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Abstract: SA-PO1030

Augmented CD36 Stimulation by Fatty Acids Promotes Macrophage Activation and Endothelial Injury in ANCA-Associated Vasculitis

Session Information

Category: Pathology and Lab Medicine

  • 1800 Pathology and Lab Medicine


  • Zhang, Xiang, UCL Department of Renal Medicine, Royal Free Hospital, London, United Kingdom
  • Ruan, Xiong Z., UCL Department of Renal Medicine, Royal Free Hospital, London, United Kingdom
  • Salama, Alan D., UCL Department of Renal Medicine, Royal Free Hospital, London, United Kingdom

ANCA-associated vasculitis (AAV) is characterised by monocyte/macrophage activation and small blood vessel inflammation leading to organ damage. In some patients, macrophage activation leads to giant cell and granuloma formation, resulting in further tissue damage. CD36 is a transmembrane glycoprotein expressed on various cells, including macrophages and endothelial cells. CD36 is crucial in the modulation of inflammatory processes. However, the role of CD36 in AAV remains understudied.


Cellular expression of CD36 and endothelial cell activation markers was assessed by FACS and immunohistochemistry on tissue sections. ELISA was used to measure soluble(s) CD36 in serum and cell supernatants. Multinucleate Giant cell(MNGC) formation was investigated using established protocols following Palmitic acid (PA) stimulation of cells with or without CD36 knockdown. Macrophage activation markers were examined using qPCR.


CD36 expression was found to be increased in AAV kidney biopsies on glomerular and tubular macrophages. Additionally, CD36 expression on classical and intermediate monocytes was significantly increased in AAV patients compared to healthy controls. Serum sCD36 was elevated in AAV patients, specifically in the PR3-ANCA subtype, in both remission and active disease. Stimulation of THP1-derived macrophages with PA resulted in an increase in CD36 expression, increased the expression of c-Myc and ATF-2, and generated M1 polarised macrophages with significant MIF production. In addition, there was an increase in MNGC formation. These findings were all attenuated by CD36 knockdown or MIF antagonism. Similarly, PA stimulation of endothelial cells increased CD36 and VCAM expression and promoted MIF production. Co-culture of endothelial cells and macrophages with PA resulted in increased migration of macrophages towards the activated endothelial cells.


AAV patients demonstrate elevated levels of monocyte and sCD36. Stimulation of CD36 by fatty acids promotes inflammatory responses in both macrophages and endothelial cells, potentially contributing to many of the features found in AAV. Targeting CD36 or its downstream effector MIF is a novel therapeutic strategy to be tested in AAV.


  • Government Support – Non-U.S.