Article thumbnail

Elevated urinary excretion of the C5b-9 complex in membranous nephropathy

By Matthias Schulze, James V. Donadio, Charles J. Pruchno, Patricia J. Baker, Richard J. Johnson, Rolf A.K. Stahl, Sandra Watkins, Donald C. Martin, Reinhard Wurzner, Otto Gotze and William G. Couser


Elevated urinary excretion of the C5b-9 complex in membranous nephropathy. In experimental membranous nephropathy, antibody binding to glomerular epithelial cell membrane antigens results in complement activation and formation of complement C5b-9 membrane attack complexes in glomeruli. During active disease, the C5b-9 complexes are shed into the urine. To test the hypothesis that a similar mechanism might be operative in human membranous nephropathy, we measured urinary excretion of C5b-9 and C5 in 146 proteinuric patients with biopsy-proven glomerular diseases or diabetes mellitus. Urinary excretion of C5b-9 relative to C5 excretion was higher in 40 patients with membranous nephropathy than in 106 patients with proteinuria due to non-membranous glomerulonephritis when analyzed by covariance analysis (P < 0.0002). Urinary C5b-9 excretion was higher in membranous nephropathy than in membranoproliferative glomerulonephritis (N = 13, P < 0.05), minimal change-focal sclerosis (N = 33, P < 0.001), mesangial proliferative glomerulonephritis (N = 9, P < 0.02) and IgA nephropathy (N = 7, P < 0.025). Urinary C5b-9 excretion was also higher in patients with lupus nephritis (N = 18, P < 0.02) compared to those with non-membranous glomerulonephritis. The lupus patients with the highest excretion had clinical or pathological features of membranous nephropathy. Nine patients with membranous nephropathy and elevated urinary C5b-9 excretion had a shorter duration of disease (P < 0.05), lower serum creatinine levels (P < 0.05) and more proteinuria (P < 0.02) than the 31 membranous nephropathy patients with normal values. The finding of increased urinary C5b-9 excretion in a subset of patients with idiopathic or lupus membranous nephropathy suggests an autoimmune basis for glomerular disease in these patients, and may indicate that these patients have ongoing immune deposit formation

Publisher: International Society of Nephrology. Published by Elsevier Inc.
Year: 1991
DOI identifier: 10.1038/ki.1991.242
OAI identifier:
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • (external link)
  • https://s3-eu-west-1.amazonaws... (external link)
  • Suggested articles

    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.