Purpose of review: Recent studies have reported an alarming increase in the incidence of obesity-related glomerulopathy, in a context of a worldwide spread of obesity.
Recent findings: Several epidemiological investigations have confirmed that obesity is a significant risk factor for the appearance of proteinuria and end-stage renal disease in a normal population. Obesity-induced hemodynamic changes and glomerular deposition of lipids (partly mediated by sterol regulatory element-binding proteins) play an important role in the pathogenesis of obesity-related renal disease. In addition, the renin-angiotensin-aldosterone system is markedly activated in obesity, adipocytes being an important source of these hormones. Weight loss induces a marked reduction in all renin-angiotensin-aldosterone system components. Patients with reduced renal mass of any origin appeared to be particularly susceptible to the detrimental influence of obesity: body mass index was the most important risk factor for the development of proteinuria and renal insufficiency in patients with unilateral renal agenesis, unilateral nephrectomy and remnant kidneys. Weight loss induces a very important reduction in proteinuria in chronic proteinuric nephropathies of different etiologies.
Summary: Prevention and treatment of obesity should be a first-line objective in the therapeutic approach of patients with diabetic and nondiabetic chronic renal diseases.