García-Carrasco Almudena, Izquierdo-Lahuerta Adriana, Medina-Gómez Gema
Área de Bioquímica y Biología Molecular, Departamento de Ciencias Básicas de la Salud, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Madrid, Spain.
Nephron. 2021;145(6):604-608. doi: 10.1159/000515419. Epub 2021 Apr 13.
There is a strong relationship between the kidney and the heart, where if one of these organs fails, so does the other, in the so-called cardiorenal syndrome (CRS). Besides, there are also interactions with the rest of the body leading to a metabolic state that establishes a feedback loop that is perpetuated. The CRS is characterized by hemodynamic changes, activation of neuro-humoral systems, natriuretic peptides, and changes in mineral metabolism. In this scenario, the kidney and heart, connected by a dysfunctional endothelium, inevitably fail. In obesity, this syndrome is exacerbated due to the complications of adipose tissue dysfunction, in the so-called cardiorenal metabolic syndrome (CRMetS). Obesity promotes adipose tissue dysfunction because it exceeds lipid storage capacity and leads to a lipotoxic state, characterized by inflammation, hypertension, insulin resistance and dyslipidemia, oxidative stress, and hyperuricemia, among others, that affect different organs other than the adipose tissue. In addition, the pro-inflammatory gut microbiota present in obese patients releases uremic toxins, contributing to oxidative stress and inflammation, perpetuating and accelerating the progression of this pathology. In this article, we describe the contribution of obesity, the factors and mechanisms implicated in the development of the CRMetS. Despite the great knowledge about the CRS, more research is needed to characterize the CRMetS given the global obesity epidemic.
肾脏与心脏之间存在着密切关系,在所谓的心肾综合征(CRS)中,若其中一个器官功能衰竭,另一个也会随之衰竭。此外,它们还与身体其他部位相互作用,导致一种代谢状态,进而形成一个持续存在的反馈回路。CRS的特征包括血流动力学变化、神经体液系统激活、利钠肽以及矿物质代谢改变。在这种情况下,由功能失调的内皮连接的肾脏和心脏不可避免地会出现功能衰竭。在肥胖症中,由于脂肪组织功能障碍的并发症,这种综合征会加剧,即所谓的心肾代谢综合征(CRMetS)。肥胖会导致脂肪组织功能障碍,因为它超过了脂质储存能力,从而导致脂毒性状态,其特征包括炎症、高血压、胰岛素抵抗和血脂异常、氧化应激以及高尿酸血症等,这些会影响除脂肪组织之外的不同器官。此外,肥胖患者体内存在的促炎性肠道微生物群会释放尿毒症毒素,加剧氧化应激和炎症,使这种病理状态持续并加速发展。在本文中,我们描述了肥胖症的作用、CRMetS发生发展中涉及的因素和机制。尽管对CRS已有很多了解,但鉴于全球肥胖流行的现状,仍需要更多研究来明确CRMetS的特征。