.
Uncertainty of measurement: C3 6%,
C4 8%.
| Age Range | Either Sex |
|---|---|
| All | 0.2 - 0.6[1] 0.8 - 1.8[2] |
C4
C3
C3 and C4 levels would be expected to be raised in systemic inflammatory response, usually up to twice their resting levels. In this setting a normal or low level may reflect utilisation, such as in an overwhelming infection. C4 levels will be depressed if utilisation by the classical pathway (e.g. in immune complex disease such as SLE and vasculitis associated with rheumatoid arthritis) exceeds production. C4 levels are low in patients with C1 inhibitor deficiency, and may be absent during an attack - normal levels effectively exclude the diagnosis. Low C3 reflects activation of either the classical or alternate pathways. Low C3 with a normal C4 occurs with isolated alternative pathway activation (e.g. type II mesangiocapillary GN, due to production of an autoantibody (C3 nephritic factor) that activates this pathway directly).
Complement pathways (classical, alternative and the newly discovered lectin pathway) are measured by an ELISA that activates each specific pathway. The activity is detected by a labelled monoclonal antibody to C5-C9 complex (MAC). The main use of complement pathways is to detect either primary or secondary complement deficiency. Homozygous deficiency of an individual component will result in an absence of the affected pathway. In secondary deficiency, complement pathways can be used to monitor disease activity.
Associate Professor Rohan Ameratunga , Immunopathologist: Ext 22106 Locator 93-5724
If the delay between taking the specimen and arrival in the testing laboratory is going to be greater than 2 days, The sample is required to be stored at -20 o C immediately after collection and transported frozen to the laboratory . Heparin samples need to be spun and the plasma separated prior to freezing.