Abstract
Sera from patients with steroid-sensitive nephrotic syndrome (SSNS) in relapse, Henoch-Schonlein purpura with nephritis (HSP) and acute post-strptococcal glomerulonephritis inhibited EAC rosette formation by normal human lymphocytes; a similar effect was seen in some patients with focal glomerulosclerosis, but not in patients with congenital neophrotic syndrome. There was significantly less inhibition by sera of SSNS and HSP patients in remission. There were fewer EAC rosette-forming cells (EAC-RFC) in the blood of three patients with SSNS in relapse, suggesting that such blockade occurred in vivo. These findings, interpreted as evidence of circulating activated C3 in the sera, provide further indirect evidence of the immunopathogenesis of these diseases. Sera of healthy adults inhibited EAC rosette formation to a small extent which correclated inversely with the numbers of EAC-RFC in their blood. The EAC rosette inhibition test may be sensitive enough to detect normal variations of complement activation in healthy individuals.
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