Background: Rapid renal function decline has been recognized as an important predictor for diabetic nephropathy (DN). Adipocyte fatty acid-binding protein (A-FABP) is a major cytoplasmic protein in adipocytes and is closely associated with metabolic syndrome and type 2 diabetes. We aim to investigate the role of adipokines including A-FABP and inflammatory cytokines in the development of rapid renal function decline in type 2 diabetes and normal renal function.

Methods: A total of 456 subjects with type 2 diabetes with normal renal function were recruited from an outpatient clinic at the Diabetes Center of Inha University Hospital and were followed up for 6 years with serial glomerular filtration rate (GFR) measurements. The serum levels of tumor necrosis factor (TNF)-a, and interleukin (IL)-6, high molecular weight (HMW) adiponectin, endogenous secretory receptor for advanced glycation end products (esRAGE), A-FABP and pentraxin-related protein (PTX3) were measured at baseline. Rapid renal function decline was defined as an eGFR decline >3.3% per year.

Results: During follow-up, 120 participants (26.3%) developed rapid renal function decline and mean annual eGFR decline was -5.4 ± 2.7% and -0.6 ± 2.4% in decliners and non-decliners, respectively. Median A-FABP levels were significantly higher in patients with rapid decliners than in non-decliners (19.1 vs. 16.8 ng/ml, p=0.011). No significant difference of three cytokines levels were observed between groups. Each log unit increase of A-FABP was independently associated with greater risk of rapid renal function decline (odds ratio [OR] = 3.60; 95% confidence interval [CI] 1.95-6.66; p < 0.001) after adjustments for sex, BMI, A1C, GFR, hypertension, presence of carotid artery plaque and urine albumin creatinine ratio.

Conclusions: High plasma A-FABP was an independent risk factor for rapid renal function decline in type 2 diabetes and normal renal function.


D. Seo: None. S. Kim: None. S. Ahn: None. S. Hong: None. M. Nam: None.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at