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Advanced Oxidation Protein Products Accelerate Renal Fibrosis in a Remnant Kidney Model

Hong Yan Li^*, Fan Fan Hou^*, Xun Zhang^*, Ping Yan Chen, Shang Xi Liu^*, Jian Xun Feng^*, Zhi Qiang Liu^*, Yue Xin Shan^*, Guo Bao Wang^*, Zhan Mei Zhou^*, Jian Wei Tian^* and Di Xie^*

^* Division of Nephrology, Nanfang Hospital, and Department of Biostatistics, Southern Medical University, Guangzhou, People’s Republic of China

Address correspondence to: Dr. Fan Fan Hou, Division of Nephrology, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou 510515, People’s Republic of China. Phone: 86-20-6164597; Fax: 86-20-87281713; E-mail: ffhou{at}public.guangzhou.gd.cn

Received for publication July 25, 2006. Accepted for publication October 26, 2006.

Accumulation of plasma advanced oxidation protein products (AOPP) has been found in patients with chronic kidney disease. However, the biologic consequences of AOPP consumption on progression of renal disease still are unclear. For testing of the hypothesis that AOPP accelerate progression of chronic kidney disease, Sprague-Dawley rats were subjected to five-sixths nephrectomy (5/6 Nx) or to sham operation. Rats in each group were randomly assigned in three subgroups (n = 30 in each group) and treated with repeated intravenous injections of AOPP-modified rat serum albumin (RSA), unmodified RSA, or vehicle for indicated period. Compared with RSA- or vehicle-treated 5/6 Nx rats, AOPP RSA–treated 5/6 Nx rats displayed greater proteinuria, higher serum creatinine, and lower creatinine clearance. AOPP challenge resulted in more renal hypertrophy, higher macrophage influx, and greater renal fibrosis in the remnant kidney. Chronic administration of AOPP in sham-operated rats increased urinary protein excretion and renal macrophage infiltration, but histologic renal fibrosis was not observed during the study period. AOPP treatment enhanced AOPP level in renal tissue. This was associated with marked increase of thiobarbituric acid reactive substances, decrease of glutathione peroxidase activity, and upregulated expression of monocyte chemoattractant protein-1 and TGF-1 in renal cortex. These data indicate that AOPP might be a new and potentially important mediator of renal fibrosis in the remnant kidney. Chronic accumulation of AOPP promotes renal fibrosis probably via a redox-sensitive inflammatory pathway.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673