Copyright: ©Author(s) 2026.
World J Transplant. Jun 18, 2026; 16(2): 117138
Published online Jun 18, 2026. doi: 10.5500/wjt.v16.i2.117138
Published online Jun 18, 2026. doi: 10.5500/wjt.v16.i2.117138
Figure 1 Recurrence of glomerular diseases.
FSGS: Focal segmental glomerulosclerosis.
Figure 2 Overlap between complement over activation and dysregulation.
C3G: C3 glomerulopathy.
Figure 3 Pathways of complement activation and inhibitors.
MBL: Mannose-binding lectin; MASP: Mannose-binding lectin-associated serine protease; C5aR: C5a receptor.
Figure 4 Alternate pathway: Activators and regulators.
MCP: Membrane cofactor protein; DAF: Decay-accelerating factor.
Figure 5 Treatment approach to C3 glomerulopathy.
C3G: C3 glomerulopathy; RAAS: Renin-angiotensin-aldosterone system; MMF: Mycophenolate mofetil; ACTH: Adrenocorticotropic hormone.
- Citation: Chutani A, Norouzi S, Lerma EV. C3 glomerulopathy in transplant “like yet unlike native”: Pathophysiology, recent advances in therapeutics and evolving paradigms. World J Transplant 2026; 16(2): 117138
- URL: https://www.wjgnet.com/2220-3230/full/v16/i2/117138.htm
- DOI: https://dx.doi.org/10.5500/wjt.v16.i2.117138