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     

心肾综合征的临床研究进展

心肾综合征一词已广泛用于进行性充血性心力衰竭引起的肾功能下降。为了概括心脏与肾脏之间复杂的因果关系,心肾综合征分为5种临床亚型:Ⅰ型:急性心肾综合征;Ⅱ型:慢性心肾综合征;Ⅲ型:急性肾心综合征;Ⅳ型:慢性肾心综合征;Ⅴ型:继发性心肾综合征。心肾综合征是慢性肾功能不全和慢性心力衰竭中治疗的难题,现就心肾综合征近年来临床研究进展进行综述。     

心肾综合征的中西医机制研究进展

心力衰竭(心衰)和肾功能不全是临床上常见的综合征.据报道[1],在因急性心力衰竭入院的患者中,19％～45％的患者出现了肾功能恶化.心力衰竭(heart failure HF)患者出现肾功能不全或使原有的肾功能不全进行性加重,即心肾综合征( cardiorenal syndrome,CRS).近年来,CRS日益引起临床医生的关注.依据其临床表现,中医多将CRS归属于水气病、心悸、喘促、胸痹、痰饮、水肿等范畴.心脏与肾脏相互影响、互相作用导致恶性循环,进一步加速了多器官的功能衰竭,使病死率增加.目前对于CRS的认识还十分有限,是临床处理的棘手问题.本文将分别从中、西医角度对心肾综合征相关机制予以阐述.     

慢性肾功能衰竭患者心律失常分析

慢性肾功能衰竭是指各种慢性肾脏疾病进行性发展，引起肾单位和肾功能不可逆地丧失，导致代谢产物和有毒物潴留、水电解质和酸碱平衡紊乱等表现的综合征，心律失常与心力衰竭为其常见死亡原因之一。本文对167例慢性肾功能衰竭患者的心律失常进行动态心电图观察，分析两者的关系。     

心-肾贫血综合征的研究进展

慢性肾功能不全的患者常有贫血、心力衰竭,贫血使心力衰竭加重,又使肾功能恶化,心力衰竭控制不好又使肾功能恶化、贫血加重,这三种状态构成心-肾贫血综合征.积极使用促红细胞生成素,纠正贫血,合理使用洋地黄制剂、降压药,适当使用碳酸氢盐透析、超滤纠正心力衰竭、肾衰竭,为临床处理心-肾贫血综合征提供了思路.     

心肾综合征临床防治进展

心肾综合征是指心力衰竭（CHF）患者出现的进行性肾功能损害，并导致肾功能不全，是一种同时伴有心肾功能异常的渐进的、严重的病理生理状态，加速单个器官的衰竭。通常认为是CHF发展到终末期的一种表现。现对其临床防治综述如下。     

肾脏和心血管系统相互影响的病理生理基础

近年来，对于慢性心力衰竭（CHF）患者治疗过程中的肾功能改变和慢性肾脏疾病（CKD）的心血管并发症认识的深入，促使人们重新评价心廊管和肾脏这两大系统的相互影响。心肾系统中某一部分的衰竭使得另一部分衰竭的治疗难度显著增加，据此提出了“心肾综合征”（cardiorenal syndrome）的概念。     

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.     

心肾综合征的研究现状

广义的心肾综合征是指心脏和肾脏中一个器官对另一个器官的功能损害不能进行代偿时,形成恶性循环,最终导致心脏和肾脏功能的共同损害.狭义的心肾综合征是特指慢性心力衰竭(CHF)患者出现的进行性肾功能损害,并导致肾功能不全.肾功能不全在CHF患者中的发生率很高,且是一个独立预后指标,其预测意义至少与左心室射血分数(LVEF)和纽约心脏病学会(NYHA)心功能分级相等.目前心肾综合征仍是临床治疗的难题.本文综述了心肾综合征的临床特点、发生机制以及防治等研究现状.     

对中国急性心力衰竭指南的几点不同意见

中华心血管病杂志2010年第3期发表了我国急性心力衰竭诊断和治疗指南[1],将心力衰竭分为急性左心衰竭、急性右心衰竭和急性非心原性心力衰竭三类,将心肾综合征和严重肺动脉高压、急性肺栓塞均归于非心原性,我个人认为有些不妥.     

Changes in Renal Function in Congestive Heart Failure

Both cardiovascular and renal diseases are common and frequently coexist in the same patient. Indeed, renal dysfunction has been shown to be a more powerful independent predictor of poor outcomes in heart failure (HF) than left ventricular ejection fraction or functional class. Furthermore, acute kidney injury is a frequent therapeutic concern in heart failure. Consequently, there has been much interest in developing new renoprotective treatments and novel biomarkers to monitor renal function. Additionally, given the crucial cardiorenal interaction and interdependence, the concept of a cardiorenal syndrome with five different subtypes has been advanced to better categorize patients and facilitate research.     

Animal models of cardiorenal syndrome: a review

The incidence of heart failure and renal failure is increasing and is associated with poor prognosis. Moreover, these conditions do often coexist and this coexistence results in worsened outcome. Various mechanisms have been proposed as an explanation of this interrelation, including changes in hemodynamics, endothelial dysfunction, inflammation, activation of renin-angiotensin-aldosterone system, and/or sympathetic nervous system. However, the exact mechanisms initializing and maintaining this interaction are still unknown. In many experimental studies on cardiac or renal dysfunction, the function of the other organ was either not addressed or the authors failed to show any decline in its function despite histological changes. There are few studies in which the dysfunction of both heart and kidney function has been described. In this review, we discuss animal models of combined cardiorenal dysfunction. We show that translation of the results from animal studies is limited, and there is a need for new and better models of the cardiorenal interaction to improve our understanding of this syndrome. Finally, we propose several requirements that a new animal model should meet to serve as a tool for studies on the cardiorenal syndrome.     

心肾综合征患者血B型钠尿肽和β2微球蛋白的意义

目的:观察晚期糖基化终产物(AGEs),B型钠尿肽(BNP)和血β2微球蛋白在心肾综合征中的意义。方法:选择2010年1月至2012年6月,我院内科就诊的心力衰竭患者291例,根据是否有肾功能异常,分为心肾综合征组(n=126)和单纯心力衰竭组(n=165),同时选择同期在我院做健康体检的自愿者30例为对照组。观察不同组别,不同肾功能和不同心功能患者的血清BNP、左心室射血分数(LVEF)、AGEs、β2微球蛋白和Scr水平的变化。结果:心肾综合征组和单纯心力衰竭组的BNP、LVEF、AGEs、β2微球蛋白和Scr水平较对照组明显增高(P0.01),而心肾功能组的增高水平明显高于单纯心力衰竭组(P0.01)。随着心功能分级的增高或肾功能恶化严重程度的增高,心肾综合征患者的BNP、LVEF、AGEs、β2微球蛋白和Scr水平出现逐渐升高(P0.01)。结论:BNP、AGEs、β2微球蛋白与心肾综合征的发病具有密切关性,并与疾病的严重程度具有相关性,参与了心肾综合征的病理生理过程。     

The cardiorenal connection in heart failure

Heart failure (HF) and renal dysfunction frequently coexist; this combination is commonly referred to as the “cardiorenal syndrome.” The intersection of cardiac and renal dysfunction has important therapeutic and prognostic implications in patients with HF. Approximately 60% to 80% of patients hospitalized for HF have at least stage III renal dysfunction; this comorbid renal insufficiency (RI) is associated with significantly increased morbidity and mortality risk. Comorbid RI can result from intrinsic renal disease and inadequate renal perfusion. HF and RI stimulate neurohormonal activation, increasing preload and afterload and reducing cardiac output. Inotropic agents augment this neurohormonal activation. Managing cardiorenal patients requires successful negotiation of the delicate balance between adequate volume reduction and adequate renal function. There is a compelling need for additional studies in this patient population.     

心肾综合征诊治进展

心肾综合征为心脏或肾脏中一个器官对另一个器官的功能损害,不能进行代偿,最终导致心脏和肾脏功能的共同损害。临床呈现心肾衰竭、肾功能恶化及利尿剂抵抗三者之一,或更多表现的进展性心肾功能调控障碍状态。发病机制尚未阐明,可能与肾内血流动力学障碍、神经介质紊乱等有关。失代偿性心力衰竭常规治疗未能奏效的容量超载患者应予超滤治疗。血管加压素受体拮抗剂及选择性腺苷A1受体拮抗剂等新制剂的相关临床试验正在进行中,近期有望在临床应用。     

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。     

Cardiorenal syndrome

The combination of decompensated heart failure and kidney failure is frequently referred to as the "cardiorenal syndrome." The cause and pathophysiology of this entity are complex and poorly understood, and treatment options are limited. This report describes 2 patients who were hospitalized for decompensated heart failure and developed diuretic resistance with rapidly worsening renal function. Understanding the underlying causes helped break the cardiorenal syndrome in the first patient but only had a transient beneficial effect in the second patient.     

Novel Renal Biomarkers to Assess Cardiorenal Syndrome

Renal dysfunction (RD) in heart failure portends adverse outcomes and often limits aggressive medical and decongestive therapies. Despite the high prevalence in this population, not all forms of RD are prognostically or mechanistically equivalent: RD can result from irreversible nephron loss secondary to diabetic or hypertensive kidney disease or it can develop secondary to heart failure (HF) itself, i.e., the cardiorenal syndrome. Furthermore, filtration is only one aspect of renal performance such that significant renal impairment secondary to cardiorenal syndrome can exist despite a normal glomerular filtration rate. Renal biomarkers have the potential to inform some of the intricacies involved in accurately assessing cardiorenal interactions. This article discusses novel biomarkers for cardiorenal syndrome and their utility in the prognosis, diagnosis, and targeted treatment of heart failure-induced RD.     

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.