Obesity has been associated with secretion of inflammatory mediators and activation of inflammation-associated signalling pathways,[26, 27] with a significant role of specific mediators such as leptin, interleukin (IL)-6, tumor necrosis factor (TNF)-a and adiponectin.[28] Because many of these cytokines have been suggested to mediate renal pathophysiology,[29] it could be speculated that progressive kidney disease could also be regulated by pro-inflammatory cytokines in the context of metabolic syndrome. This evidence concerns the gene LEP and obesity due to melanocortin 4 receptor deficiency.