CORRELATIONS BETWEEN SERUM FACTOR-B AND FACTOR-C3B INACTIVATOR LEVELS IN NORMAL SUBJECTS AND IN PATIENTS WITH INFECTIONS, NEPHROSIS AND HYPOCOMPLEMENTEMIC GLOMERULONEPHRITIS

  • 1 January 1977
    • journal article
    • research article
    • Vol. 28  (1) , 61-71
Abstract
In normal subjects factor B and C3b [b fragment of the 1st complement component] inactivator (KAF) levels were linearly related (r [correlation coefficient] = 0.71); factor B levels in subjects with low normal levels of KAF were significantly lower than in those with high normal levels of KAF. This relationship is probably due to modulation by the level of KAF of the availability of nascent, spontaneously formed, C3b, in turn responsible for a constant low-grade activation of the C3b feedback which determines in part the level of factor B. This correlation was not obtained in patients with infections; levels of KAF and, to a greater extent, factor B were elevated. In patients with glomerulonephritis and hypocomplementemia (due to in vivo classical pathway activator), KAF and factor B levels were also poorly correlated, presumably because many factors influenced the levels of these proteins transcending the modulating effect of the concentration of KAF. In patients with nephrosis and with type 2 MPGN [membranoproliferative glomerulonephritis], KAF and factor B levels were low but were directly correlated. In nephrosis the correlation may be the combined result of an equal rate of catabolism of these proteins and of modulation of factor B levels by the level of KAF as in normal subjects. In type 2 MPGN, the correlation may reflect the fact that with alternative pathway activation, the level of KAF influences the extent of factor B and C3 conversion to a greater extent than when complement is activated by the classical pathway.