Perspectiva 282 Obesity and kidney disease - C. P. Kovesdy et al Rev Med Chile 2017; 145: 281-291 In 2014, over 600 million adults worldwide, 18 years and older, were obese. Obesity is a potent risk factor for the development of kidney disease. It increases the risk of developing major risk factors for Chronic Kidney Disease (CKD), like diabetes and hypertension, and it has a direct impact on the development of CKD and end-stage renal disease (ESRD). In individuals affected by obesity, a (likely) compensatory mechanism of hyperfiltration occurs to meet the heightened metabolic demands of the increased body weight. The increase in intraglomerular pressure can damage the kidney structure and raise the risk of developing CKD in the long-term. The good news is that obesity, as well as the related CKD, are largely preventable. Education and awareness of the risks of obesity and a healthy lifestyle, including proper nutrition and exercise, can dramatically help in preventing obesity and kidney disease. This article reviews the association of obesity with kidney disease on the occasion of the 2017 World Kidney Day. Epidemiology of obesity in adults and children Over the last 3 decades, the prevalence of overweight and obese adults (BMI ≥ 25 kg/m2) worldwide has increased substantially1. In the US, the age-adjusted prevalence of obesity in 2013- 2014 was 35% among men and 40.4% among women2. The problem of obesity also affects children. In the US in 2011-2014, the prevalence of obesity was 17% and extreme obesity 5.8% among youth 2-19 years of age. The rise in obesity prevalence is also a worldwide concern3,4, as it is projected to grow by 40% across the globe in the next decade. Low- and middle-income countries are now showing evidence of transitioning from normal weight to overweight and obesity as parts of Europe and the United States did decades ago5. This increasing prevalence of obesity has implications for cardiovascular disease (CVD) and also for CKD. A high body mass index (BMI) is one of the strongest risk factors for new-onset CKD6,7. Definitions of obesity are most often based on BMI (i.e. weight kilograms divided by the square of his or her height meters). A BMI between 18.5 and 25 kg/m2 is considered by the World Health Organization (WHO) to be normal weight, a BMI between 25 and 30 kg/m2 as overweight, and a BMI of >30 kg/m2 as obese. Although BMI is easy to calculate, it is a poor estimate of fat mass distribution, as muscular individuals or those with more subcutaneous fat may have a BMI as high as individuals with larger intraabdominal (visceral) fat. The latter type of high BMI is associated with substantially higher risk of metabolic and cardiovascular disease. Alternative parameters to more accurately capture visceral fat include waist circumference (WC) and a waist hip ratio (WHR) of > 102 cm and 0.9, respectively, for men and > 88 cm and > 0.8, respectively, for women. WHR has been shown to be superior to BMI for the correct classification of obesity in CKD. Association of obesity with CKD and other renal complications Numerous population based studies have shown an association between measures of obesity and both the development and the progression of CKD (Table 1). Higher BMI is associated with the presence8 and development9-11 of proteinuria in individuals without kidney disease. Furthermore, in numerous large population-based studies, higher BMI appears associated with the presence8,12 and development of low estimated GFR9,10,13, with more rapid loss of estimated GFR over time,14 and with the incidence of ESRD15-18. Elevated BMI levels, class II obesity and above, have been associated with more rapid progression of CKD in patients with pre-existing CKD19. A few studies examining the association of abdominal obesity using WHR or WC with CKD, describe an association between higher girth and albuminuria20, decreased GFR8 or incident ESRD21 independent of BMI level. Higher visceral adipose tissue measured by computed tomography has been associated with a higher prevalence of albuminuria in men22. The observation of a BMI-independent association between abdominal obesity and poorer renal outcomes is also described in relationship with mortality in patients with ESRD23 and kidney transplant24, and suggests a direct role of visceral adiposity. In general, the associations between obesity and poorer renal outcomes persist even after adjustments for possible mediators of obesity’s cardiovascular and metabolic effects, such as high blood pressure and diabetes mellitus, suggesting that obesity may affect kidney function through mechanisms in part unrelated to these complications (vide infra).
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