Copyright
©The Author(s) 2015.
World J Nephrol. May 6, 2015; 4(2): 169-184
Published online May 6, 2015. doi: 10.5527/wjn.v4.i2.169
Published online May 6, 2015. doi: 10.5527/wjn.v4.i2.169
Table 1 Representative abnormalities in complement leading to renal disease
Components/related molecules | Diseases |
Complement C3 | C3 glomerulopathy (DDD), aHUS |
Factor H | C3 glomerulopathy (DDD/C3GN), aHUS |
Factor I | C3 glomerulopathy (C3GN), aHUS |
MCP | aHUS |
Factor B | aHUS |
CFHR5 | Familial C3 glomerulopathy (CFHR5 nepropathy) |
CFHR3-1 | Familial C3 glomerulopathy |
CFHR1/3 | IgA nephropathy, aHUS |
Factor B autoantibody | C3 glomerulopathy (DDD) |
Factor H autoantibody | C3 glomerulopathy (DDD/C3GN) |
Bb (activated factor B) | HUS, ANCA-associated vasculitis |
C3Nef | C3 glomerulopathy (DDD, C3GN) |
Soluble C5b-9 | HUS, TTP, ANCA-associated vasculitis |
C3a | ANCA-associated vasculitis, TTP |
C5a | ANCA-associated vasculitis |
C1q/C1qR | C1q nephropathy |
Properdin | TI injury due to massive proteinuria |
C5 | ANCA-associated vasculitis |
Factor B | ANCA-associated vasculitis |
CRaR | TI inflammation, IRI |
C5aR | IRI |
Factor H | IRI |
C5b-9 | IRI |
CD59 | IRI |
- Citation: Salvadori M, Rosso G, Bertoni E. Complement involvement in kidney diseases: From physiopathology to therapeutical targeting. World J Nephrol 2015; 4(2): 169-184
- URL: https://www.wjgnet.com/2220-6124/full/v4/i2/169.htm
- DOI: https://dx.doi.org/10.5527/wjn.v4.i2.169