2012年第1期中文目录

心肾综合征特指在心力衰竭的治疗过程中,由于患者的肾功能出现明显下降,而导致心力衰竭治疗效果欠佳.目前,其诊断尚无统一标准,有学者将诊断标准确定为,在急性心力衰竭时血清肌酐升高3.0～5.0 mg/dl或者肾小球滤过率下降15 ml/min以上.心肾综合征确切发病率仍不清楚,但有研究显示,其在心力衰竭患者中的发病率可达30％左右.心肾综合征的病理生理机制比较复杂,中心静脉淤血、神经内分泌激活、贫血、氧化应激和肾交感神经过度激活可能是导致心肾综合征的重要原因.心肾综合征的治疗仍是一个很大的难题.原则上首先应纠正心肾综合征的可逆性诱因;其次,需要确定患者肾灌注状态,保证收缩压在80mmHg以上,平均压在60mmHg以上,对于低心排血量患者,可尝试使用硝酸酯类药物,降低心脏前后负荷;此外,还需及时停用影响肾功能的药物.具体讲,利尿剂、血管紧张素转换酶抑制剂/血管紧张素Ⅱ受体拮抗剂、血液滤过、重组人B型利钠肽和加压素拮抗剂均可考虑应用.本文就心肾综合征的上述相关问题做一综述.     

肾功能不全并发心力衰竭的诊治策略

肾功能衰竭和心力衰竭常并存,可以互为因果,临床上称此状态为心肾综合征。心肾综合征共分五类,其中3型和4型心肾综合征分别由急性和慢性肾功能不全导致的心力衰竭。我院对一组心力衰竭患者的回顾性分析表明,肾功能不     

心肾综合征的最新进展

心脏和肾脏之间的关系越来越得到医学界的广泛关注,心力衰竭与肾功能衰竭常常合并存在并相互影响,互为因果,这两者共存的情况称为心肾综合征.心肾综合征的病理生理学机制极为复杂,迄今尚未阐明.当心力衰竭与肾功能衰竭两者并存时,不仅处理困难,而且预后亦差.现着重对于心肾综合征的最新研究进展、治疗策略方面进行讨论.     

心肾综合征的研究进展

心肾综合征（CRS）广泛定义为心肾的病理生理紊乱。心脏和肾脏中一个器官的慢性或急性功能不全可能诱发另一个器官的慢性或急性功能不全,急性（或慢性）心脏或肾脏功能不全相互影响、相互加重,导致心肾功能急剧恶化。     

心肾综合征炎症机制的研究进展

心肾综合征（cardiorenalsyndrome，CRS）是近年就心肾联合损害提出的新诊断，是临床上一种常见的疾病组合，病程进展快，预后凶险。2007年，Ronco等^[1]提出了心。肾综合征的定义，即心肾功能在病理生理上的紊乱，其中一个器官的急性，慢性病变导致另一器官的急性／慢性病变。流行病学数据显示，30％的慢性心力衰竭（chronicheartfailure，     

高龄老年心肾综合征患者按心功能分级治疗：50例报道

心肾综合征（cardiorenal syndrome,CRS）最早由Ledoux于1951年提出,当时仅指心功能不全时引起肾功能不全。2004年美国国立卫生研究院国立心肺和血液研究所召开专家会议,将CRS定义为慢性心力衰竭引起进行性肾功能损害、利尿剂抵抗、心脏容量负荷过重而使心力衰竭治疗受限等情况[1]。随着对心肾功能相互作用认识的加深,Ronco等[2,3]于2008年提出了目前被大多数人认可的CRS定义,即心肾功能在病理生理上的紊乱,其中一个器官的急／慢性病变可以导致另一器官的急／慢性病变,强调了心／肾双向作用。根据心肾疾病发病的急慢和先后,将CRS分为5个亚型：I型CRS（急性CRS）,主要是急性心功能障碍导致急性肾损伤;     

心肾综合征治疗分析

近年来慢性心力衰竭病人出现肾功能不全即心肾综合征的问题，逐渐引起人们的注意。广义的心肾综合征是指心脏和肾脏中的一个器官对另一个器官的共同损害。狭义的心肾综合征是特指慢性心力衰竭引起的进行性肾脏损害，并导致肾功能不全，通常认为是慢性心力衰竭的终末期的一种表现。近年来，随着老年化社会的逐步形成和人民生活水平的提高，慢性心血管病（如高血压、冠心病）和代谢紊乱性疾病（如糖尿病、高脂血症、高尿酸血症）的发病率明显升高，内外科治疗的进展使许多心血管疾病病人在疾病的急性期得到了有效的治疗，病情发展到终末期的病人也明显增加，并常存在肾功能不全，出现心肾综合征，预后差。现将湖北省当阳市长坂坡医院2001年-2005年收治的40例心肾综合征病人分析报道如下。     

沙库巴曲缬沙坦用于Ⅱ型心肾综合征治疗的研究进展

心肾综合征共分为5型,以Ⅱ型心肾综合征最为常见。沙库巴曲缬沙坦属于钠盐复合物,由沙库巴曲和缬沙坦以1:1的比例构成,是一种血管紧张素受体脑啡肽酶抑制剂（angiotensin receptor enkephalinase inhibitor,ARNI）,其可同时抑制肾素-血管紧张素-醛固酮系统（renin-angiotensin-aldosterone system,RAAS）和脑啡肽酶（enkephalinase,NEP）,延缓脑啡肽的降解,脑啡肽中的利钠肽在心力衰竭中具有重要作用。因此,通过抑制脑啡肽降解提高体内利钠肽浓度,可能成为治疗Ⅱ型心肾综合征的新靶点。本文着重介绍ARNI用于Ⅱ型心肾综合征治疗的最新进展,以期为广大临床医生提供参考。     

心肾综合征的研究进展

心力衰竭和慢性肾衰竭的发病率日益上升,这两种疾病的相伴出现即“心肾综合征”。“心肾综合征”会加重单个器官的衰竭程度,预后极差。新近的研究把肾素-血管紧张素系统活性增加、氧化应激反应、炎症、交感神经活性增高认为是心肾综合征的病理生理学基础,其中任何一个发生紊乱都会导致心肾综合征恶性循环的发生。     

II型心肾综合征患者肾功能损害及预后影响因素

目的:慢性心力衰竭（Chronic heart failure, CHF）合并肾功能不全（RI）即II型心肾综合征（type II cardiorenal syndrome, type II CRS）时其死亡率及再入院率均升高明显。本研究探讨II型CRS患者肾功能损害及预后影响因素。方法: 收集并整理2010年3月至2015年3月就诊于南京市胸科医院的II型CRS患者共95例,根据改良MDRD公式计算肾小球滤过率估计值（estimated glomerular filtration rate,eGFR）并将患者分为轻度RI组（60 ml /min?1.73m2≤eGFR＜90 ml/min?1.73m2）以及中重度RI组（eGFR＜60 ml/min?1.73m2）两组。分别记录两组患者的一般临床资料、实验室检查资料以及超声心动图参数,随访观察5年。结果:II型CRS中重度RI组的年龄、肌酐、尿酸、NT-proBNP高于轻度RI组,差异具有统计学意义（P值均＜0.05）,而高密度脂蛋白胆固醇（High density lipoprotein- cholesterol, HDL-C）水平显著低于对照组,差异具有统计学意义（P值＜0.05）。多因素Logistic回归分析显示年龄（OR=1.071）与HDL-C水平（OR=0.161）与eGFR独立相关（P＜0.05）。II型CRS中重度RI组生存率显著低于轻度RI组;校正eGFR水平后Logistic回归分析显示HDL-C浓度（OR=0.027）与II型CRS患者预后显著相关（P＜0.05）。结论:II型心肾综合征患者年龄越大,NT-proBNP、肌酐、尿酸水平越高,HDL-C水平越低,提示肾功能损害程度越重;HDL-C水平不仅与II型CRS患者肾功能独立相关,也是评估肾损严重程度及临床预后的重要指标。     

Síndrome cardiorrenal na insuficiência cardíaca aguda: um círculo vicioso?

Introduction and ObjectiveWorsening renal function has an unquestionably negative impact on prognosis in patients with acute heart failure (HF). In Portugal there is little information about the importance of this entity in HF patients admitted to hospital. The objective of this work was to assess the prevalence of cardiorenal syndrome and to identify its key predictors and consequences in patients admitted for acute HF.MethodsThis was a retrospective study of 155 patients admitted for acute HF. Cardiorenal syndrome was defined as an increase in serum creatinine of ≥26.5 μmol/l. Clinical, laboratory and echocardiographic parameters were analyzed and compared. Mortality was assessed at 30 and 90 days.ResultsCardiorenal syndrome occurred in 46 patients (29.7%), 5.4±4.4 days after admission; 66.7% (n=24) did not recover baseline creatinine levels. The factors associated with cardiorenal syndrome were older age, chronic renal failure, moderate to severe mitral regurgitation, higher admission blood urea nitrogen, creatinine and troponin I, and lower glomerular filtration rate. Patients who developed cardiorenal syndrome had longer hospital stay, were treated with higher daily doses of intravenous furosemide, and more often required inotropic support and renal replacement therapy. They had higher in‐hospital and 30‐day mortality, and multivariate analysis identified cardiorenal syndrome as an independent predictor of in‐hospital mortality.ConclusionsRenal dysfunction is common in acute HF patients, with a negative impact on prognosis, which highlights the importance of preventing kidney damage through the use of new therapeutic strategies and identification of novel biomarkers.     

Managing acute renal failure in patients with acute decompensated heart failure: The cardiorenal syndrome

In patients with acute decompensated heart failure, worsening renal function during conventional decongestive therapy (cardiorenal syndrome) affects prognosis and the initiation of therapies with known benefit in chronic heart failure. Potential strategies for decongestion in patients who develop cardiorenal syndrome include invasive hemodynamic monitoring to guide therapy, use of continuous diuretic infusions, ultrafiltration, or novel therapy with adenosine or vasopressin receptor antagonists. Clinical trials by the National Heart, Lung, and Blood Institute’s Heart Failure Network are currently underway to validate such therapies in patients with acute decompensated heart failure with worsening renal function and to establish novel biomarkers for the early identification of patients who develop cardiorenal syndrome.     

The Cardiorenal Syndrome: Lessons from the ADHERE Database and Treatment Options

Significant renal dysfunction is common in patients hospitalized for heart failure and carries a grim prognosis. Patients with heart failure who have or develop renal dysfunction while being treated for heart failure are said to have the cardiorenal syndrome. The Acute Decompensated Heart Failure National Registry (ADHERE®) database, which enrolled nonselected patients admitted to the hospital for acute decompensated heart failure (ADHF), was used to determine the causes for this renal dysfunction and whether treatment can optimize outcomes. Results show that the average patient admitted for ADHF is older than those typically enrolled in clinical trials and has at least moderate kidney damage, with significantly impaired glomerular filtration rates. Renal dysfunction in patients with heart failure is complex and often multifactorial in origin, but the syndrome may be reversible in some patients. Reduction of angiotensin II levels with angiotensin-converting enzyme (ACE) inhibitors may prevent glomerular hyperfiltration and ultimately preserve renal function; however, patients who are volume-depleted may be especially sensitive to ACE inhibitor–induced efferent arteriolar dilation, so ACE inhibitor therapy in patients with renal dysfunction should be initiated when the patient is volume replete. In conclusion, impaired renal function is common in heart failure patients and may be a key cause of the cascade involving fluid retention, decompensation, and eventual hospital admission. Future pharmacologic research should focus on therapies aimed at maintaining or improving renal function in heart failure patients to reduce the high mortality associated with the cardiorenal syndrome.Supported by an unrestricted educational grant from Scios Inc.     

Epidemiology of cardiorenal syndrome

The interdependence of cardiac and renal dysfunction has emerged as a focus of intense interest in heart failure management due to the substantial associated morbidity and mortality. Captured in the clinical entity known as cardiorenal syndrome, recent definitions afford discussion of the acute and longitudinal evaluation and management of these patients. This article discusses potential pathophysiologic mechanisms of cardiorenal syndrome, epidemiology, inpatient and long-term care (including investigational therapies and mechanical fluid removal), and end-of-life and palliative care.     

2型心肾综合征患者血清CysC及血浆Hcy水平变化及意义

目的探讨胱抑素C(CysC)、同型半胱氨酸(Hcy)在2型心肾综合征患者体内水平变化及意义。方法回顾性分析2018年6-12月在我院就诊的心力衰竭患者,根据是否合并肾功能异常分为单纯心力衰竭组(50例)及心肾综合征组(50例),本研究肾功能异常定义为肾小球滤过率(GFR)<60mL/min,另选取30例在我院健康体检正常的人群作为健康对照组。观察不同组别,不同心功能患者的CysC、Hcy、左室射血分数(LVEF)等指标的水平变化。结果心肾综合征组及单纯心力衰竭组患者血清CysC、血浆Hcy水平高于健康对照组(P<0.05);心肾综合征组患者血清CysC、血浆Hcy水平高于单纯心力衰竭组的患者(P<0.05);心肾综合征患者随着心功能分级的增高,血清CysC及血浆Hcy水平逐渐升高(P<0.05);心肾综合征患者血清CysC及血浆Hcy水平变化与LVEF水平变化呈负相关(P<0.05);ROC曲线表明CysC及Hcy对诊断心肾综合征有意义(AUC分别为0.610、0.707,95%CI分别为0.500~0.652、0.596~0.812,P=0.001)。结论血清CysC及血浆Hcy水平有助于2型心肾综合征诊断,且在一定程度上能够反映疾病的严重程度。     

The nephrologist and the role of ultrasound imaging in the diagnosis of cardiorenal syndrome

The term cardiorenal syndrome (CRS) refers to multiple possible clinicopathological correlations between heart and kidney failure. The most recent classification recognizes five types of CRS: types I and II originate from heart failure (acute and chronic, respectively), type III and IV from kidney failure (again acute and chronic), while type V originates from a range of systemic diseases. Echocardiography and renal ultrasound are important means to arrive at a correct diagnosis. Basic echocardiography (defined by some as "echocardioscopy") allows the assessment of the left and right ventricles (diastolic and systolic function), atrial size, pulmonary circulation markers such as systolic pulmonary arterial pressure (PAPs) and tricuspid annular plane excursion (TAPSE), pericardial effusions, valve dysfunctions, and volume repletion. Renal ultrasound is of help in distinguishing between chronic and acute renal failure (kidney volume, parenchymal thickness, echogenicity) and excluding obstructive kidney disease.     

The severe cardiorenal syndrome: 'Guyton revisited'.

The incidence of cardiac failure and chronic renal failure is increasing and it has now become clear that the co-existence of the two problems has an extremely bad prognosis. We propose the severe cardiorenal syndrome (SCRS), a pathophysiological condition in which combined cardiac and renal dysfunction amplifies progression of failure of the individual organ, so that cardiovascular morbidity and mortality in this patient group is at least an order of magnitude higher than in the general population. Guyton has provided an excellent framework describing the physiological relationships between cardiac output, extracellular fluid volume control, and blood pressure. While this model is also sufficient to understand systemic haemodynamics in combined cardiac and renal failure, not all aspects of the observed accelerated atherosclerosis, structural myocardial changes, and further decline of renal function can be explained. Since increased activity of the renin-angiotensin system, oxidative stress, inflammation, and increased activity of the sympathetic nervous system seem to be cornerstones of the pathophysiology in combined chronic renal disease and heart failure, we have explored the potential interactions between these cardiorenal connectors. As such, the cardiorenal connection is an interactive network with positive feedback loops, which, in our view, forms the basis for the SCRS.     

The Acute Cardiorenal Syndrome Type I: Considerations on Physiology,Epidemiology, and Therapy

Acute cardiorenal syndrome, also known as cardiorenal syndrome type 1, is defined as an abrupt worsening of cardiac function that occurs in at least 30 % of patients with acute decompensated heart failure and can lead to the development of acute kidney injury. The changes in renal function that occur in this setting have variable prognostic implications, as both poorer and better outcomes have been reported when renal function worsens during treatment of heart failure decompensation. Furthermore, it remains unclear when worsening renal function is actually a manifestation of true acute kidney injury or simply an indicator of hemoconcentration. Given these gaps in the understanding of the significance of renal function changes in the setting of decompensated heart failure, it is not surprising that studies on the effects of available therapies, including diuretics, vasoactive drugs, and mechanical fluid removal have yielded inconsistent results. The purpose of this review is to analyze critically the current knowledge on the pathophysiology, epidemiology, prognosis, and treatment of acute cardiorenal syndrome.