Epidemiology of contrast-associated acute kidney injury in ICU patients: a retrospective cohort analysis

Purpose  

Intensive care unit (ICU) patients frequently undergo contrast-enhanced radiographic examinations, which carries a risk for development of contrast-associated acute kidney injury (CA-AKI). Data on this in ICU patients are scarce. The aim of this study was therefore to evaluate the epidemiology and short- and long-term outcomes of CA-AKI in ICU patients.     

重症监护病房住院患者急性肾损伤的发病及预后分析

目的：分析重症监护病房(ICU)住院患者并发急性肾功能损伤(AKI)的发病及影响预后的危险因素,为临床更好的预防 AKI 的发生、改善预后提供依据。方法调查本院2010年1月至2013年12月所有 ICU 住院患者1100例,以急性肾损伤网(AKIN)推荐的 AKI 定义筛选出病史完整的 AKI 患者105例,回顾性分析 AKI 患者的一般临床资料、病因、临床特点,采用 logistic 回归分析影响其预后的危险因素。结果符合入选标准的住院 AKI 患者105例,肾前性、肾性、肾后性 AKI 分别占71.4%、23.8%、4.8%,肾前性病因中,脓毒症是 ICU 患者 AKI 发生的最主要的原因(占45.0%),随着 AKI 程度的增加,AKI 患者 ICU 住院时间明显延长(F =3.450,P <0.05),28天病死率亦明显增高(χ2=16.500,P <0.01)。应用多因素 logistic 逐步回归分析法显示 AKI 患者基础疾病的严重程度[相对比值比(OR )=3.259,95%可信区间(95% CI )=1.453~5.087,P <0.01]、肾外器官衰竭数(OR =1.275,95% CI =1.071~1.421,P <0.01)、年龄(OR =2.315,95% CI =1.015~3.684,P <0.01)、行肾替代(CRRT)治疗与否(OR=2.018,95% CI =1.852~3.014,P <0.01)是 AKI 患者肾功能未恢复的独立危险因素。结论 AKI 是 ICU 住院患者的常见并发症之一。脓毒症是住院 AKI 最常见的原因。合并严重基础疾病、肾外器官衰竭、年龄、行 CRRT 治疗与否是 AKI 患者肾功能未恢复的独立危险因素。     

Six-month outcome in acute kidney injury requiring renal replacement therapy in the ICU: a multicentre prospective study

Objective  

To assess quality of life (QOL), mortality rate and renal function 6 months after onset of renal replacement therapy (RRT) for acute kidney injury (AKI) in the ICU.     

Bench-to-bedside review: Functional hemodynamics during surgery - should it be used for all high-risk cases?

The administration of a fluid bolus is done frequently in the perioperative period to increase the cardiac output. Yet fluid loading fails to increase the cardiac output in more than 50% of critically ill and surgical patients. The assessment of fluid responsiveness (the slope of the left ventricular function curve) prior to fluid administration may thus not only help in detecting patients in need of fluids but may also prevent unnecessary and harmful fluid overload. Unfortunately, commonly used hemodynamic parameters, including the cardiac output itself, are poor predictors of fluid responsiveness, which is best assessed by functional hemodynamic parameters. These dynamic parameters reflect the response of cardiac output to a preload-modifying maneuver (for example, a mechanical breath or passive leg-raising), thus providing information about fluid responsiveness without the actual administration of fluids. All dynamic parameters, which include the respiratory variations in systolic blood pressure, pulse pressure, stroke volume and plethysmographic waveform, have been repeatedly shown to be superior to commonly used static preload parameters in predicting the response to fluid loading. Within their respective limitations, functional hemodynamic parameters should be used to guide fluid therapy as part of or independently of goal-directed therapy strategies in the perioperative period.     

What every Intensivist should know about COVID-19 associated acute kidney injury

Acute kidney injury (AKI) is a serious complication in critically ill patients with COVID-19 with a reported incidence ranging from <5% to >25%. Proposed aetiologies include hypovolemia, hemodynamic disturbance and inflammation but also specific factors like direct viral invasion, microvascular thrombosis, and altered regulation of the renin-angiotensin-aldosterone system. To date, there are no confirmed specific therapies, and prevention and management of AKI should follow established guidelines. Novel therapies specifically targeting COVID-19 related pathologies are under investigation. The incidence of renal replacement therapy (RRT) is variable, ranging from 0-37%. In a pandemic, RRT practice is likely to be determined by the number of patients, availability of machines, consumables and staff, clinical expertise, and acceptable alternatives. Close collaboration between critical care and renal services is essential.In this article, we describe the epidemiology and pathophysiology of COVID-19 associated AKI, outline current management and suggest strategies to provide RRT during a pandemic when resources may be scarce.     

ICU急性肾损害患者血清肝细胞生长因子浓度变化及临床意义

目的 探讨血清肝细胞生长因子(HGF)在急性肾损害(AKI)发展过程中的浓度变化及临床意义.方法 检测62例AKI患者血清HGF浓度(每2天1次),分析其与评估肾小球滤过率(eGFR)、肾功能衰竭指数、病程、脏器损伤数目及近期预后间的关系.结果 一定时间内血清HGF浓度随病程延长、脏器损害数目增多而进行性升高(P=0.000),第9天达峰值,而后下降;死亡组较肾功能未恢复组升高,后者较肾功能恢复组升高(均P<0.05);合并肝损害者各时间点均明显高于不伴肝损害者(均P<0.05).HGF浓度与肾功能衰竭指数正相关(r=0.580～0.821,均P<0.05),与eGFR负相关(r=-0.943～-0.703,均P<0.05).结论 AKI患者血清HGF浓度异常升高,其升高的程度反映AKI病情和近期预后.     

NGAL和KIM-1在重症监护室危重患者早期急性肾损伤中的诊断价值

目的探讨尿液、血清中性粒细胞明胶酶转运蛋白(NGAL)和尿肾损伤分子-1(KIM-1)在重症监护室(ICU)危重症患者急性肾损伤(AKI)中的早期诊断价值。方法选取2010年6月至2011年5月本院以各种原发病于ICU病房治疗,且继发AKI的危重症患者23例,同期于ICU治疗的非AKI患者24例和健康者21例,用定量酶联免疫吸附试验(ELISA)检测尿液、血清NGAL和尿KIM-1水平,用常规生化方法检测血清尿素氮(BUN)、肌酐(Cr),用乳胶增强免疫比浊法检测血清胱抑素C(Cys C)。健康对照组、AKI患者入院时,AKI患者组、ICU非AKI患者组组间比较采用两独立样本t检验;应用受试者操作特征曲线(ROC曲线)评价各指标对AKI的诊断价值。结果 AKI患者组血清NGAL、尿NGAL、尿KIM-1、BUN、Cr和Cys C水平显著高于健康对照组,差异有统计学意义(P<0.01);AKI患者组与其入院时各研究指标比较,血清NGAL、尿NGAL、尿KIM-1、BUN和Cr水平差异有统计学意义(P<0.01);AKI患者组与非AKI患者组间血清NGAL、尿NGAL、尿KIM-1和Cr水平差异有统计学意义(P<0.01);血清NGAL、尿液NGAL、尿液KIM-1、Cr、Cys C、BUN的ROC曲线下面积依次为1.00、0.97、1.00、0.98、0.98、0.99。结论 AKI患者组与其他各研究组间血清NGAL、尿NGAL、尿KIM-1水平差异有统计学意义,血清NGAL、尿NGAL、尿KIM-1作为新的肾损伤标志物,对AKI具有早期诊断价值。     

Transfusion-related acute lung injury and the ICU

Transfusion-related acute lung injury (TRALI) has been the leading cause of transfusion-related deaths reported to the United States Food and Drug Administration for three consecutive years. Although traditionally TRALI has been viewed as having a one event pathogenesis (passive donor anti-leukocyte antibody interacting with a cognate antigen on the recipients leukocytes), emerging evidence suggests that TRALI is a multifactorial syndrome, and a true two-event subtype of ALI. Both recipient predisposition and biological response modifiers, generated during storage of cellular blood products, appear to play major pathogenetic roles. This review highlights recent advances in our knowledge of the pathophysiology of TRALI and recent progress towards a consensus definition of TRALI. It also guides the reader as to the recognition, investigation, and clinical management of TRALI.