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To assess the role of circulating immune complexes in the pathogenesis of acute rejection, sera were measured for such complexes by the (125)I-C1(q) binding assay in 45 normal subjects, 24 allografted patients undergoing acute rejection, and in 11 allografted patients in a quiescent phase. Increased C1(q)-binding activity (C1(q)-BA) was detected in 14 patients with acute rejection, 9 of whom had renal biopsies showing fibrin deposition in the vasculature together with cellular infiltrates in the tubulo-interstitial structures; renal histology was not available in the other 5 patients. The other 10 patients with acute rejection, whose biopsies showed only cellular infiltrates, and the 11 patients in a quiescent phase posttransplantation did not have increased levels of serum C1(q)-BA. Of the group with increased serum C1(q)-BA, serial studies in eight patients showed a correlation between increased serum C1(q)-BA and the occurrence of rejection; with reversal by therapy, serum C1(q)-BA returned to within normal levels. Complexes from six patients were analyzed by sucrose density gradient ultracentrifugation to have sedimentation coefficients ranging from 15S to 18.4S. After acid dissociation and analysis by double-diffusion techniques, C1(q)-reactive complexes were shown to contain IgG. Immunofluorescent studies done in five renal biopsies from this group revealed granular deposits of immunoglobulin, and (or) less frequently, of complement in the glomeruli or the tubular basement membranes. The findings suggest that circulating immune complexes may mediate the type of acute rejection characterized by fibrin deposition in the kidney. The role of circulating immune complexes arising from the recipient's original kidney disease could be excluded in 10 patients with humoral rejection, inasmuch as the underlying renal pathology was of a "nonimmunologic" nature; this was corroborated by sequential studies in six patients in whom circulating immune complexes could not be demonstrated before rejection. The participation of administered antilymphocyte globulin (ALG) as an antigen also appears to be excluded in four patients, two who were not given ALG, and in two of whom episodes of rejection occurred unrelated temporally to ALG administration.
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
May 1979,
Nihon Jinzo Gakkai shi,
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
May 1976,
The Journal of clinical investigation,
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
June 1977,
The Journal of clinical investigation,
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
January 1981,
Gastroenterologia Japonica,
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
October 1979,
Nihon Jinzo Gakkai shi,
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
April 1976,
Transplantation,
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
January 1980,
Gastroenterologia Japonica,
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
January 1980,
Scandinavian journal of urology and nephrology. Supplementum,
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
January 1981,
Nephron,
Y M Ooi, and
B S Ooi, and
E H Vallota, and
M R First, and
V E Pollak
April 1979,
Journal of comparative pathology,
