The progression of metabolic and cellular dysfunction both systemically and locally within kidney tissue is linked to many diverse and complex pathways currently being elucidated; these include factors mentioned, and in particular the heightened production of proinflammatory cytokines, IL-1β, -6, -8, TNFα and interferon gamma (IFNγ), oxidative stress and abnormalities in glucose and lipid metabolism (e.g. impaired glucose tolerance, glycemia and dyslipidemia) (see Figure 1). This evidence concerns the gene IL1B and metabolic syndrome.