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The clustering of insulin resistance, dysglycaemia, dyslipidaemia, hypertension and central obesity represents the major features of metabolic syndrome. These clusters of factors may share common aetiology, each of which is a risk factor for cardiovascular disease. The metabolic syndrome seems to affect between 10% and 25% of adult populations worldwide. Several studies have described the association between metabolic syndrome, and diabetes and cardiovascular disease.1 Although obesity is often associated with diabetes and hypertension, which are two of the most common risk factors for the development of end‐stage renal disease (ESRD), it has been suggested that obesity in itself is an independent risk factor.
The prevalence of obesity‐related glomerulopathy (ORG), which may lead to end‐stage renal disease, has increased 10‐fold over the past 15 years as a consequence of the spread of the obesity epidemic. The increasing prevalence of ESRD, with its associated high annual mortality and rates of cardiovascular complications, is a worldwide problem.2 In the US alone, the prevalence of ESRD has more than doubled in the past decade and the population living with ESRD is projected to increase to 650000 persons by the year 2010, with associated Medicare expenditures of $28 billion.3 Identifying new and potentially modifiable risk factors for ESRD is critical in order to devise effective, population‐based preventive strategies.
Massive obesity has been shown to produce nephrotic syndrome, and it has been reported that proteinuria and segmental glomerulosclerosis can be present in obese patients, even in the absence of diabetes.2 In addition, a large‐scale study including 6818 renal biopsies from 1986 to 2000 showed a 10‐fold increase in renal lesion, such as glomerulomegaly and focal segmental glomerulosclerosis, which were associated with obesity.2 ORG was recently defined morphologically as glomerulomegaly with or without focal segmental glomerulosclerosis. The syndrome constitutes the triad of morbid obesity, marked proteinuria without oedema and normal serum albumin concentration. It can occur in any degree of obesity but is more common in the morbidly obese group—that is, body mass index >40 kg/m2. It often presents as proteinuria on urinary dipsticks, followed by the confirmation of gross proteinuria of up to 32 g/dl. ORG should be diagnosed by excluding the presence of hypertension or undetected type 2 diabetic renal diseases.2 The pathogenesis is unknown (thought to be due to low renal nitric oxide production) and most of the available information comes from studies in Zucker fa/fa rats which often die from ESRD. These rats are a genetic model of obesity that results from a mutation in the leptin receptor gene.4 Homozygous Zucker fa/fa rats exhibit most of the metabolic picture seen in human obesity, including hypercholesterolaemia, hypertriglyceridaemia, hyperinsulinaemia and proteinuria.
Although the condition is said to be benign, a small proportion of patients will progress towards end‐stage renal failure requiring replacement therapy, a further addition to the cost. The condition is readily reversible and ameliorated with weight loss, an important consideration in the management of this condition. In association with increasing prevalence of chronic kidney disease, this will inevitably result in increasing proportions of deaths from cardiovascular disease as well as increased prevalence and associated consequences of other complications of chronic kidney disease. A concerted, global initiative is required to deal with the ORG epidemic.
Competing interests: None declared.