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Abstract: FR-PO013

Leucine Rich α-2 Glycoprotein Is a Novel Urinary and Serum Biomarker for AKI

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials


  • Eguchi, Tomohiro, Kochi University, Nankoku city, Japan
  • Terada, Yoshio, Kochi University, Nankoku city, Japan
  • Taniguchi, Yoshinori, Kochi University, Nankoku city, Japan
  • Nishikawa, Hirofumi, Kochi University, Nankoku city, Japan

Leucine-rich α-2 glycoprotein (LRG) is one of serum glycosylated proteins with 347 amino acids, and reported that serum LRG is a novel disease activity biomarker for rheumatoid arthritis and inflammatory bowel disease. However, little is known about the role of LRG in acute kidney injury (AKI) pathogenesis. We examined renal LRG expression and urinary LRG level using mice AKI model and clinical samples.


We evaluated LRG mRNA and protein expression in kidney in the bilateral renal ischemia-reperfusion injury (IRI) mice AKI model. We also examined immunohistological examination of LRG localization by confocal microscopy, and measured serum and urinary LRG levels. We evaluate the mechanism of LRG regulation using cultured renal tubular cells (NRK-52E cells). In clinical study, we measured urinary LRG in contrast media-induced AKI patients using ELISA, and immunohistological examination of LRG in AKI and minimal change renal biopsy samples.


In mice with IRI-induced AKI, renal mRNA and protein expression of LRG were induced from 6 h and 12 h and peaked at 24 h and 48 h after IRI, respectively. In control mice kidney, only a very few expression of LRG was observed. Immunohistological examination showed that LRG expression was observed mainly on renal tubular cells in AKI mice. The LRG positive tubular cells are mainly co-stained with AQP1 using confocal microscopy. We also find that serum and urinary LRG levels were up-regulated in IRI-induced AKI from 12h. In NRK-52E cells, TNF-alpha and LPS stimulated LRG expression. Notably, in contrast media-induced AKI patients, urinary LRG levels were increased from 6 h. LRG staining were enhanced in AKI renal-biopsy samples mainly at proximal tubules. In contrast, only a few LRG staining was observed in minimal change renal biopsy samples.


Our results demonstrate that LRG is up-regulated in renal tissues in both mice and human AKI, and that urine and serum LRG are increased in early phase of AKI. Inflammatory cytokines such as TNF-alpha stimulates expression of LRG in renal tubular cells. Thus, urine and serum LRG could serve as a potential early biomarker in AKI.