Pazos Fernando
Department of Medicine, Medicine Faculty, Cantabria University, Valdecilla Hospital, Santander 39080, Cantabria, Spain.
World J Diabetes. 2020 Aug 15;11(8):322-350. doi: 10.4239/wjd.v11.i8.322.
Obesity and obesity-related co-morbidities, diabetes mellitus, and hypertension are among the fastest-growing risk factors of heart failure and kidney disease worldwide. Obesity, which is not a unitary concept, or a static process, ranges from alterations in distribution to the amount of adiposity. Visceral adiposity, which includes intraabdominal visceral fat mass and ectopic fat deposition such as hepatic, cardiac, or renal, was robustly associated with a greater risk for cardiorenal morbidity than subcutaneous adiposity. In addition, morbid obesity has also demonstrated a negative effect on cardiac and renal functioning. The mechanisms by which adipose tissue is linked with the cardiorenal syndrome (CRS) are hemodynamic and mechanical changes, as well neurohumoral pathways such as insulin resistance, endothelial dysfunction, nitric oxide bioavailability, renin-angiotensin-aldosterone, oxidative stress, sympathetic nervous systems, natriuretic peptides, adipokines and inflammation. Adiposity and other associated co-morbidities induce adverse cardiac remodeling and interstitial fibrosis. Heart failure with preserved ejection fraction has been associated with obesity-related functional and structural abnormalities. Obesity might also impair kidney function through hyperfiltration, increased glomerular capillary wall tension, and podocyte dysfunction, which leads to tubulointerstitial fibrosis and loss of nephrons and, finally, chronic kidney disease. The development of new treatments with renal and cardiac effects in the context of type 2 diabetes, which improves mortality outcome, has highlighted the importance of CRS and its prevalence. Increased body fat triggers cellular, neuro-humoral and metabolic pathways, which create a phenotype of the CRS with specific cellular and biochemical biomarkers. Obesity has become a single cardiorenal umbrella or type of cardiorenal metabolic syndrome. This review article provides a clinical overview of the available data on the relationship between a range of adiposity and CRS, the support for obesity as a single cardiorenal umbrella, and the most relevant studies on the recent therapeutic approaches.
肥胖及肥胖相关的合并症、糖尿病和高血压是全球范围内心力衰竭和肾脏疾病增长最快的危险因素。肥胖并非单一概念或静态过程,其范围涵盖脂肪分布改变至脂肪量变化。内脏脂肪,包括腹内内脏脂肪量以及肝脏、心脏或肾脏等部位的异位脂肪沉积,与心肾发病风险增加的关联比皮下脂肪更为紧密。此外,病态肥胖对心脏和肾脏功能也有负面影响。脂肪组织与心肾综合征(CRS)相关的机制包括血流动力学和机械变化,以及诸如胰岛素抵抗、内皮功能障碍、一氧化氮生物利用度、肾素 - 血管紧张素 - 醛固酮、氧化应激、交感神经系统、利钠肽、脂肪因子和炎症等神经体液途径。肥胖及其他相关合并症会引发不良的心脏重塑和间质纤维化。射血分数保留的心力衰竭与肥胖相关的功能和结构异常有关。肥胖还可能通过超滤、肾小球毛细血管壁张力增加和足细胞功能障碍损害肾功能,进而导致肾小管间质纤维化和肾单位丧失,最终发展为慢性肾脏病。在2型糖尿病背景下开发具有肾脏和心脏作用的新治疗方法以改善死亡率结果,凸显了CRS的重要性及其患病率。体内脂肪增加会触发细胞、神经体液和代谢途径,从而产生具有特定细胞和生化生物标志物的CRS表型。肥胖已成为一种单一的心肾总括或心肾代谢综合征类型。本文综述提供了一系列肥胖与CRS之间关系的现有数据的临床概述、支持肥胖作为单一心肾总括的依据,以及近期治疗方法的最相关研究。