Glomerulonephritis complement levels

Serum complement levels are often decreased in patients with PSGN in whom hemolytic complement activity and C3 levels are reduced in more than 90% of the patients for 4 to 6 weeks. If the C3 level is depressed for more than 6 to 8 weeks, MPGN, lupus nephritis, or glomerulonephritis related to endocarditis or occult visceral abscess should be suspected. 

Serum complement levels are useful to distinguish between various forms of acute nephritis that may be due to either a primary renal disorder or a systemic disease. Glomerular diseases associated with decreased complement levels include systemic diseases such as systemic lupus erythematosus, subacute bacterial endocarditis, and cryoglobulinemia, and renal diseases such as acute poststreptococcal glomerulonephritis. Glomerular diseases in which serum complement levels are normal include systemic diseases such as Goodpasture s syndrome and renal diseases such as IgG-IgA nephropathy, antiglomerular basement membrane disease, and immune-complex disease. 

Herman [67] published a case report of a patient with hairy cell leukemia who developed membrano-prohferative glomerulonephritis during treatment with IFN-a. He developed hematuria, pyuria, and depressed complement levels. Renal biopsy revealed foot process effacement and subendothelial deposits. 

Type III hypersensitivity is due to the presence of elevated levels of antigen-antibody complexes that deposit on basement membranes in tissues and vessels. Immune complex deposition activates complement to produce components with anaphylatoxic and chemotactic activities (C5a, C3a, C4a) that increase vascular permeability and recruit neutrophils to the site of complex deposition. Complex deposition and the action of lytic enzymes released by neutrophils can cause skin rashes, glomerulonephritis, and arthritis in these individuals. If patients have type III hypersensitivity against a particular antigen, clinical symptoms usually occur 3-4 days after exposure to the antigen. 

---