[Renal consequences of obesity].

The steady increase in the prevalence of obesity contributes to the increase in the prevalence of chronic kidney disease, through renal damages associated with type-2 diabetes and hypertension. Obesity is also an independent risk factor for the kidney, since it is associated with an increased risk of albuminuria and glomerulosclerosis, and worsens the course of chronic kidney disease regardless of the primary renal disease. The existence of a metabolic syndrome, constant in type-2 diabetes, and associated with abdominal obesity, is not the only requirement for renal anomalies of which the translation is a functional hyperfiltration, a clinical microalbuminuria and histologically a glomerulomegaly and glomerulosclerosis. The estimated glomerular filtration rate (GFR) in obese patients is strongly influenced by the weight or indexation to body surface area, and it is logical to take into account the value of non-indexed GFR to assess renal risk and treatment effects, especially if they lead to weight loss. Hypertension is promoted by salt sensitivity, potentially reversible, and overactivity of the renin-angiotensin system (RAS) in part due to adipose tissue. The cytokines secreted by adipose tissue (adipokines), induce sympathetic hyperactivity through leptin, and low-grade inflammatory state that contributes to the development of glomerular sclerosis lesions, especially because a resistance to adiponectin. The treatment relies on weight loss, possibly through bariatric surgery, and antagonists of the RAS.