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目的:探讨吉西他滨致溶血尿毒综合征（HUS）的临床和病理特点。方法:检索国外相关数据库（截至2018年11月12日），收集吉西他滨致HUS的病例报告与临床研究论文，记录患者一般情况、吉西他滨用药情况、HUS症状、相关实验室指标检测结果、肾组织活检结果、用药至出现HUS时间以及HUS治疗与转归情况，采用描述性统计方法分析吉西他滨致HUS的临床和病理特点。结果:纳入分析的患者共61例，男性22例，女性35例，性别不明4例；年龄25~81岁；原发疾病为胰腺癌者22例，肺癌18例，胆管癌7例，乳腺癌5例，卵巢癌4例，非霍奇金淋巴瘤2例，软组织肉瘤、膀胱癌、肾癌各1例；HUS发生在首次应用吉西他滨后2~34个月，中位时间6个月；发生HUS时吉西他滨累积剂量为4 000~99 540 mg/mn 2，中位累积剂量19 100 mg/mn 2。61例患者中54例出现HUS症状，主要表现为高血压（43例，79.6%）、外周性水肿（31例，57.4%）和呼吸困难（20例，37.0%）；7例无症状。61例患者均出现不同程度血清肌酐、乳酸脱氢酶水平升高和血小板、血红蛋白减少。15例患者做了肾活检，均可见血栓性微血管病变。发生HUS后均停用吉西他滨，给予对症或血浆置换或血液透析治疗，或对症+血浆置换、对症+糖皮质激素治疗，或在上述基础上再加利妥昔单抗或依库珠单抗治疗。61例患者中34例（55.7%）好转；27例（44.3%）在发生HUS后1~65个月内死亡，其中13例（21.3%）因HUS死亡。n 结论:吉西他滨致HUS的临床表现主要为高血压、外周性水肿和呼吸困难，少数可无症状，但均出现与尿毒症和溶血相关的实验室指标异常，肾脏主要病理学改变为血栓性微血管病变。HUS预后较差，严重者可导致患者死亡。“,”Objective:To explore the clinical and pathological characteristics of heomlytic-uremic syndrome (HUS) induced by gemcitabine.Methods:The relevant databases abroad were searched up to November 12, 2018. Case reports and clinical research papers about HUS induced by gemcitabine were collected. The patient′s general situation, use of gemcitabine, symptoms of HUS, relevant laboratory test results, renal biopsy results, time from medication to HUS onset, and the treatments and outcomes of HUS were recorded. The clinical and pathological characteristics of HUS induced by gemcitabine were analyzed by descriptive statistical method.Results:A total of 61 patients were enrolled in the study, including 22 males and 35 females with 4 unknown gender. The age of patients ranged from 25 to 81 years. The primary diseases included pancreatic cancer in 22 cases, lung cancer in 18 cases, cholangiocarcinoma in 7 cases, mammary cancer in 5 cases, ovarian cancer in 4 cases, non-Hodgkin′s lymphoma in 2 cases, soft tissue sarcoma in 1 case, bladder cancer in 1 case, and kidney cancer in 1 case. HUS occurred in 2-34 months after the first application of gemcitabine, and the median time was 6 months. The cumulative dose of gemcitabine was 4 000-99 540 mg/mn 2 when HUS occurred, and the median cumulative dose was 19 100 mg/mn 2. Of the 61 patients, 54 patients developed HUS symptoms, including hypertension (43 cases, 79.6%), peripheral edema (31 cases, 57.4%), and dyspnea (20 cases, 37.0%), and 7 patients were asymptomatic. There were different degrees of increase in serum creatinine and lactate dehydrogenase and decrease in platelet and hemoglobin in 61 patients. Fifteen patients performed renal biopsy and the thrombotic microangiopathy were found in all cases. Gemcitabine were stopped after the occurrence of HUS in all patients, and therapies such as symptomatic treatments, plasmapheresis, hemodialysis, symptomatic treatments+plasmapheresis, symptomatic treatments+glucocorticoid, or rituximab or ikuzumab treatment on the basis of above-mentioned therapy were given. Of the 61 patients, HUS was improved in 34 (55.7%) cases, but 27 patients (44.3%) died within 1-65 months after the occurrence of HUS, of which 13 cases (21.3%) died of HUS.n Conclusions:The main clinical manifestations of HUS caused by gemcitabine are hypertension, peripheral edema, and dyspnea. A few patients may be asymptomatic, but all develop abnormal laboratory indicators related to toxuria and hemolysis. The main pathological changes in the kidney are thrombotic microangiopathy. The prognosis of HUS is poor. Severe cases can lead to death.