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Kidney Week

Abstract: TH-PO757

Autotaxin Early Predicts Progressive Renal Fibrosis in CKD

Session Information

  • Pediatric CKD
    November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Pediatric Nephrology

  • 1700 Pediatric Nephrology


  • Lin, Ching-Yuang, Children's Hospital, China Medical University, Taiwan, Taichung, Taiwan

Single-kidney FUBI (Failure of Ureteric Bud Invasion) mice in susceptible animals causes glomerular sclerosis and interstitial fibrosis in the remnant kidney. To identify potential biomarker, we applied cDNA microarray.


We examined serial changes with aging and investigated the single-kidney-FUBI mice for 15 months. Using microarray, gene expression and validation workflow, we identified potential biomarkers and validation using plasma samples from 146 patients with chronic kidney disease (CKD) of diverse etiologies.


We identified autotaxin that were shared by FUBI mice and CKD patients. Autotaxin (ATX) protein expression expressed dramatically after age of 12 months in the single-kidney compared with double-kidney-FUBI mice. During the progression of human CKD, a gradual increase of plasma autotaxin level became significant in stage 3 CKD with the amplification of CKD severity. ATX was absent in normal human renal tissue but detected immunohistologically in the human specimen of renal dysplasia. ATX also contributed a drastic increase in the expression of fibrotic components including: fibronection, α-smooth muscle actin, collagen I and TGF-β in aging. Also fibrotic proteins upregulated in cultured human podocytes treated by ATX in a dose dependent manner.


Our results indicated that ATX might serve as a novel tool for monitoring the progression of CKD. ATX might also be as a possible therapeutic target to slow progression of CKD.