The kidney is an organ where complement-mediated tissue injuries take
place by various stimuli. To assess how the kidney is protected from t
he autologous complement attack, comparative localization of decay acc
elerating factor (DAF), membrane cofactor protein (MCP) and 20 kDa hom
ologous restriction factor (HRF20) was studied in the normal human kid
ney. Specific monoclonal antibodies to DAF, MCP and HRF20 were used fo
r the study. Studies by immunofluorescence and immunoelectron microsco
py showed that the distribution of each protein in the kidney was comp
lementary to each other in most parts. MCP and HRF20 were clearly seen
in the glomerular capillaries, while DAF was only faintly observed. J
uxtaglomerular apparatus was abundant in DAF and MCP but not in HRF20.
HRF20 was most strongly expressed in the peritubular capillaries wher
e MCP was not detectable. Basolateral membranes of the proximal tubule
s and collecting ducts expressed MCP strongly, while there was no expr
ession of DAF in the proximal tubules. Interestingly, both DAF and MCP
, which inhibit complement activation at C3/C4 level, were not express
ed in the apical portion of the tubular cells including proximal tubul
e brush border. In contrast, HRF20 was expressed on the apical part of
the tubules. Medullary interstitium strongly expressed MCP but not DA
F. Based on these observations, we conclude that each segment of the k
idney is protected from the complement attack by the different combina
tion of complement regulatory proteins. We speculate that the tubular
cells might be fragile when complements are activated inside the tubul
ar lumen, because there is no expression of complement regulatory prot
eins which inhibit C3 convertase.