In addition to conventional treatment with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) agents, participants were randomly assigned to receive Tangshen formula (TSF) or matching placebo for 24 weeks. The urinary

and plasmic L-FABP, renal function, UAER for patients with microalbuminuria, 24 h urinary protein level (24 h UP) for patients with macroalbuminuria were measured. Results: In microalbuminuria patients, TSF displayed a significant decrease in UAER (TSF 97.89 ± 52.89 ug/min VS placebo 109.03 ± 75.62 ug/min, P < 0.05) after 24-week treatment. Levels of urinary L-FABP in TSF group were significant lower than that in Placebo group both after 12 weeks and 24 weeks treatment (6.83 ± 2.87 ug/ml VS 11.08 ± 3.29 ug/ml, P < 0.01 and 6.04 ± 2.95 ug/ml VS 9.21 ± 4.38 ug/ml, P < 0.05, respectively).

In macroabluminuria patients, 24 h UP at 12th week obviously decreased Selleckchem CHIR 99021 than baseline in TSF group (12th week 0.37(0.06,0.90)g/24 h VS baseline 0.73(0.50,1.07)g/24 h, P < 0.05). TSF group showed a significant decreased in urinary L-FABP (12 weeks, 1.21 ± 0.26 ug/ml VS 1.65 ± 0.33 ug/ml, P < 0.05; 24 weeks, 1.42 ± 0.46 ug/ml VS 1.91 ± 0.48 ug/ml, P < 0.05). Levels of urinary L-FABP significantly increased according to the severity of diabetic kidney disease (normoalbuminuria patients 5.916(5.152,7.824)ug/ml VS microalbuminuria patients 11.444(6.775,13.441)ug/ml VS macroabluminuria patients 18.471(10.873,23.391)ug/ml, P < 0.05). Conclusion: Urinary L-FABP levels appear to be associated with the severity of DKD, and administration LY294002 of TSF in addition to conventional therapy is demonstrated to be effective in reducing urinary protein and urinary L-FABP. Acknowledgements: This work was supported by the International Science and Technology Cooperation Program of China (Grant no.2011DFA31860, Grant no.2006DFB31480), the National Basic Research Program of China (973 Program, Grant ID-8 no.2006CB504602) and the National Natural Science Foundation of China (Grant no.81130066). GUAN SIAO-SYUN1,2, SHEU MEEI-LING3, WU CHENG-TIEN1,

CHIANG CHIH-KANG4,5, LIU SHING-HWA1 1Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan; 2Institute of Nuclear Energy Research, Atomic Energy Council, Executive Yuan, Taoyuan, Taiwan; 3Biomedical Sciences, College of Life Sciences, National Chung Hsing University, Taichung, Taiwan; 4Departments of Integrated Diagnostics & Therapeutics, National Taiwan University Hospital, Taiwan; 5Departments of Internal Medicine, National Taiwan University College of Medicine, Taiwan Introduction: Diabetic nephropathy is known to be the most common cause of chronic kidney disease. Advanced glycation end products (AGEs) have been suggested to play an important role in diabetic nephropathy, including renal fibrosis.