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首页> 外文会议>Conference on Biomarkers in AKI (Acute Kidney Injury) >Pathophysiology of the Cardiorenal Syndromes: Executive Summary from the Eleventh Consensus Conference of the Acute Dialysis Quality Initiative (ADQI)
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Pathophysiology of the Cardiorenal Syndromes: Executive Summary from the Eleventh Consensus Conference of the Acute Dialysis Quality Initiative (ADQI)

机译：生物综合征的病理生理学：急性透析质量倡议的第十一协商会大会（ADQI）执行摘要

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摘要

Cardiorenal syndromes (CRS) have been recently classified into five distinct entities, each with different major pathophysiologic mechanisms. CRS type 1 most commonly occurs in the setting of acutely decompensated heart failure where approximately 25% of patients develop a rise in serum creatinine and a reduction of urine output after the first several doses of intravenous diuretics. Altered cardiac and renal hemodynamics are believed to be the most important determinants of CRS type 1. CRS type 2 is the hastened progression of chronic kidney disease (CKD) in the setting of chronic heart failure. Accelerated renal cell apoptosis and replacement fibrosis is considered to be the dominant mechanism. CRS type 3 is acutely decompensated heart failure after acute kidney injury from inflammatory, toxic, or ischemic insults. This syndrome is precipitated by salt and water overload, acute uremic myocyte dysfunction, and neurohormonal dysregulation. CRS type 4 is manifested by the acceleration of the progression of chronic heart failure in the setting of CKD. Cardiac myocyte dysfunction and fibrosis, so-called 'CKD cardiomyopathy', is believed to be the predominant pathophysiologic mechanism. Type 5 CRS is simultaneous acute cardiac and renal injury in the setting of an overwhelming systemic insult such as sepsis. In this scenario, the predominant pathophysiological disturbance is microcirculatory dysfunction as a result of acutely abnormal immune cell signaling, catecholamine cellular toxicity, and enzymatic activation which result in simultaneous organ injury often extending beyond both the heart and the kidneys. This paper will summarize these and other key findings from an international consensus conference on the spectrum of pathophysiologic mechanisms at work in the CRS.
机译：心肾综合征（CRS）最近被分为五个不同的实体，各有不同的主要病理生理机制。 CRS 1型最常发生在急性失代偿心脏衰竭，其中患者大约25％发展血清肌酸酐的上升和第一几个剂量静脉内利尿剂的后减少尿量的设置。改变心脏和肾脏的血流动力学被认为是CRS型的最重要的决定因素1. CRS 2型是慢性心脏衰竭的设置慢性肾脏病（CKD）的进展加速。加速肾脏细胞凋亡和更换纤维化被认为是主要的机制。 CRS 3型急性失代偿心脏衰竭的炎症，中毒，或缺血性损伤急性肾损伤后。这种综合征是由盐和水的过载，急性肌细胞尿毒症功能障碍，和神经激素失调沉淀。 CRS类型4由慢性心脏衰竭的CKD的设定进展的加速度表现。心肌细胞功能障碍和纤维化，所谓的“CKD心肌病”，被认为是主要的病理生理机制。 5型CRS是压倒性的系统性侮辱如败血症设置同时急性心脏和肾损伤。在这种情况下，主要的病理生理紊乱是微循环功能障碍如急性异常免疫细胞信号传导，儿茶酚胺的细胞毒性，和酶激活的结果，其导致同时器官损伤经常延伸超过心脏和肾脏两者。本文将总结这些和其他重要发现从上在CRS工作病理生理机制频谱的国际共识会议。

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