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


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: SA-PO835

Identification of Anti-Peroxidasin Antibodies in Human and Experimental Glomerulonephritis

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: From Inflammation to Fibrosis


  • Costa, Lyndon H., Imperial College London, London, London, United Kingdom
  • Dhutia, Amrita, Imperial College London, London, London, United Kingdom
  • Pusey, Charles D., Imperial College London, London, London, United Kingdom
  • McAdoo, Stephen Paul, Imperial College London, London, London, United Kingdom
  • Prendecki, Maria, Imperial College London, London, London, United Kingdom

Peroxidasin (Pxdn) is an extracellular matrix (ECM) haem peroxidase critical for forming sulfilimine bonds which crosslink type 4 collagen. Sulfilimine bonds contribute to structural integrity and stability of the ECM and act to sequester the Goodpasture antigen giving it immune privilege. Autoantibodies to peroxidasin have previously been identified in patients with anti-glomerular basement (GBM) disease and MPO-ANCA associated vasculitis (MPO-AAV).


Circulating anti-Pxdn IgG was measured by ELISA in serum from patients (anti-GBM disease, AAV, and healthy volunteers) and rats with experimental autoimmune glomerulonephritis (EAG), an autoimmune model of anti-GBM disease. For coating, recombinant rat peroxidasin was expressed in HEK293 cells and purified; human peroxidasin was from a commercial source (Origene). Antibody specificity was confirmed using immunoblotting. Expression of Pxdn, deposited IgG, and smooth muscle actin (SMA) in kidney tissue was assessed by indirect immunofluorescence (IF).


Circulating anti-Pxdn IgG antibodies were detected in 29.4% of (15/51) patients with anti-GBM disease, 14.2% (2/14) of patients with active MPO-AAV, and 0% (0/6) patients with active PR3-AAV (Fig 1A). Circulating anti-Pxdn IgG antibodies were detectable at day 28 after induction of EAG (peak glomerular injury) in 86.7% (13/15) of rats (Fig 1B). Anti-PXDN antibodies were detectable at low titre from day 18 suggesting they may arise later than anti-α3(IV)NC1 antibodies which are detected from day 7. IF staining of kidney tissue in EAG identified Pxdn at areas of glomerular injury and crescent formation. Pxdn co-localised with SMA but not with deposited rat IgG (Fig 1C).


We confirm the presence of anti-Pxdn antibodies in patients with glomerular disease. In EAG, anti-Pxdn antibodies were evident after the development of antibodies against α3(IV)NC1 and glomerular Pxdn expression was only detected after disease onset: thus we suggest anti-Pxdn antibodies may arise by a process of inter-molecular epitope spreading in the diseased glomerulus.