Complement deficiency is an immunodeficiency of absent or suboptimal functioning of one of the complement system proteins. Because of redundancies in the immune system, many complement disorders are never diagnosed. Some studies estimate that less than 10% are identified. Hypocomplementemia may be used more generally to refer to decreased complement levels, while secondary complement disorder means decreased complement levels that are not directly due to a genetic cause but secondary to another medical condition. Signs and symptoms
The following symptoms (signs) are consistent with complement deficiency in general:

Complications
Vaccinations for encapsulated organisms (e.g., Neisseria meningitidis and Streptococcus pneumoniae)  is crucial for preventing infections in complement deficiencies. Among the possible complications are the following:

Deficiencies of the terminal complement components increases susceptibility to infections by Neisseria. Causes
The cause of complement deficiency is genetics (though cases of an acquired nature do exist post infection). The majority of complement deficiencies are inherited as autosomal recessive conditions, while properdin deficiency occurs through X-linked inheritance. MBL deficiency can be inherited by either manner. Inherited
Properdin deficiency is an X-linked disorder that also causes susceptibility to Neisseria infections. C1-inhibitor deficiency or hereditary angioedema will have low C4 with normal C1 levels. Acquired
Acquired hypocomplementemia may occur in the setting of bone infections (osteomyelitis), infection of the lining of the heart (endocarditis), and cryoglobulinemia. Systemic lupus erythematosus is associated with low C3 and C4. Membranoproliferative glomerulonephritis usually has low C3. Mechanism
The mechanism of complement deficiency consists of:

C2: In regard to C2 deficiency, about 5 different mutations in the C2 gene are responsible.
It may develop several days or weeks later in premature babies.The rash has a variable appearance, ranging from a few blotchy red spots to many yellow-white bumps and boils. The classic presentation is 1–3 mm, firm, yellow-white bumps with a surrounding red halo. The rash is often described as "flea-bitten." There may be only a few or many lesions, and they may be clustered or widespread. The rash often appears on the cheeks first and may later spread throughout the face, trunk, arms, and legs. Lesions most often appear on the thighs, buttocks, and trunk. The palms and soles are not affected, likely because the skin in these areas does not have hair follicles.Individual lesions may grow and shrink over hours or days. They usually fade within a week or two. The rash may recur within the next few weeks, but this is rare. Cause
Erythema toxicum neonatorum is related to activation of the immune system, but its exact cause is unknown. Many inflammatory factors have been detected in erythema toxicum neonatorum lesions, including IL-1alpha, IL-1beta, IL-8, and eotaxin. These molecules cause redness and swelling in the skin and attract immune cells.Eosinophils and other immune cells are found in the upper layer of the skin in erythema toxicum neonatorum lesions. Immune cells tend to cluster around hair follicles in particular. The leading hypothesis about the cause of erythema toxicum neonatorum is that bacteria activate the immune system when they enter hair follicles for the first time.