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The understanding how complement relates to glomerular diseases has
evolved considerably during the last years. Substantial evidence
has accumulated that explain how a defective or deregulated
complement system results in kidney diseases. The combination and
close interaction of basic research with clinical medicine has
demonstrated an important role of complement effector and
regulatory proteins in pathological settings of the kidney. A large
panel of distinct human kidney diseases such as hemolytic uremic
syndrome (HUS), membrano proliferative glomerulonephritis (MPGN),
systemic lupus erythematosus (SLE) and in ischemic reperfusions
injury and transplantation are caused by defective complement
control. Genetic analyses have identified mutations in complement
regulators that are associated with these diseases. Mutations have
been identified in the fluid phase alternative pathway regulator
Factor H and the membrane regulator Membrane Cofactor Protein MCP
(CD46). The functional characterization of the mutant proteins
allows to define the pathophysiological events on a molecular
level. These new concepts and data on disease mechanisms already
allowed to establish new diagnostic and novel promising therapeutic
approaches for several human kidney diseases.
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