Key result
Altered levels of adipokines, oxidative stress, and inflammation mediate the effects of obesity and metabolic syndrome on renal physiology and cardiovascular risk.
Highlights the role of adipokines, oxidative stress, and inflammation in the pathophysiology linking obesity and metabolic syndrome to chronic kidney and cardiovascular diseases.
No immediate practice changes for obesity or metabolic syndrome; leaves open targeted interventional trials on these mediators.
Obesity is a chronic disease, whose incidence is alarmingly growing. It is associated with metabolic abnormalities and cardiovascular complications. These complications are clustered in the metabolic syndrome (MetS) leading to high cardiovascular morbidity and mortality. Obesity predisposes to diabetic nephropathy, hypertensive nephrosclerosis, and focal and segmental glomerular sclerosis and represents an independent risk factor for the development and progression of chronic kidney disease (CKD). Albuminuria is a major risk factor for cardiovascular diseases (CVDs). Microalbuminuria has been described as early manifestation of MetS-associated kidney damage and diabetic nephropathy. Obesity and MetS affect renal physiology and metabolism through mechanisms which include altered levels of adipokines such as leptin and adiponectin, oxidative stress, and inflammation. Secretory products of adipose tissue also deeply and negatively influence endothelial function. A better understanding of these interactions will help in designing more effective treatments aimed to protect both renal and cardiovascular systems.
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Tesauro et al. (2011) conducted a review in Obesity, Metabolic Syndrome, Chronic Kidney Disease, Cardiovascular Diseases. Adipokines was evaluated. Altered levels of adipokines, oxidative stress, and inflammation mediate the effects of obesity and metabolic syndrome on renal physiology and cardiovascular risk.
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