Article ID Journal Published Year Pages File Type
2805941 Metabolism 2013 7 Pages PDF
Abstract

ObjectiveTo explore the relationship between adiponectin and albuminuria in a large group of overweight and obese nondiabetic individuals after controlling for potential confounders.Material and MethodsDetailed anthropometry, computed tomography-measured visceral abdominal adipose tissue, 24-h albuminuria, adiponectin and a series of biochemical parameters were assessed. Four hundred forty patients, predominantly of Caucasian origin, were included (80.2% female). A multiple linear regression model was developed, with albuminuria as the dependent variable and potential predictors as independent variables.ResultsThe mean age was 40 ± 13 years, the mean body mass index was 35.7 ± 6.6 kg/m2, and the median visceral abdominal adipose tissue was 142.4 (92.3–194.0) cm2. 10.9% of subjects exhibited microalbuminuria. The median adiponectin level was 9.08 (6.23–12.94) μg/ml, and the median fasting serum glucose level was 83 (77–89) mg/dl. The strongest significant univariate correlations with albuminuria were visceral abdominal adipose tissue (r = 0.258, p < 0.001), adiponectin (r = − 0.265, p < 0.001), waist circumference (r = 0.250, p < 0.001), waist-to-hip ratio (r = 0.236, p < 0.001) and high-density lipoprotein cholesterol (r = − 0.211, p < 0.001). The multiple linear regression model revealed a significant positive independent correlation between visceral abdominal adipose tissue and albuminuria (r = 0.134, p = 0.033), between fasting glucose levels and albuminuria (r = 0.390, p = 0.029) and between gender and albuminuria (r = 0.107, p = 0.038). A significant independent negative correlation was identified between adiponectin and albuminuria (r = − 0.255, p = 0.022).ConclusionsWe observed an independent inverse relationship between adiponectin and albuminuria in overweight and obese nondiabetic individuals. Further investigations are needed to confirm this finding and to clarify whether adiponectin is a risk marker or plays a causative role in developing obesity-induced nephropathy.

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