The antiphospholipid syndrome (APS) is characterized by antibodies directed against either phospholipids or plasma proteins bound to anionic phospholipids. Patients with the APS may display a constellation of clinical features including venous and arterial thrombosis, recurrent fetal losses, and thrombocytopenia. This disorder is referred to as the primary APS when it occurs alone; however, it can also be found in association with systemic lupus erythematosus (SLE), other rheumatic diseases, and with certain infections and drugs.
Four types of antiphospholipid antibodies have been characterized:
- Antibodies causing a false positive VDRL
- Lupus anticoagulants
- Anticardiolipin antibodies
- Antibodies to beta2-glycoprotein I
There appears to be a relationship between the isotype and titer of antiphospholipid antibody, and the risk of thrombotic events. Higher titers of IgG antiphospholipid antibody, for example, have been reported to be associated with a greater incidence of thrombotic events .
The kidney is one of the organs that can be compromised in patients with antiphospholipid antibodies (aPL). Renal complications directly resulting from thrombotic events associated with these antibodies include glomerular disease, large vessel renal involvement, and coagulation problems relating to dialysis and renal transplants [2-8].