Introduction:

The prevalence of overweight and obese adults has increased substantially worldwide, in the last three decades. The accumulation of abdominal and visceral fat is highly correlated with renal adverse effects, through the accumulation of adipose tissue in and around the kidneys and the intrarenal accumulation of extracellular matrix. This obesity-related glomerulopathy is characterized in early stages by glomerular hypertrophy with or without secondary focal segmental glomerulosclerosis.

Objective:

To review the mechanisms involved in the obesity related renal illness.

Methods:

A bibliographical search on this topic was carried out in PubMed and Academic Google databases from 2013 to 2017.

Conclusions:

The harmful effects of obesity on the renal vasculature are due to increased blood pressure, inflammation, hyperglycemia, lipotoxicity caused by an excess of non-β-oxidative metabolism of fatty acids, oxidative stress and activation of multiple neurohumoral systems. Excess visceral fat is a source of cytokines and other factors that create a means of oxidative stress and inflammation contributing to endothelial dysfunction, vascular stiffness and the development of atherosclerosis. Hyperfiltration and glomerular hypertrophy cause kidney damage associated with obesity. Compensatory hyperfiltration, which preserves the glomerular filtration rate, is accompanied by glomerular volume expansion, an increase in the components of the glomerular matrix, endothelial and mesangial cells. Following inflammation, neovascularization occurs, a compensatory mechanism to maintain perfusion of injured or ischemic tissues.

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