Range of adiposity and cardiorenal syndrome

Abstract

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.

The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

“…Uremic toxicity is an indication for the initiation of renal replacement therapy and can manifest itself in the form of anorexia, nausea, vomiting, bleeding diathesis, pericarditis, uremic neuropathy or encephalopathy, seizures, coma, and death [ 9 , 10 ]. Advanced age, smoking, obesity, and other unhealthy lifestyle factors [ 5 , 11 , 12 , 13 ], along with genetic susceptibility [ 14 , 15 ], are all risk factors for the development of CKD preceding ESRD.…”

Modulation of insulin resistance by renin angiotensin system inhibitors: implications for cardiovascular prevention

“…MS and obesity are two manifestations of IR and are also independent determinants of structural and functional CV diseases [61][62][63]. In addition, both often are associated with abnormalities of renal function such us CKD and microalbuminuria [64,65] which represents independent risk factors for CV diseases [66,67]. Adipose tissue acts as an endocrine organ, secreting hormones and other substances that create a proinflammatory state and promote formation of atherosclerotic plaques [68,69].…”

Adiponectin protects obesity-related glomerulopathy by inhibiting ROS/NF-κB/NLRP3 inflammation pathway

“…Different adipose tissue depots play different roles in the development of other diseases, such as cardiovascular disease and renal disease. Morbid obesity has been shown to adversely affect cardiac and renal function [ 2 ]. Obesity-related glomerulopathy (ORG) is a well-characterized renal complication of obesity, referring to proteinuria and glomerulomegaly in obese patients who show no clinical and histopathological evidence of other renal diseases [ 3 ].…”