急性肾损伤患者尿肾损伤分子1水平与APACHEⅡ评分的相关性研究

急性肾损伤(AKI)是重症医学科的常见病症,早期发现与治疗可防止其病情恶化,阻止其发展成肾衰竭.目前,在临床研究领域中十分注重转移医学,即临床-基础相结合研究,临床生物学标志物是其中的研究重点[1].近年来发现的肾损伤分子1(Kim-1)位于近曲小管上皮细胞膜上,缺血性损伤时可从尿中排出[2],可作为肾损伤早期监测的一个生物指标.我们回顾性收集并观察了62例AKI患者及36例非AKI患者的临床资料,研究其尿液中Kim-1浓度与APACHEⅡ评分及预后的关系.     

尿NGAL、NAG及KIM-1联合检测在高龄老年急性肾损伤早期诊断中的价值

目的探讨尿中性粒细胞明胶酶相关脂质运载蛋白(uNGAL)、尿N-乙酰β-D氨基葡萄糖苷酶(uNAG)及尿肾损伤分子-1(uKIM-1)的联合检测老年急性肾损伤中的诊断价值。方法选择2016年6月至2018年6月在泰山疗养院住院的老年患者184例,根据急性肾损伤网络(AKIN)标准为诊断标准,诊断AKI组116例(1期55例、2期39例、3期24例),非AKI组68例,检测并比较各组尿NGAL、NAG、KIM-1水平,用受试者工作特征曲线(ROC)及曲线下面积(AUC)分析3项生物学标志物对AIK的诊断价值。结果①AKI组尿NGAL、NAG、KIM-1明显高于对照组(P<0.05),3期尿NGAL、NAG、KIM-1明显高于2期和1期,2期明显高于1期(P<0.05);②尿NGAL、NAG、KIM-1单独诊断AKI的AUC分别为0.734、0.804、0.705;③3项标志物联合诊断AKI的灵敏度、特异度分别为84.9%、90.7%,高于各单项诊断。结论尿NGAL、NAG、KIM-1是诊断AKI的较好指标,联合诊断对高龄老年急性肾损伤的早期诊断有着更重要的价值。     

重症感染合并急性肾损伤中NGAL的变化

目的探讨尿中性粒细胞明胶酶相关载脂蛋白在重症感染合并急性。肾损伤中的诊断价值。方法选择2010年1月--2011年6月在新疆自治区人民医院ICU住院的重症感染患者79例,按急性肾损伤的诊断标准分为急性肾损伤组和非急性肾损伤组。分别测定尿中性粒细胞明胶酶相关载脂蛋白、N-乙酰-β-D-氨基葡萄糖苷酶、微量白蛋白和血肌酐的浓度。通过受试者工作特征曲线及曲线下面积评价各项指标的敏感性。结果急性肾损伤组中各项指标的测定浓度明显高于非急性肾损伤组,其中尿中性粒细胞明胶酶相关载脂蛋白的敏感性和特异性分别为0．95和0．90,曲线下面积=0．986（0．9681．004）;血肌酐的敏感性和特异性分别为0．75和0．69,曲线下面积=0．776（0．705～0．852）,差异具有统计学意义（P〈0．001）。结论’尿中性粒细胞明胶酶相关载脂蛋白的敏感性高于血肌酐,可以作为重症感染合并急性肾损伤的早期诊断标记物。     

尿肾损伤分子1与白细胞介素18对急性肾损伤患者的诊断价值

目的：观察尿肾损伤分子1（kidney inj ury molecule-1,Kim-1）与白细胞介素18（inter-leukin-18,IL-18）在急性肾损伤（acute kidney injury,AKI）患者中的变化,探讨其对 AKI的诊断价值。方法选择我院确诊为AKI患者71例（AKI组）,并根据AKI分期,分为AKI 1期组23例、AKI 2期组25例和 AKI 3期组23例;另选择同时期我院体检中心健康体检者30名（健康对照组）,分别检测2组患者尿Kim-1、尿 IL-18及血肌酐（SCr）水平。结果 AKI组 SCr、尿Kim-1较健康对照组明显升高（P〈0.01）,尿 IL-18亦升高（P〈0.05）,与健康对照组比较,SCr、尿 Kim-1在 AKI 1期组、AKI 2期组、AKI 3期组均明显升高（P〈0.01）,尿 IL-18在 AKI 2期组、AKI 3期组亦明显升高（P〈0.01）,在 AKI 1期组虽升高,但差异无统计学意义（P〉0.05）;与 AKI 1期组比较,SCr、尿 Kim-1在 AKI 2期组、AKI 3期组均明显升高（P〈0.01）,尿IL-18在AKI 2期升高（P〈0.05）,在AKI 3期组亦升高（P〈0.01）,与 AKI 2期组比较,SCr、尿 Kim-1及尿 IL-18在 AKI 3期组均明显升高（P〈0.01）;而且相关性分析显示,尿 Kim-1与 SCr 呈正相关（r=0.842,P〈0.01）;尿 IL-18与 SCr 呈正相关（r=0.785,P〈0.01）;尿Kim-1与尿 IL-18呈正相关（r=0.756,P〈0.01）。而 ROC 曲线下面积比较结果显示,尿Kim-1（0.915）明显大于尿 IL-18（0.807）（P〈0.05）。结论尿 Kim-1、尿 IL-18在 AKI患者中升高,二者均可能作为 AKI的诊断标准,且尿Kim-1诊断价值可能更高。     

尿NGAL在儿童急性肾损伤诊断中的作用研究

目的：探讨尿中性粒细胞明胶酶相关脂质记载蛋白（neutrophil gelatinase-associate dlipocalin,NGAL）在儿童急性肾损伤诊断中的敏感性,特异性以及在鉴别肾前性氮质血症和急性肾损伤中的作用。方法：收集急性肾损伤的患儿36例,肾前性氮质血症患儿28例,正常对照组52例。所有入选患儿均常规测血压,检测血常规、肝功、肾功及离子、尿常规、尿钠、尿肌酐、尿NAG、尿α1-MG。每个入选患儿收集3～5ml尿液,离心后-80℃冰箱冻存,ELISA方法检测尿NGAL。结果：急性肾损伤组患儿尿NGAL值明显高于肾前性氮质血症组和正常对照组（399μg/g creatinine[SD,366];P〈0.01）。绘制ROC曲线后,NGAL在截断值为100μg/g creatinine时,其诊断儿童急性肾损伤的敏感性为0.91（CI：0.74～0.98）,特异性为0.98（CI0.97～0.99）;阳性似然比为155.33（CI56.34～464.75）,阴性似然比为0.08（CI0.03～0.27）,明显好于尿NAG,尿α1-MG和血肌酐。结论：尿NGAL在儿童急性肾损伤的诊断中,敏感性和特异性,阳性似然比和阴性似然比均明显好于血肌酐,并且可以在一定程度上鉴别肾前性氮质血症和急性肾损伤。     

血胱抑素C、尿肾损伤分子-1水平和血清肌酐在急性肾损伤患者肾功能评估中的比较研究

目的:探讨肾功能状态标志物血胱抑素C、尿肾损伤分子-1水平相较于血清肌酐在评估急性肾损伤中的价值。方法:本研究以2014年2月~2015年6月我院收治的49例急性肾损伤患者以及40例健康体检者为研究对象,采用生化仪测定血胱抑素C以及血清肌酐的浓度变化、双抗体夹心酶标免疫分析法测定尿肾损伤分子-1水平;分析血胱抑素C、尿肾损伤分子-1水平相较于血清肌酐在急性肾损伤患者肾功能状态评估中的价值。结果:在急性肾损伤患者肾功能状态评估中血胱抑素C以及尿肾损伤分子-1的准确性、阳性以及阴性预测值显著高于血清肌酐(P0.05),其余指标不存在统计学差异(P0.05);全部患者以及Ⅰ期患者的血胱抑素C与尿肾损伤分子-1的检测灵敏度要优于血清肌酐(P0.05),而Ⅱ期及Ⅲ期患者无显著差别(P0.05)。结论:血胱抑素C、尿肾损伤分子-1水平均可作为评估急性肾损伤患者肾功能状态的内源性标志物,有助于尽早识别急性肾损伤患者肾功能的损害。     

乌司他丁对重症急性胰腺炎并发急性肾损伤的临床干预观察

目的:研究乌司他丁对重症急性胰腺炎合并急性肾损伤的临床干预效果,同时观察乌司他丁对急性肾损伤发生及发展过程中肾损伤因子-1(kim-1)、尿中性粒细胞明胶酶相关载脂蛋白(NGAL)的影响。方法:将我院普外科56例重症急性胰腺炎并发急性肾损伤的患者随机分为对照组和治疗组,每组28例。两组均给予常规治疗,治疗组在此基础上加用乌司他丁,疗程7 d。观察两组患者治疗前与治疗7天血尿素氮、血肌酐变化,两组患者少尿期持续时间及7 d死亡率,同时监测两组患者入院1 h及12 h尿kim-1和NGAL的水平。结果:治疗7 d后,治疗组患者血尿素氮及血肌酐低于对照组(P0.05),少尿期持续时间缩短(P0.05);两组患者7 d死亡率差异无统计学意义;两组患者入院1 h所测尿kim-1差异无统计学意义,尿NGAL差异无统计学意义;治疗组在入院12 h尿kim-1及NGAL所测值均较对照组低,差异有统计学意义(P0.05)。结论:乌司他丁对重症急性胰腺炎并发急性肾损伤患者具有一定治疗作用,通过抑制急性期某些细胞因子表达,减轻肾小管损伤而保护肾功能,可辅助治疗重症急性胰腺炎。     

尿白细胞介素-18在慢性肾脏病基础上急性肾损伤诊断中的意义

目的：研究尿液白细胞介素-18（IL-18）在慢性肾脏病基础上急性肾损伤（AonC）诊断中的应用价值。方法：入选住院的AonC患者（AonC组）、稳定的慢性肾脏疾病（CKD对照组）患者及体检中心无CKD的体检者（正常对照组）各28例,分别收集各组的临床、实验室检查资料及尿液标本;采用ELISA方法检测尿IL-18水平,用比色法检测尿N-乙酰-β-D氨基葡萄糖酐酶（NAG）水平,进行综合分析。结果：尿IL-18水平在AonC组、CKD对照组和正常对照组分别为343.10（230.76～721.78）ng/L、205.97（137.06～319.62）ng/L、44.44（12.42～107.19）ng/L。AonC组尿IL-18水平显著高于CKD对照组和正常对照组（P〈0.01）。相关性分析显示,AonC组尿IL-18水平与血清肌酐水平呈正相关（r=0.665,P〈0.01）。ROC曲线分析提示,尿IL-18在AonC诊断中特异性较高,曲线下面积为0.886,P〈0.01;当以212.4ng/L为截点时,其在诊断AonC时的敏感性和特异性分别为85.7%和76.8%。3组患者尿液NAG水平亦存在统计学意义（P〈0.01）,但尿NAG水平与Scr无显著性相关。ROC曲线分析显示,曲线下面积为0.67。当检测的截点为10.5U/L时,其诊断的敏感性和特异性分别为74.1%和58.9%。结论：尿IL-18水平在慢性肾脏病基础上急性肾损伤时明显上升,在慢性肾脏病基础上急性肾损伤诊断中的意义值得进一步研究。     

泌尿系结石相关急性肾损伤早期监测的生物学标记物研究进展

泌尿系结石的存在及外科处理有诱发急性肾损伤(AKI)的风险。AKI与许多不良结果的风险增加有关,早期发现和干预是降低AKI危害的关键。生物学标记物肾损伤分子-1(KIM-1)、人中性粒细胞明胶酶相关脂质运载蛋白(NGAL)、神经导向因子(Netrin-1)、N-乙酰-β-D氨基葡萄糖苷酶(NAG)、人肝型脂肪酸结合蛋白...     

ESWL前后肾内血管阻力和尿中GAL与NAG活性变化的意义

观测体外冲击波碎石(ESWL)治疗50例单侧肾结石病人过程中,肾内血管阻力指数(RI)和尿液中β-D半乳糖苷醇(GAL)与N-乙酰-β-D氨基葡萄糖苷醇(NAG)水平的变化,探讨三者与ESWL所致肾脏损伤及修复过程的关系。结果ESWL后较ESWL前肾内血管RI显著升高(P<0.01);伴尿中NAG水平也明显上升(P<0.05)。而ESWL后1～2周时尿中GAL水平开始升高,且GAL/NAG值呈明显的上升趋势。提示ESWL后所致肾损伤程度与肾内血管RI和尿中NAG水平呈正相关;肾修复时限长短与尿中GAL水平的变化相关,GAL/NAG值的变化可能是肾损伤和修复过程中最有效的临床检测指标。     

联合尿液标记物检测在高血压早期肾损害诊断中的临床应用研究

目的 探讨尿视黄醇结合蛋白(RBP)、尿N-乙酰-β-D-氨基葡萄糖苷酶(NAG)、尿胱蛋白酶抑制剂C(Cystatin C)和微量白蛋白(mALB)的联合测定对原发性高血压早期肾损害诊断的敏感性及临床意义.方法 选择2014年9月至2015年6月在新疆自治区人民医院肾病科住院的原发性高血压患者52例作为观察组,另设健康体检者30例为对照组.尿RBP、Cys-tatin C和mALB测定采用酶联免疫法(ELISA)检测,尿NAG测定采用对硝基苯酚(PNP)比色法检测.结果 观察组中尿RBP、NAG、Cystatin C和mALB的含量明显高于正常对照组(P＜0.001),通过ROC曲线、诊断试验结果显示:尿NAG、RBP的曲线下面积分别为0.952、0.932,95％可信区间分别为0.911 ～0.993、0.875 ～0.981,较尿Cystatin C和mALB更具有敏感性(P＜0.001).联合尿RBP、NAG、Cystatin C和mALB检测的曲线下面积为0.971,95％可信区间分别为0.946 ～1.000,差异具有统计学意义(P＜0.001).结论 联合检测尿NAG、RBP、CystatinC和mALB有助于高血压肾损害的早期监测,对预防高血压性肾病的发生、发展具有重要的临床价值.     

尿N-乙酰-β-D-氨基葡萄糖苷酶水平与新生儿窒息后肾损伤关系

目的探讨新生儿窒息后尿 N-乙酰-β-D-氨基葡萄糖苷酶（N-acetyl-beta-D-glu-cosaminidase,NAG）、血清中α1微球蛋白（α1-microglobulin,α1-MG）、β2-MG 值水平变化以及与窒息程度和急性肾损伤（acute kidney inj ury,AKI）之间的关系,阐述其在窒息新生儿肾损伤中的诊断价值。方法选择围产期窒息新生儿40例（窒息组）,按照新生儿窒息Apgar评分标准分为轻度窒息者22例（轻度窒息组）,重度窒息者18例（重度窒息组）;根据有无发生 AKI 将40例窒息新生儿分为AKI组25例和无 AKI组15例;记录入选新生儿 Apgar评分、胎龄、日龄、体质量。另外选择20例无窒息史新生儿为对照组。所有纳入对象在出生后24 h内采取外周静脉血,同时收集尿液。采用胶乳增强免疫比浊法测定血清中α1-MG、β2-MG的含量;采用 ELISA法测定尿液中 NAG含量;同时用全自动生化仪检测尿素氮及血肌酐水平。结果（1）本研究40例窒息后新生儿 AKI 总发生率为62.5%（25/40）,并且轻度窒息与重度窒息对 AKI 影响不同,重度窒息患儿更易发生严重的肾损伤。（2）窒息组尿 NAG及血清中β2-MG、α1-MG明显高于对照组[（25.48±12.45）U/L 比（8.62±2.49） U/L,（4.82±1.32）mg/L比（2.92±0.89）mg/L,（29.85±5.59）mg/L 比（25.23±5.26）mg/L]。（3）重度窒息组尿 NAG及血清中β2-MG、α1-MG 明显高于轻度窒息组[（32.21±24.32）U/L、（5.89±1.59）mg/L、（34.32±7.64）mg/L]明显高于轻度窒息组[（17.25±7.32）U/L、（2.92±0.89）mg/L、（26.94±5.57）mg/L]。（4）AKI组尿 NAG及血清中β2-MG、α1-MG[（28.24±21.25）U/L、（5.79±1.49）mg/L、（31.32±5.28）mg/L]明显高于无 AKI组[（16.34±6.72））U/L、（2.82±0.79）mg/L、（26.49±5.52）mg/L]。（5）按照对照组尿 NAG及血清中β2-MG、α1-MG值设定在x＋2SD为对照上限值,窒息组中尿 NAG异常率达65%,明显高于血清中β2-MG、α1-MG 异常率（分别为32.5%和7     

Mitochondrial dysfunction in the process of cisplatin-induced acute kidney injury in mice

Objective To assess the characteristics of different doses of cisplatin-induced acute kidney injury, further to understand mitochondrial dysfunction and its role in acute kidney injury (AKI). Methods Male C57BL/6J mice were first randomly divided into two groups: control group (n＝6) and AKI group (n＝12). Then, AKI group was subsequently divided into other two groups according to different dose of cisplatin (10 mg/kg or 20 mg/kg). AKI group received intraperitoneal injection of cisplatin. All mice were sacrificed after 72 h of injection. Renal biochemical function, renal pathological changes, renal injury markers, kidney mitochondrial function and structural changes were observed. Results (1) After 72 hours of injection, the AKI group performed significant kidney injury changes compared to control group, thereinto 20 mg/kg group was more serious than 10 mg/kg group. With the cisplatin dose increasing, renal function markers such as serum creatinine, urine protein gradually increased. (2)Kidney biopsy showed tubular structural damage, the formation of protein casts, kidney injury molecule-1 (KIM-1) gradually increased(P＜0.05). (3)Electron microscopy found tubular mitochondrial structural damage, mtDNA copy number decreased, the level of peroxisome proliferator-activated receptor -gamma coactivator-1alpha (PGC-1α), ATP synthase β decreased(P＜0.05), and Western blotting manifested cytochrome C was released from mitochondria to the cytoplasm. These data all exhibited significant difference between different groups(P＜0.05). Conclusions Cisplatininduces acute kidney injury in dose-dependent manner. Mitochondrial dysfunction participates in kidney injury, and is also related to the kidney pathological damage.     

联合生物标志物检测在慢性肾脏疾病中的临床研究

目的 探讨尿微量白蛋白（mALB）、尿β2-微球蛋白（β2-MG）、尿视黄醇结合蛋白（RBP）、尿转铁蛋白（TRF）、尿半胱氨酸蛋白酶抑制剂C（Cystatin C）及尿N-乙酰-β-D-氨基葡萄糖苷酶（NAG）在慢性肾脏疾病中的临床研究及诊断价值.方法 选择2012年8月～2013年1月在本院住院的慢性肾脏病患者121例为病例组,健康体检者60例为对照组.尿mALB、β2-MG、RBP、TRF及Cystatin C采用酶联免疫吸附法检测,尿NAG采用对硝基苯酚（PNP）比色法检测,并对两组检测结果进行比较及统计学分析,以受试者工作特征（ROC）曲线及曲线下面积（AUC）评价各项标志物单—及联合应用时在慢性肾脏疾病中的诊断价值.结果 病例组中121例患者的尿液生物标志物测定含量明显高于对照组.通过ROC曲线、诊断试验结果显示：病例组中尿mALb、TRF、Cystatin C、NAG、RBP及β2-MG的敏感性显著高于血肌酐（Scr）和血尿素氮（BUN）.尿mALb、TRF、Cystatin C、NAG、RBP及β2-MG的曲线下面积分别为：0.988、0.984、0.974、0.947、0.915、0.897,95％可信区间分别是0.973—1.000、0.963～1.000、0.956 ～0.992、0.910～0.984、0.877～0.954、0.851 ～0.944,联合这6种尿液标志物得到的曲线下面积为0.990,95％可信区间是0.976 ～0.998,差异具有统计学意义（P＜0.001）.结论 病例组中各项尿液标志物的敏感性明显高于Scr和BUN,可以作为慢性肾脏病的诊断标志物.尿nALb、TRF、Cystatin C及NAG的曲线下面积最大,尿RBP和β2-MG也显示了较好的诊断价值.联合应用尿液标志物可以更好地预测临床上急性和慢性肾脏损害的发生,对预防慢性肾脏病的发展具有重要的临床价值.     

Urinary biomarkers in the early diagnosis of acute kidney injury

A change in the serum creatinine is not sensitive for an early diagnosis of acute kidney injury. We evaluated urinary levels of matrix metalloproteinase-9 (MMP-9), N-acetyl-beta-D-glucosaminidase (NAG), and kidney injury molecule-1 (KIM-1) as biomarkers for the detection of acute kidney injury. Urine samples were collected from 44 patients with various acute and chronic kidney diseases, and from 30 normal subjects in a cross-sectional study. A case-control study of children undergoing cardio-pulmonary bypass surgery included urine specimens from each of 20 patients without and with acute kidney injury. Injury was defined as a greater than 50% increase in the serum creatinine within the first 48 h after surgery. The biomarkers were normalized to the urinary creatinine concentration at 12, 24, and 36 h after surgery with the areas under the receiver-operating characteristic curve compared for performance. In the cross-sectional study, the area under the curve for MMP-9 was least sensitive followed by KIM-1 and NAG. Combining all three biomarkers achieved a perfect score diagnosing acute kidney injury. In the case-control study, KIM-1 was better than NAG at all time points, but combining both was no better than KIM-1 alone. Urinary MMP-9 was not a sensitive marker in the case-control study. Our results suggest that urinary biomarkers allow diagnosis of acute kidney injury earlier than a rise in serum creatinine.     

Analysis of risk factors for progression of acute kidney injury to acute kidney disease

Objective To investigate the risk factors of clinically diagnosed acute kidney injury (AKI) patients progressing to acute kidney disease (AKD). Methods The clinical data of AKI patients admitted to the First Affiliated Hospital of Zhengzhou University from January 1, 2018 to December 31, 2018 were retrospectively analyzed. According to the outcome of the patients, AKI patients were divided into non-acute kidney disease (NAKD) group and AKD group. Clinical characteristics and laboratory data of two groups were compared. The risk factors of AKD in patients with AKI were analyzed by logistic regression, and then the receiver operating characteristic curve (ROC) was drawn to evaluate the predictive value of these risk factors. Results A total of 254 patients with AKI were enrolled, and 186 patients developed AKD with an incidence of 73.2%. The incidences of AKD in stage 1, stage 2 and stage 3 of AKI were 20.0%, 46.7% and 83.5% respectively. Multivariate logistic regression analysis showed increased peak serum creatinine (within 7 days after AKI diagnosis) (OR=2.561, 95%CI 1.584-4.140, P＜0.001), proteinuria (OR=2.952, 95%CI 1.162-7.500, P=0.023) and increased intact parathyroid hormone (OR=1.757, 95%CI 1.104-2.797, P=0.017) were independent risk factors for progression to AKD in patients with AKI. The ROC showed that increased peak serum creatinine (within 7 days after AKI diagnosis) was an important predictor of AKD in patients with AKI (AUC=0.798, P＜0.001). Conclusion Increased peak serum creatinine (within 7 days after AKI diagnosis), proteinuria and increased intact parathyroid hormone are independent risk factors for progression to AKD in patients with AKI, providing new evidences and ideas for clinical preventions and treatments of AKD.     

Value of levels of biomarkers at the time of nephrologists consultation in predicting the prognosis of acute kidney injury patients

Objective To investigate the value of biomarker levels at the time of nephrologists consultation in predicting the prognosis of acute kidney injury (AKI) patients. Methods A total of 103 hospitalized patients with AKI were enrolled at the time of nephrologists consultation. Blood and urine samples were collected when patients were diagnosed as AKI. ELISA was used to detect the concentration of urinary biomarkers including neutrophil gelatinase?associated lipocalin (NGAL), IL?6 and IL?18. Colorimetric method was used to measure urinary N?acetyl?β?D?glucosaminidase (NAG). Turbidimetry and enzymic method were applied to examine the concentration of serum cystatin C (Cys C), baseline Scr (bScr), Scr at consultation (cScr) and the peak of Scr (pScr) respectively. Patients were followed?up to evaluate the prognosis at 28 days after consultation, including patient survival and kidney survival. The levels of biomarkers between different groups, including patient survival or death, kidney recovery or lose and renal replacement therapy (RRT) or not, were compared. Area under curve (AUC) of receiver operating characteristic (ROC) curve of these biomarkers were used to evaluate the sensitivity and specificity in predicting prognosis. AKI was defined as the Scr at the time of consultation increased more than 50% of baseline Scr within 48 hours. Results (1)Mean age of 103 hospitalized AKI patients was (54.28±19.05) years old and ratio of male to female was 1.86 to 1. (2)Patient mortality was 25.2% at 28 days after consultation. The bScr, cScr and pScr were similar between survival and death group, while the concentration of urinary NGAL in death group was significantly higher than that of survival group [147.00(31.59, 221.87) mg/L vs 22.43(6.48, 89.77) mg/L, P＝0.001]. The serum Cys C, urinary IL?6 and NAG were similar between survival and death group (P＞0.05). Logistic regression analysis showed urinary NGAL was an independent risk factor of patient survival (OR＝1.011, 95%CI 1.004?1.018, P＝0.001) with AUC of 0.723. (3)Kidney lose rate was 20.4% at 28 days after consultation. The bScr, cScr and pScr were similar between patients with kidney survival and lose. The levels of urinary NAG, IL?6, NGAL and IL?18 were significantly higher in patients with kidney lose than those of kidney survival. Logistic regression analysis showed urinary IL?6 was an independent risk factor of renal survival (OR＝1.056, 95%CI 1.009?1.105, P＝0.018) with AUC of 0.705. (4)The median time from consultation to RRT was 2.17 (0?3) days. The concentrations of cScr, pScr, serum Cys C, urinary IL?6 and NGAL were significantly higher in RRT patients than thosein non?RRT patients (P＜0.05). Logistic regression analysis showed urinary NGAL was an independent risk factor of RRT (OR＝1.012, 95%CI 1.005?1.019, P＜0.01) with AUC of 0.775. Conclusions Urinary NGAL can predict the prognosis of AKI patients, including patient prognosis and RRT. Urinary IL?6 may predict kidney prognosis in hospitalized patients with AKI. More study with large samples should be done for further estimation of the results.