Viswanathan Gautham, Gilbert Scott
Division of Nephrology, Tufts Medical Center, 800 Washington Street, P.O. 391, Boston, MA 02111, USA.
Int J Nephrol. 2010 Oct 4;2011:283137. doi: 10.4061/2011/283137.
The heart and the kidneys share responsibility for maintaining hemodynamic stability and end-organ perfusion. Connections between these organs ensure that subtle physiologic changes in one system are tempered by compensation in the other through a variety of pathways and mediators. In the setting of underlying heart disease or chronic kidney disease, the capacity of each organ to respond to perturbation caused by the other may become compromised. This has recently led to the characterization of the cardiorenal syndrome (CRS). This review will primarily focus on CRS type 1 where acute decompensated heart failure (ADHF) results in activation of hemodynamic and neurohormonal factors leading to an acute drop in the glomerular filtration rate and the development of acute kidney injury. We will examine the scope and impact of this problem, the pathophysiology associated with this relationship, including underperfuson and venous congestion, diagnostic tools for earlier detection, and therapeutic interventions to prevent and treat this complication.
心脏和肾脏共同负责维持血流动力学稳定和终末器官灌注。这些器官之间的联系确保一个系统中细微的生理变化会通过各种途径和介质在另一个系统中得到代偿调节。在存在基础心脏病或慢性肾脏病的情况下，每个器官对另一个器官引起的扰动的反应能力可能会受到损害。这最近导致了心肾综合征（CRS）的特征描述。本综述将主要关注1型CRS，即急性失代偿性心力衰竭（ADHF）导致血流动力学和神经激素因子激活，进而导致肾小球滤过率急性下降和急性肾损伤的发生。我们将研究这个问题的范围和影响、与这种关系相关的病理生理学，包括灌注不足和静脉淤血、早期检测的诊断工具，以及预防和治疗这种并发症的治疗干预措施。
