ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: FR-PO972

Detection of Autotaxin and Lysophosphatidic Acid Receptors in Glomerular Diseases within Glomerulus

Session Information

Category: Pathology and Lab Medicine

  • 1800 Pathology and Lab Medicine

Authors

  • Kumagai, Naonori, Fujita Ika Daigaku, Toyoake, Aichi, Japan
  • Hirayama, Masaya, Fujita Ika Daigaku, Toyoake, Aichi, Japan
  • Ando, Takuma, Fujita Ika Daigaku, Toyoake, Aichi, Japan
  • Kondo, Tomomi, Fujita Ika Daigaku, Toyoake, Aichi, Japan
  • Matsumoto, Yuji, Fujita Ika Daigaku, Toyoake, Aichi, Japan
  • Ikezumi, Yohei, Fujita Ika Daigaku, Toyoake, Aichi, Japan
Background

Lysophosphatidic acid (LPA) is a lysophospholipid that acts as a chemical mediator. It acts through six dedicated receptors, LPA receptor 1-6 (LPAR1-6). LPA is mainly produced by autotaxin (ATX) in blood from lysophospholipids in blood as a substrate. Moreover, LPA is produced by mPA-PLA within cells from phosphatidic acid in the cells as a substrate. be. The Pathophysiological role of the LPA and ATX in glomerular diseases within glomerulus remains unclear.

Methods

Immunostaining for LPAR1-5 and ATX was performed on renal biopsy specimens of pediatric glomerular diseases such as lupus nephritis, membranous nephropathy, idiopathic nephrotic syndrome, IgA nephropathy, and mesangioproliferative glomerulonephritis (MPGN). Moreover, ATX mRNA was detected by in situ hybridization.

Results

LPAR1-5 and ATX were strongly stained in lupus nephritis and membranous nephropathy. They were stained negative to weakly positive in the other glomerular diseases. ATX mRNA was detected in mesangial cells in IgA nephropathy and MPGN, however, was hardly detected in lupus nephritis and membranous nephropathy.

Conclusion

In systemic lupus erythematosus and lupus nephritis, ATX is assumed to be produced in macrophage and released into blood, resulting in elevated concentration in blood and urine. Taken together with the present study, these findings imply that in systemic lupus erythematosus and lupus nephritis ATX in blood is deposited in the glomerulus and LPA is produced in situ. Produced LPA acts in an autocrine and/or paracrine manner through LPA receptors and are involved in pathophysiological role. Conversely, in IgA nephropathy and MPGN, ATX is produced in situ within the glomerulus and is involved in the pathophysiological role. It is needed to elucidate the pathophysiological role of LPA and ATX in each glomerular disease within glomerulus.

Funding

  • Government Support – Non-U.S.