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目的:探讨重症监护病房（ICU）重症泛耐药革兰阴性菌（XDR-GNB）感染患者使用多黏菌素B治疗后急性肾损伤（AKI）的发生率和危险因素。方法:回顾性分析2018年4月1日至2020年1月31日南京大学医学院附属鼓楼医院重症医学科接受多黏菌素B治疗3 d以上重症感染患者的临床资料。AKI依据改善全球肾脏病预后组织（KDIGO）标准诊断。比较AKI组与非AKI组基线、治疗期间及预后相关指标，将单因素分析中差异有统计学意义的因素和重要的临床因素纳入Logistic回归模型，分析发生AKI的危险因素。结果:研究期间有72例患者接受多黏菌素B治疗>3 d，最终49例患者符合纳入标准，其中32例发生多黏菌素B相关性AKI，发生率为44.4%。AKI组与非AKI组基线资料均衡，且预后比较差异也无统计学意义〔死亡或自动出院（例）：14比6，好转出院（例）：18比11，χn 2＝0.329，n P＝0.566〕。多黏菌素B相关性AKI发生于用药后1～14 d，平均（6.8±3.8） d。32例AKI患者中，2例好转出院后肾功能失访，18例肾功能恢复，12例未恢复；肾功能未恢复者预后明显差于肾功能恢复者〔死亡或自动出院（例）：12比2，好转出院（例）：0比16，n P＝0.000〕。单因素分析显示：AKI组多黏菌素B日剂量高于非AKI组（mg：151.6±23.7比132.4±30.3）；日剂量≥150 mg、使用血管活性药物、严重低蛋白血症（白蛋白≤25 g/L）的例数均显著多于非AKI组（例：29比10，18比4，9比0），差异均有统计学意义（均n P<0.05）。多因素Logistic回归分析显示，多黏菌素B日剂量≥150 mg、使用血管活性药物是多黏菌素B相关性AKI的独立危险因素〔优势比（n OR）＝37.466，95%可信区间（95%n CI）为2.676～524.586，n P＝0.007；n OR＝22.960，95%n CI为1.710～308.235，n P＝0.018〕。n 结论:发生多黏菌素B相关性AKI者较未发生者更多合并严重低蛋白血症，且使用血管活性药物和多黏菌素B日治疗剂量更高；多黏菌素B日剂量≥150 mg、使用血管活性药物为多黏菌素B相关性AKI的独立危险因素。“,”Objective:To investigate the incidence and risk factors of polymyxin B-associated acute kidney injury (AKI) in patients with severe infections caused by extensive drug resistance Gram negative bacteria (XDR-GNB)in intensive care unit (ICU).Methods:A retrospective study of adult patients with severe infection who received polymyxin B for more than 3 days in the department of critical care medicine of Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School from April 1st 2018 to January 31st 2020 were performed. AKI was diagnosed by Kidney Disease: Improving Global Outcomes (KDIGO) criteria. The baseline data, indicators during treatment period and prognostic factors were compared between AKI group and non-AKI group. Factors with statistically significant difference in univariate analysis and important clinical factors were included in the Logistic regression model to analyze the risk factors of AKI.Results:Seventy-two patients were treated with polymyxin B for more than 3 days. Forty-nine patients were finally enrolled, with 32 patients developing polymyxin B-associated AKI, and the incidence was 44.4%. The baseline data was balanced in AKI group and non-AKI group, and there was no significant difference in the prognosis [death or discharge without medial order (cases): 14 vs. 6, discharged for improvement (cases): 18 vs. 11, χ n 2 = 0.329, n P = 0.566]. Polymyxin B-associated AKI occurred from 1 day to 14 days after treatment, with an average of (6.8±3.8) days. Among the 32 AKI patients, 2 cases were lost to follow up after discharge, while renal function recovered in 18 cases and unrecovered in 12 cases. The prognosis of patients without recovery of renal function was significantly worse than that of patients with renal function recovery [death or discharge without medial order (cases): 12 vs. 2, discharged for improvement (cases): 0 vs. 16, n P = 0.000]. Single factor analysis showed that daily dosage of polymyxin B in AKI group was higher than that in non-AKI group (mg: 151.6±23.7 vs. 132.4±30.3), numbers of patients with daily polymyxin B dose ≥ 150 mg, using vasoactive drugs, or severe hypoalbuminemia (albumin≤25 g/L) were higher than those in non-AKI group (cases: 29 vs. 10, 18 vs. 4, 9 vs. 0), with statistically significant differences (all n P < 0.05). Multivariate Logistic regression analysis showed that daily dosage of polymyxin B ≥ 150 mg and use of vasoactive drugs were independent risk factors for polymyxin B-associated AKI [odds ratio ( n OR) = 37.466, 95% confidence interval (95%n CI) was 2.676-524.586, n P = 0.007; n OR = 22.960, 95%n CI was 1.710-308.235, n P = 0.018].n Conclusions:Comparing with non-AKI patients, more patients with polymyxin B-associated AKI had severe hypoalbuminemia, and the probability of using vasoactive drugs and the daily dose of polymyxin B were higher than non-AKI patients. Daily dose of polymyxin B ≥ 150 mg and using vasoactive drugs were independent risk factors for polymyxin B-associated AKI.