SAGE-Hindawi Access to Research Cardiology Research and Practice Volume 2011, Article ID 653182, 11 pages doi:10.4061/2011/653182 Review Article Metabolic Syndrome, Chronic Kidney, and Cardiovascular Diseases: Role of Adipokines Manfredi Tesauro,1, 2 Maria Paola Canale,1 Giuseppe Rodia,1 Nicola Di Daniele,1 Davide Lauro,1 Angelo Scuteri,3 and Carmine Cardillo4 1 Department of Medicina Interna, Universita` di Tor Vergata, Viale Oxford 81, 00133 Rome, Italy 2 Laboratory of Molecular Medicine, Department of Internal Medicine, University of Rome Tor Vergata, Viale Oxford 81, 00133 Rome, Italy 3 UOC Geriatria INRCA, POR Roma, 00189 Rome, Italy 4 Universita` Cattolica del Sacro Cuore, 00168 Rome, Italy Correspondence should be addressed to Manfredi Tesauro, mtesauro@tiscali.it Received 1 October 2010; Revised 30 November 2010; Accepted 7 January 2011 Academic Editor: Ken Ichi Aihara Copyright © 2011 Manfredi Tesauro et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Obesity is a chronic disease, whose incidence is alarmingly growing. It is associated with metabolic abnormalities and cardiovascu- lar 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. 1. Introduction The prevalence of obesity, among both adults and children, has worldwide increased over the past two decades; a phe- nomenon which is predominantly attributed to the change in dietary habits and lifestyle modiﬁcations [1, 2]. It is clearly knows that central obesity is an independent risk factor for CVD and is associated with Mets. Insulin resistance (IR) is a key feature of the Mets and consists in a decreased sensitivity or responsiveness of peripheral tissues to the metabolic action of insulin [3]. IR as well as all components of the Mets are associated with altered functions of endothelium which lead to CVD [4]. Hyperlipemia and coronary artery disease are also consequences of obesity which through a cascade of various reactions lead to kidney dysfunction. Moreover, obesity-induced sleep apnoea activates sympathetic nervous system increasing the tone of the glomerular eﬀerent arteri- oles and the secretion of renin and angiotensin [5]. In the last decade, obesity has been suggested as a risk factor for chronic kidney disease, decline of renal function, and low- grade albuminuria, but conﬂicting results have been reported [6–10]. Yet obesity, per se, even in the absence of the above- mentioned medical complications alters renal physiology and metabolism. In this paper, we will examine the role of adipose tissue-secreted factors and the mechanisms of obesity-induced renal and vascular injury leading to chronic kidney and cardiovascular diseases. 2. Epidemiology of Mets, CKD, and CVD CVD accounts for premature death in about 50% of dialysis patients [11]. As early as 1974, Lindner et al. demonstrated that dialysis patients have a higher prevalence of CVD com- pared to the general population [12]. The strong association between mild CKD and CVD has been shown, and recently Henry et al. reported that mild to moderate CKD is strongly