The role of obesity on chronic kidney disease development, progression, and cardiovascular complications

The complex links between obesity, chronic kidney disease (CKD) and cardiovascular disease (CVD) are not completely understood. The objective of this review is to describe and discuss the anatomy, physiology, and biochemistry of the adipose tissue, as well as its involvement in the pathophysiology of CVD and CKD. We searched for original articles in PubMed. The search terms used were “obesity”, “CKD”, and “CVD”. In addition, we also identified publications from our personal databases of literature about obesity, CKD and CVD to identify any important studies that might have been missing from the PubMed search. We further searched the reference lists of identified articles for further relevant papers. Epidemiological studies show that obesity is associated with obesity-related glomerulopathy (ORG) as well as an increase in the risk of CKD in the general population. A number of pathophysiological mechanisms, including renal hemodynamic changes, neurohumoral pathways that activate the sympathetic and renin-angiotensin-aldosterone systems, proinflammatory and profibrotic effects of various adipokines, and insulin resistance may explain the excessive risk of CKD development and progression in obese patients. In patients with mild to moderate CKD, obesity per se contributes a modest increase in cardiovascular risk, while the effect of obesity on the cardiovascular risk of patients with advanced CKD is probably due to the concurrent metabolic syndrome and coexisting cardiovascular risk factors, but the effect of obesity on the cardiovascular risk of patients with advanced CKD is probably the result of the concomitant metabolic syndrome and coexisting cardiovascular risk factors. There are recent data suggesting that subcutaneous and visceral adipose tissue have different and probably opposite effects on the CVD risk in CKD. Further studies are necessary to distinguish the specific clinical implication of different adipose tissue compartments, and to determine the principal mediators that connect obesity, CKD and CVD