotics (GPs), which are strongly associated with drug-induced AKI and CKD. We performed logistic regression analysis using patients' background, laboratory test results, and concomitant drug use, among other such factors as explanatory variables and drug-induced AKI or CKD onset as objective variables to explore the risk factors for drug-induced AKI and CKD. Our results showed that co-administration of amphotericin B, piperacillin-tazobactam and other AGs and GPs, increased serum creatinine (Scr) and chloride concentrations, serum lactate dehydrogenase activity, and decreased serum albumin concentration were risk factors for drug-induced AKI onset. Moreover, a reduced blood urea nitrogen : Scr ratio at drug-induced AKI onset served as a risk factor for CKD. 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引用次数: 0
摘要
药物诱发的急性肾损伤(AKI)是一种严重的药物不良反应,会导致肾功能显著下降,并有可能发展为慢性肾病(CKD)。因此,适当的药物治疗对于避免药物诱发 AKI 和 CKD 的风险非常重要,这也是临床实践中严重关切的问题。在本研究中,我们利用滨松大学医院的医疗信息数据库,调查了接受氨基糖苷类抗生素(AGs)或糖肽类抗生素(GPs)治疗的患者中加速药物性 AKI 发病或进展为 CKD 的风险因素,这两种抗生素与药物性 AKI 和 CKD 密切相关。我们以患者的背景、实验室检查结果和同时使用药物等因素为解释变量,以药物诱发的 AKI 或 CKD 发病为客观变量,进行了逻辑回归分析,以探讨药物诱发 AKI 和 CKD 的风险因素。我们的研究结果表明,联合使用两性霉素 B、哌拉西林-他唑巴坦及其他 AGs 和 GPs、血清肌酐(Scr)和氯化物浓度升高、血清乳酸脱氢酶活性升高以及血清白蛋白浓度降低是药物诱发 AKI 发病的风险因素。此外,药物诱导性 AKI 发病时血尿素氮与 Scr 的比值降低也是导致 CKD 的危险因素。这些结果表明,仔细监测上述因素对于确保使用 AGs 和 GPs 治疗的患者适当使用这些药物非常重要。
[Exploration of Risk Factors of the Onset of Antibiotics-induced Acute Kidney Injury and Its Transfer to Chronic Kidney Disease Using the Medical Information Database].
Drug-induced acute kidney injury (AKI) is a serious adverse drug reaction, which results in a significant decline in renal function and is known to progress to chronic kidney disease (CKD). Therefore, appropriate drug therapy is important to avoid the risk of drug-induced AKI and CKD, which are serious concerns in clinical practice. In this study, using the medical information database of Hamamatsu University Hospital, we investigated the risk factors that accelerate the onset of drug-induced AKI or its progression to CKD in patients who received aminoglycoside antibiotics (AGs) or glycopeptide antibiotics (GPs), which are strongly associated with drug-induced AKI and CKD. We performed logistic regression analysis using patients' background, laboratory test results, and concomitant drug use, among other such factors as explanatory variables and drug-induced AKI or CKD onset as objective variables to explore the risk factors for drug-induced AKI and CKD. Our results showed that co-administration of amphotericin B, piperacillin-tazobactam and other AGs and GPs, increased serum creatinine (Scr) and chloride concentrations, serum lactate dehydrogenase activity, and decreased serum albumin concentration were risk factors for drug-induced AKI onset. Moreover, a reduced blood urea nitrogen : Scr ratio at drug-induced AKI onset served as a risk factor for CKD. These results suggest that careful monitoring of the aforementioned factors is important to ensure appropriate usage of these drugs in patients treated with AGs and GPs.