急性心肌梗死患者家庭功能及社会支持与急性应激状态的相关性

<正>急性应激反应(acute stress response,ASR)是描述个体在亲历、目击具有死亡威胁和严重伤害的创伤事件后的2天至4周内所表现的应激反应~[1]。急性心肌梗死(acute myocardial infarction,AMI)的患者急性期有不同程度的精神应激反应,严重者可发展为急性应激障碍(acute stress disorder,ASD),严重影响疾病的康复和预后~[1]。目前国内关于临床急性心肌梗死患者的ASR研究鲜为报道。本研究旨在了解急性心肌梗死患者的急性应激及相关因     

急性胰腺炎发病机制及相关治疗的研究进展

<正>急性胰腺炎(acute pancreatitis,AP)是多种病因引起胰酶激活,以胰腺局部炎症反应为主要特征,伴或不伴有其它器官功能改变的疾病,是临床上常见的急腹症。重者起病急骤、病情危重,称为重症急性胰腺炎(severe acute pancreatitis,SAP)。AP的发病     

急性冠脉综合征患者血清IL-8、hs-CRP及ox-LDL的变化

<正>急性冠状动脉综合征(acute coronary syndrome,ACS)是一组由急性心肌缺血引起的临床综合征,包括急性心肌梗死(acute myocardial infarction,AMI)及不稳定型心绞痛(unstable angina pectoris,UAP),冠状动脉内斑块的破裂而导致血栓形成是ACS的主要原因[1]。其早期的诊断及对疾病的严重程度的了解对于临床有效的治疗起着积极的作用。本实验通过     

LDH及sTfR在成人急性溶血性贫血中的意义

目的 探讨血清乳酸脱氢酶(lactic dehydrogenase,LDH)及可溶性血清转铁蛋白受体(soluable transferritin receptor,sTfR)在无慢性贫血史成人急性溶血性贫血(acute hemolutic anemia,AHA)诊断中的意义.方法 无慢性溶血性疾病史的32例成人急性溶贫患者采用酶标比色法测定血清LDH水平,ELISA方法检测血清sTfR水平并与正常体检者进行比较分析.结果 急性溶贫患者血清sTfR水平为49.3±13.1 nmol/L,对照组为15.5 ±2.1 nmol/L,两组比较有统计学差异(P＜0.05);急性溶贫患者血清LDH水平为531.1 ±111.2 IU/L,对照组为105.5 ±42.1 IU/L,两组比较有统计学差异(P＜0.05);不同程度AHA患者血清LDH及sTfR不同.结论 血清LDH、sTfR活性可作为无慢性溶血性疾病成人AHA诊断筛选.     

凝血和纤溶失衡在急性肺损伤中的作用

急性肺损伤(acute lung injury,ALI),以肺泡上皮细胞和血管内皮屏障损伤、急性炎症反应、富含蛋白的肺水肿为特征,是一种临床常见的危重病症,可进一步发展为急性呼吸窘迫综合症(acute respiratory distress syndrome,ARDS).     

运用组织学知识提高急性放射病教学效果

急性放射病（acute radiation sickness,ARS）是核武器爆炸以及核事故中因受到放射性核素过量外照射而引起的一种急性全身性疾病。在防原医学知识体系中,     

SARS患者机械通气的管理

SARS(Server acute respiratory syndrome),是2002年底在全世界范围内流行的一种以肺炎为主要表现的突发的、传染性较强的疾病,世界卫生组织(W H O)将其命名为“严重急性呼吸综合征”,我国将这种疾病将之为“传染性非典型肺炎”。它的主要传播途径是距离飞沫传播或密切接触传播     

免疫炎症反应在对比剂急性肾损伤发病机制中的作用

对比剂急性肾损伤(contrast-induced acute kidney injury,CI-AKI)是医院获得性急性肾损伤的常见原因之一。对CIAKI发病机制的研究发现,免疫炎性细胞与介质可通过不同机制调控其功能和细胞因子的表达,在CI-AKI的发生和发展中起重要作用。深入研究肾脏固有细胞与免疫细胞及其因子在CI-AKI疾病中的作用机制将有助于发现新的临床防治靶点,为治疗CI-AKI提供新的理论依据。     

急性呼吸窘迫综合征的药物治疗

急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)的防治是多途径、综合性的救治过程.目前尚无治疗急性肺损伤(acute lung injury,ALI)/ARDS的特效药物,对其有缓解作用的药物主要针对其的急性渗出期、炎症反应或氧化损伤以及纤维增生期.联合多种药理因素...     

南方汉族KIR-HLA系统分子遗传多态性与急性白血病的相关性

目的:探讨中国南方汉族人群KIR-HLA系统分子遗传多态性与急性淋巴细胞白血病(acute lymphoblastic leukemia, ALL)、急性髓系白血病(acute myelocytic leukemia, AML)的相关性。方法:对323份成年ALL、350份成年AML患者以及745份随机健康对照的样本,...     

Biomarkers in acute kidney injury – pathophysiological basis and clinical performance

Various biomarkers of acute kidney injury (AKI) have been discovered and characterized in the recent past. These molecules can be detected in urine or blood and signify structural damage to the kidney. Clinically, they are proposed as adjunct diagnostics to serum creatinine and urinary output to improve the early detection, differential diagnosis and prognostic assessment of AKI. The most obvious requirements for a biomarker include its reflection of the underlying pathophysiology of the disease. Hence, a biomarker of AKI should derive from the injured kidney and reflect a molecular process intimately connected with tissue injury. Here, we provide an overview of the basic pathophysiology, the cellular sources and the clinical performance of the most important currently proposed biomarkers of AKI: neutrophil gelatinase‐associated lipocalin (NGAL), kidney injury molecule‐1 (KIM‐1), liver‐type fatty acid‐binding protein (L‐FABP), interleukin‐18 (IL‐18), insulin‐like growth factor‐binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinase 2 (TIMP‐2) and calprotectin (S100A8/9). We also acknowledge each biomarker's advantages and disadvantages as well as important knowledge gaps and perspectives for future studies.     

单核巨噬细胞介导急性肾损伤发病的研究进展

急性肾损伤 (Acute Kidney Injury,AKI) 和慢性肾脏病 (Chronic Kidney Disease,CKD) 是最常见的肾损伤形式,已成为新的“公共健康问题”。高效识别肾脏高危易损者是目前临床精准监测、精准防治的迫切需要。肾损伤后的信号分子,特别是肾小管上皮细胞损伤后表达的小分子蛋白,能释放至尿液中,尿中水平与肾损伤程度密切相关,是新的肾损伤指标。本文围绕主要的尿液肾损伤生物标志物,介绍它们从基础发现到临床验证,再到临床应用的全过程,最后初步探讨尿液肾损伤标志物研究的未来方向。     

Identification of phosphorylated MYL12B as a potential plasma biomarker for septic acute kidney injury using a quantitative proteomic approach

Acute kidney injury (AKI) is a common and increasingly encountered complication in hospitalized patients with critical illness in intensive care units (ICU). According to the etiology, Sepsis-induced AKI (SAKI) is a leading contributor to AKI and significantly has very poor prognosis, which might be related to the late detection when the elevation of BUN and serum creatinine (SCr) is used. Many genes are up-regulated in the damaged kidney with the corresponding protein products appearing in plasma and urine. Some of these are candidate biomarkers for more timely diagnosis of SAKI. Therefore, extensive research efforts over this past decade have been directed at the discovery and validation of novel SAKI biomarkers to detect injury prior to changes in kidney function, a number of serum and urinary proteins, including NGAL, KIM-1, cystatin-C, IL-18, and L-FABP, have been identified for predicting SAKI before a rise in BUN and serum creatinine in several experimental and clinical trainings. Unfortunately, an ideal biomarker of SAKI with highly sensitivity and specificity has not been identified yet. Recent progresses in quantitative proteomics have offered opportunities to discover biomarkers for SAKI. In the present study, kidney tissue samples from SAKI mice were analyzed by two-dimensional differential gel electrophoresis (2D-DIGE), and 4 up-regulated proteins, which were actin (ACTB), myosin regulatory light chain 12B (MYL12B), myosin regulatory light polypeptide 9 (MYL9), and myosin regulatory light chain 12A (MYL12A) were identified by matrix assisted laser desorption ionization-time of flight/time of flight mass spectrometry (MALDI-TOF/TOF MS). Among all the varied proteins, MYL12B was validated by western blot. Interestingly, there was no change between the SAKI and control kidney tissues, however, phosphorylated MYL12B was detected to be consistent with the proteomics data. Furthermore, phosphorylated MYL12B was found similarly to be increased in SAKI plasma, while MYL12B was changeless in plasma of control group. Taking together, phosphorylated MYL12B may be employed as a potential plasma biomarker for the early diagnosis of SAKI.     

Fibrinogen excretion in the urine and immunoreactivity in the kidney serves as a translational biomarker for acute kidney injury

Fibrinogen (Fg) is significantly up-regulated in the kidney after acute kidney injury (AKI). We evaluated the performance of Fg as a biomarker for early detection of AKI. In rats and mice with kidney tubular damage induced by ischemia/reperfusion (I/R) or cisplatin administration, respectively; kidney tissue and urinary Fg increased significantly and correlated with histopathological injury, urinary kidney injury molecule-1 (KIM-1) and N-acetyl glucosaminidase (NAG) corresponding to the progression and regression of injury temporally. In a longitudinal follow-up of 31 patients who underwent surgical repair of abdominal aortic aneurysm, urinary Fg increased earlier than SCr in patients who developed postoperative AKI (AUC-ROC = 0.72). Furthermore, in a cohort of patients with biopsy-proven AKI (n = 53), Fg immunoreactivity in the tubules and interstitium increased remarkably and was able to distinguish patients with AKI from those without AKI (n = 59). These results suggest that immunoreactivity of Fg in the kidney, as well as urinary excretion of Fg, serves as a sensitive and early diagnostic translational biomarker for detection of AKI.     

Acute Kidney Injury in Children after Hematopoietic Cell Transplantation Is Associated with Elevated Urine CXCL10 and CXCL9

Acute kidney injury (AKI) is nearly universally associated with worse outcomes, especially among children after hematopoietic stem cell transplant (HCT). Our objective was to examine urinary immune biomarkers of AKI after HCT to provide insights into novel mechanisms of kidney injury in this population. Studying patients undergoing allogeneic HCT provides a unique opportunity to examine immune markers of AKI because the risk of AKI is high and the immune system newly develops after transplant. Children (>2 years old) and young adults undergoing their first allogeneic HCT and enrolled in a prospective, observational cohort study at 2 large children's hospitals had urine collected pre-HCT and monthly for the first 4 months after HCT. Urine samples at each monthly time point were assayed for 8 immune-related biomarkers. AKI was defined as a 1.5-fold increase in the monthly serum creatinine value, which was recorded ±1 day from when the research urine sample was obtained, as compared with the pre-HCT baseline. Generalized estimating equation regression analysis evaluated the association between the monthly repeated measures (urinary biomarkers and AKI). A total of 176 patients were included from 2 pediatric centers. Thirty-six patients from 1 center were analyzed as a discovery cohort and the remaining 140 patients from the second center were analyzed as a validation cohort. AKI rates were 18% to 35% depending on the monthly time point after HCT. Urine CXCL10 and CXCL9 concentrations were significantly higher among children who developed AKI compared with children who did not (P < .01) in both cohorts. In order to gain a better understanding of the cellular source for these biomarkers in the urine, we also analyzed in vitro expression of CXCL10 and CXCL9 in kidney cell lines after stimulation with interferon-γ and interferon-α. HEK293-epithelial kidney cells demonstrated interferon-induced expression of CXCL10 and CXCL9, suggesting a potential mechanism driving the key finding. CXCL10 and CXCL9 are associated with AKI after HCT and are therefore promising biomarkers to guide improved diagnostic and treatment strategies for AKI in this high-risk population.     

Acute Kidney Injury after Using Contrast during Cardiac Catheterization in Children with Heart Disease

Acute kidney injury (AKI) is closely associated with the mortality of hospitalized patients and long-term development of chronic kidney disease, especially in children. The purpose of our study was to assess the evidence of contrast-induced AKI after cardiac catheterization in children with heart disease and evaluate the clinical usefulness of candidate biomarkers in AKI. A total of 26 children undergoing cardiac catheterization due to various heart diseases were selected and urine and blood samples were taken at 0 hr, 6 hr, 24 hr, and 48 hr after cardiac catheterization. Until 48 hr after cardiac catheterization, there was no significant increase in serum creatinine level in all patients. Unlike urine kidney injury molecule-1, IL-18 and neutrophil gelatinase-associated lipocalin, urine liver-type fatty acid-binding protein (L-FABP) level showed biphasic pattern and the significant difference in the levels of urine L-FABP between 24 and 48 hr. We suggest that urine L-FABP can be one of the useful biomarkers to detect subclinical AKI developed by the contrast before cardiac surgery.

Graphical Abstract

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Tissue kim-1 and urinary clusterin as early indicators of Cisplatin-induced acute kidney injury in rats

The kidney is one of the main targets of drug toxicity, and early detection of renal damage is critical in preclinical drug development. A model of cisplatin-induced nephrotoxicity in male Sprague Dawley rats treated for 1, 3, 5, 7, or 14 days at 1 mg/kg/day was used to monitor the spatial and temporal expression of various indicators of kidney toxicity during the progression of acute kidney injury (AKI). As early as 1 day after cisplatin treatment, positive kidney injury molecule-1 (Kim-1) immunostaining, observed in the outer medulla of the kidney, and changes in urinary clusterin indicated the onset of proximal tubular injury in the absence of functional effects. After 3 days of treatment, Kim-1 protein levels in urine increased more than 20-fold concomitant with a positive clusterin immunostaining and an increase in urinary osteopontin. Tubular basophilia was also noted, while serum creatinine and blood urea nitrogen levels were elevated only after 5 days, together with tubular degeneration. In conclusion, tissue Kim-1 and urinary clusterin were the most sensitive biomarkers for detection of cisplatin-induced kidney damage. Thereafter, urinary Kim-1 and osteopontin, as well as clusterin immunostaining accurately correlated with the histopathological findings. When AKI is suspected in preclinical rat studies, Kim-1, clusterin, and osteopontin should be part of urinalysis and/or IHC can be performed.     

Incidence and Risk Factors for Acute and Chronic Kidney Injury after Adult Cord Blood Transplantation

Although cord blood transplantation (CBT) extends allograft access, patient comorbidities, chemoradiation, and nephrotoxic medications all contribute to acute kidney injury (AKI) risk. We analyzed AKI in adult myeloablative CBT recipients who underwent transplantation from 2006 to 2017 for hematologic malignancies using cyclosporine A (CSA)/mycophenolate mofetil immunosuppression. Maximum grades of AKI were calculated using Kidney Disease: Improving Global Outcomes (grade 1, 1.5 to <2-fold; grade 2, 2 to <3-fold; or grade 3, ≥3-fold over baseline) definitions. In total, 153 patients (median 51 years [range, 23-65], 114/153 [75%] acute leukemia, 27/153 [18%] African, 88/153 [58%] cytomegalovirus seropositive, median age-adjusted hematopoietic cell comorbidity index 3 [range, 0-9], median pretransplant albumin 4.0 g/dL [range, 2.6-5.2]) underwent transplantation. The day 100 cumulative incidence of grade 1-3 AKI was 83% (95% confidence interval [CI], 77%-89%) (predominantly grade 2, median onset 40 days, range 0 to 96), and grade 2-3 AKI incidence was 54% (95% CI, 46%-62%) (median onset 43 days, range 0 to 96). Mean CSA level preceding AKI onset was high (360 ng/mL, target range 300-350). In multivariate analysis, African ancestry, addition of haploidentical CD34⁺ cells, low day –7 albumin, critical illness/intensive care admission, and nephrotoxic drug exposure (predominantly CSA and/or foscarnet) were associated with AKI. In a day 100 landmark analysis, 6% of patients with no prior AKI had chronic kidney disease (CKD) at 2 years versus 43% with prior grade 1 and 38% with prior grade 2-3 AKI (overall P= .02). Adult CBT recipients are at significant AKI risk, and AKI is associated with increased risk of CKD. Prevention strategies, early recognition, and prompt intervention are critical to mitigate kidney injury.     

Noninvasive evaluation of renal pH homeostasis after ischemia reperfusion injury by CEST‐MRI

Acute kidney injury (AKI) in mice caused by sustained ischemia followed by reperfusion is associated with acute tubular necrosis and renal dysfunctional blood flow. Although the principal role of the kidney is the maintenance of acid–base balance, current imaging approaches are unable to assess this important parameter, and clinical biomarkers are not robust enough in evaluating the severity of kidney damage. Therefore, novel noninvasive imaging approaches are needed to assess the acid–base homeostasis in vivo. This study investigates the usefulness of MRI‐chemical exchange saturation transfer (CEST) pH imaging (through iopamidol injection) in characterizing moderate and severe AKI in mice following unilateral ischemia reperfusion injury. Moderate (20 min) and severe (40 min) ischemia were induced in Balb/C mice, which were imaged at several time points thereafter (Days 0, 1, 2, 7). A significant increase of renal pH values was observed as early as one day after the ischemia reperfusion damage for both moderate and severe ischemia. MRI‐CEST pH imaging distinguished the evolution of moderate from severe AKI. A recovery of normal renal pH values was observed for moderate AKI, whereas a persisting renal pH increase was observed for severe AKI on Day 7. Renal filtration fraction was significantly lower for clamped kidneys (0.54–0.57) in comparison to contralateral kidneys (0.84–0.86) following impairment of glomerular filtration. The severe AKI group showed a reduced filtration fraction even after 7 days (0.38 for the clamped kidneys). Notably, renal pH values were significantly correlated with the histopathological score. In conclusion, MRI‐CEST pH mapping is a valid tool for the noninvasive evaluation of both acid–base balance and renal filtration in patients with ischemia reperfusion injury.     

体外循环心脏手术后尿mAlb、β2-m和NAG、KIM-1与急性肾损伤的关系

目的:探讨体外循环心脏手术后尿微量白蛋白(mAlb)、β2-微球蛋白(β2-m)和N-乙酰-β-D-氨基葡萄糖苷酶(NAG)、肾损伤分子-1(KIM-1)与急性肾损伤(AKI)的关系.方法:根据AKI的诊断标准,将91例体外循环心脏手术患者分为AKI组和非AKI组,分别留取术前及术后不同时间点的血液和尿标本,测定尿mA...