Complement and glomerular disease - a natural history study.
Over a 5-year period we have performed sequential measurements of a range of complement components in 127 patients. Each had a well-characterised glomerular lesion and there was no evidence of an underlying connective tissue disorder. In 17 patients with varied histopathology, who did not have C3 nephritic factor, there was a persisting complement defect which was present during remission in the patients we were able to study. The finding of such defects is consistent with the thesis that primary complement system abnormalities predispose to the development of glomerular lesions. Interestingly, these abnormalities did not influence the prognosis of our patients. In 12 other cases without C3 nephritic factor, complement levels were below the normal range when the glomerular lesion was active but returned to it in remission; these were secondary changes. We showed by discriminant analysis that some circulating complement component levels, assessed in relation to each other and without reference to a statistically derived 'normal' range, discriminated between histological subgroups and had prognostic significance as well. These patterns could not be distinguished until the data were stored and analysed by computer.
D000704:Analysis of Variance; D003178:Complement C3 Nephritic Factor / Q000032:analysis; D003179:Complement C3b / Q000172:deficiency; D003165:Complement System Proteins / Q000032:analysis / Q000172:deficiency*; D005921:Glomerulonephritis / Q000276:immunology*; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology / Q000276:immunology; D007678:Kidney Glomerulus / Q000473:pathology; D011507:Proteinuria / Q000503:physiopathology
D003178:Complement C3 Nephritic Factor; D003179:Complement C3b; D003165:Complement System Proteins