Although not completely understood, the primary mechanism of tissue injury in SLE and related autoimmune disease is the formation of antigen–antibody immune complexes. Not all ANAs are pathogenic. For the few that are harmful, pathogenicity depends on the specific immunoglobulin class, ability to activate complement, size of the immune complex, and site of tissue deposition. For example, studies of immune complex–mediated tissue injury in the kidney have shown a clear relation between deposition of immune complexes and glomerular disease.

The anti-dsDNA test is done specifically to identify or differentiate native (i.e., double-stranded) DNA antibodies found in 40%–60% of patients with SLE during the active phase of their disease from other, nonnative DNA antibodies found in other rheumatic diseases. The presence of antibodies to double-stranded DNA (dsDNA) generally correlates with lupus nephritis. An anti-dsDNA test supports a diagnosis, allows monitoring of disease activity and response to therapy, and establishes a prognosis for SLE.

• Negative: <25 IU by ELISA

• Borderline: 25–30 IU

• Positive: 31–200 IU

• Strongly positive: >200 IU

1. Collect a 7-mL blood serum sample in a red-topped tube. Observe standard precautions.

2. Label the specimen with the patient’s name, date, and test(s) ordered and place in a biohazard bag for transport to the laboratory.

1. Anti-dsDNA concentrations may decrease with successful therapy and may increase with an acute recurrence of SLE.

2. DNA–anti-dsDNA immune complexes play a role in SLE pathogenesis through the deposit of these complexes in the kidney and other tissues.

See Antinuclear Antibody (ANA) Test.

1. The Farr assay, a radioimmunoassay (RIA) method, detects both single-stranded DNA (ssDNA) and dsDNA antibodies.

2. Antibodies to ssDNA are nonspecific but are associated with various other rheumatic diseases.