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Nephrol Dial Transplant (2002) 17: 1157-1159
© 2002 European Renal Association-European Dialysis and Transplant Association


Editorial Comments

Obesity—a neglected culprit in renal disease

Manuel Praga

Servicio de Nefrología, Hospital 12 de Octubre, Madrid, Spain

Keywords: body mass index; focal and segmental glomerulosclerosis; obesity; obesity-related glomerulopathies; renin–angiotensin system; renal disease

The first 10% of the full text of this article appears below.

Obesity-related glomerulopathies—clinical features and epidemiology

Proteinuria is a recognized complication of morbid obesity, although it develops only in a minority of patients. Renal biopsies and autopsy studies have shown that focal and segmental glomerulosclerosis (FSG) is the commonest histologic lesion in proteinuric obese patients [1]. Obesity-related FSG can be distinguished from idiopathic cases of FSG by glomerulomegaly and by less severe foot process effacement. From a clinical point of view, patients with obesity-related glomerulopathies (ORG) do not develop the nephrotic syndrome (hypoalbuminaemia, oedema) even when there is massive and sustained proteinuria. This clinical characteristic (that is also observed in other renal diseases related to hyperfiltration such as reflux nephropathy or proteinuria related to renal mass reduction) is very useful to distinguish these patients from idiopathic FSG in which a complete nephrotic syndrome usually accompanies the presence of . . . [Full Text of this Article]

How could obesity induce proteinuria and glomerulosclerosis?

Glomerular hyperfiltration
Hyperlipidaemia
Role of leptin and other adipocyte-derived hormones
Therapeutic interventions
Influence of obesity on the evolution of other renal diseases

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