OBJECTIVES: I. Determine whether allelic differences associated with the fourth component of
complement, type-1 complement receptor expressed on erythrocytes, and Fc receptor FcgRIII
contribute to the pathogenesis of IgA glomerulonephritis (IgA-N).
II. Compare genetic anomalies of these key components in immune complex processing and
clearance between juvenile vs adult onset IgA-N vs normal controls.
Participants undergo qualitative genetic analysis of complement-related proteins. Studies
include: genomic re-arrangement of 4-gene unit, C4 DNA sequence and RNA expression, type-1
complement receptor DNA sequence, Fc-gamma receptor IIIA isoform analysis, classical and
alternative complement activation pathway assays, plasma C4 and C4d protein levels, and
immunoglobulin patterns in glomerular deposits.