In this study, we demonstrate that central obesity is significantly associated with albuminuria in middle-aged Chinese, even with adjustment for general obesity, hsCRP, renal function and lifestyle factors. We also found that subjects with central obesity tend to develop albuminuria, independently of BMI. These findings were most pronounced in women.
The association between central obesity and albuminuria has been previously reported 
. For example, in the Look AHEAD (Action for Health in Diabetes) Study, increased BMI and abdominal obesity (measured by waist circumference) were found to be associated with albuminuria in overweight and obese adults with type 2 diabetes 
. de Boer et al. also found that waist circumference predicts the subsequent development of microalbuminuria in type 1 diabetes 
. Thoenes et al found that abdominal obesity is associated with microalbuminuria and an elevated cardiovascular risk profile in patients from 26 countries with hypertension 
. Chandie Shaw et al. also reported that central obesity (measured by waist-to-hip ratio) is independent risk factor for increased albuminuria in normoglycemic South Asian subjects 
. A similar finding was observed in the Copenhagen City Heart Study 
. These studies provide an agreement that adiposity is associated with albuminuria. However, these studies are either cross-sectional studies or focused on specific conditions or diseases, such as diabetes or hypertension subjects. Our study is a population-based cohort survey which demonstrates that central obesity is associated with an increased risk of prevalence and incidence of albuminuria in Chinese. In addition, this study provides confirmatory data that the reduced cut-points for abdominal obesity specific to Asian populations are sensitive predictors of albuminuria, similar to thresholds used in Caucasians.
Sex difference is another point worthy of mention in this study. Foster et al. reported that, in the Framingham Heart Study, visceral adipose tissue is associated with microalbuminuria in men but not in women 
. Our result showed that central obesity is more strongly associated with albuminuria in women than in men. Our previous study also found that hsCRP is closely associated with metabolic syndrome in women than in men 
. Sullivan et al. reported that the renal protection afforded to female hypertensive rats is associated with lower blood pressure, decreased macrophage infiltration, and decreased levels of oxidative stress 
. In this gender difference, sex hormones may play an important role on the inflammatory mechanism which links central obesity and albuminuria, and these merit further study.
Several mechanisms link central obesity to albuminuria have been proposed. Firstly, compared to general obesity, central obesity is more strongly associated with inflammatory markers and oxidative stress which may increase the risks of CVD and other chronic diseases, such as hypertension or diabetes 
. These chronic diseases are closely related to microalbuminuria 
. In the current study, we also found that subjects with central obesity or albuminuria had higher hsCRP level than non-central obesity or normoalbuminuria. Second, studies reported that the adipocyte hormone adiponectin and leptin, which can regulate podocyte function, may play an important role in the development of obesity-related albuminuria 
. A possible mechanism by which central obesity promotes glomerular damage and induces microalbuminuria is through decreasing serum adiponectin and increasing serum leptin levels 
. Third, central obesity is an underlying feature of insulin resistance. Subjects with insulin resistance may increase urinary albumin excretion, leading progressively to chronic kidney disease 
. Therefore, central obesity may, through insulin resistance, increase the risk of albuminuria and glomerular damage. Fourth, central obesity may activate the transforming growth factor beta (TGF-β)-related mechanisms, leading to glomerular hyperfiltration. Glomerular hyperfiltration causes renin-angiotensin-system (RAS) activation which leads to renal damage 
. Previous studies reported that the use of angiotensin-converting-enzyme inhibition in patients with uncomplicated type 1 DM results in a significant decline in hyperfiltration 
. Obesity also increases renal tubular sodium reabsorption which impaired renal pressure natriuresis 
. Fifth, central obesity may induce hyperleptinemia through sympathetic nervous system activation, thus stimulating the hypothalamic pro-opiomelanocortin pathway to cause renal damage 
A strength of this study is that it uses a population-based prospective cohort not limited to specific conditions or diseases, and as such may be more representative of the general population than previous studies. Second, we demonstrate the strong association between central obesity and albuminuria in the baseline population using a cross-sectional design. Our study design enabled us to infer causality of central obesity on albuminuria incidence after 3 years of follow-up. Third, our sample size is large enough to enable adjustment of potential confounders to minimize bias. One limitation associated with this study was that the diagnosis of albuminuria was depended on a spot urine sample, which may not represent the true level of urinary albumin excretion. The potential misclassification, however, is likely non-differential with our results. Second, our findings may not be generalizable to young adults because we recruited subjects aged 40 and older. Third, the purely Chinese sample may limit the generalizability of our results to other races or ethnic populations.
In summary, subjects with central obesity had increased prevalence and incidence of albuminuria in a population-based middle-aged Chinese cohort. This association was stronger in women than in men. Albuminuria may be one of the major complications of central obesity. Obesity-associated renal disease should be prevented or treated by weight reduction.