Renal localization of the membrane attack complex in systemic lupus erythematosus nephritis.

G Biesecker, S Katz, D Koffler - Journal of Experimental Medicine, 1981 - rupress.org
G Biesecker, S Katz, D Koffler
Journal of Experimental Medicine, 1981rupress.org
Materials and Methods Tissues. Renal tissue was obtained at autopsy (15 cases) and
biopsy (7 cases) from patients with clinical and laboratory findings that fulfilled the American
Rheumatism Association criteria for SLE (20). SLE renal disease was classified as
mesangial nephropathy (2 cases), focal proliferative glomerulonephritis (7 eases), diffuse
proliferative glomerulonephritis (10 cases), and membranous nephropathy (3 cases). The
categorization of renal disease (21-23) was based on microscopic review of hematoxylin …
Materials and Methods Tissues. Renal tissue was obtained at autopsy (15 cases) and biopsy (7 cases) from patients with clinical and laboratory findings that fulfilled the American Rheumatism Association criteria for SLE (20). SLE renal disease was classified as mesangial nephropathy (2 cases), focal proliferative glomerulonephritis (7 eases), diffuse proliferative glomerulonephritis (10 cases), and membranous nephropathy (3 cases). The categorization of renal disease (21-23) was based on microscopic review of hematoxylin-eosin-and periodic acid-Schiff (PAS)-stained sections of autopsy tissues and renal biopsies performed before reference to the immunofluorescence data. Clinical Data. 20 of 22 patients fulfilled previously described clinical criteria for active renal disease (24). One of two patients classified as mesangial nephropathy exhibited mild proteinuria (< 1 g/24 h) and the second patient had no clinical evidence of renal dysfunction. One of the three patients with membranous nephropathy also had mild proteinuria and two patients had moderate to severe proteinuria (> 3 g protein/24 h). Two patients manifested signs of acute renal failure, but microscopic examination of the kidneys obtained at autopsy did not show evidence of acute tubular necrosis, and no differences were observed between these and other patients with SLE nephritis with respect to interstitial and peritubular mononuclear infiltration. Four patients with diffuse proliferative glomerulonephritis were uremic before death and manifested signs of advanced diffuse proliferative glomerulonephritis on microscopic examination of their kidneys.
Antisera. Monospecific goat antisera to IgG, IgM, C3, and rabbit antisera to Clq (25) and C9 (26) were prepared and labeled with fluorescein (27). Antiserum titers were determined before labeling and expressed as the dilution of serum that produced a reaction of equivalence with 0.2 mg/ml of purified antigen: anti-IgG-1: 5, anti-IgM-1: 1, anti-C3-1: 2, anti-C 1 q-1: 1, and anti-C9-1: 1, using agar gel double diffusion.
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