Figure 1

A range of ‘obesity and obesity-related’ factors have been suggested to be implicated in the progression of chronic kidney disease, CKD. These include; general insulin resistance and progressive hyperglycemia. Heightened free fatty acids, FFAs common in obesity may lead to further insulin resistance and FA/TG fatty acid/triglyceride accumulation locally within tissues –which may be implicated in cellular dysfunction (e.g. the promotion of cell death pathways). Hypertension is common in obesity and metabolic syndrome and may be due to a range of factors including heightened sympathetic nervous system activation and angiotensinogen release from adipose tissue. The hypertension may have a direct damaging effect on microvasculature within renal tissues and via the actions of heightened renin angiotensin aldosterone system, RAAS activity. The dysregulation of adipose tissue-derived adipocytokines such as leptin and adiponectin and proinflammatory cytokine release may strengthen obesity-related factors including insulin resistance, dyslipidemia and oxidative stress. Other factors potentially implicated may include resistin, corticosteroids (potentially via increased adipose tissue production and hypothalamic pituitary stimulation), hypovitamin D status and other nutritional and genetic factors (e.g. gene polymorphisms). Note that the precise mechanisms in human in vivo CKD are yet to be fully elucidated, and is speculation at present, based upon association studies, cell and animal studies and pharmacological manipulation.