Abstract
Abstract Nephritic factor (C3NeF) occurring in the serum of patients with hypocomplementemic chronic glomerulonephritis is known to activate complement via the alternate pathway. Addition of isolated C3NeF to normal serum resulted in assembly of the membrane attack mechanism of complement, the stable 22.5S C5b-9 complex. In the presence of normal serum C3NeF caused lysis of erythrocytes from patients with paroxysmal nocturnal hemoglobinuria or of glutathione-treated normal human erythrocytes. The extent of cell lysis was proportional to the amount of C3NeF employed. Sera from patients with hypocomplementemic chronic nephritis containing C3NeF were shown to be hemolytically inactive because of lack of C3. Cell lysis induced by C3NeF ensued upon addition of isolated C3 to nephritic sera. The results show that C3NeF is capable of initiating cell injury through activation of the alternate pathway, and that the impairment of this pathway in C3NeF-containing sera is due to C3 deficiency. Lysis of glutathione-treated erythrocytes initiated by C3NeF may be used as an alternative assay for C3NeF.
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