Lupus anticoagulants, autoantibodies to phospholipids, long thought to represent clinically irrelevant inhibitors of in vitro coagulation tests, are now strongly linked to in vivo thrombotic events, to thrombocytopenia, and to recurrent abortions. Patients with these problems may not have signs, symptoms, or serological evidence of classic systemic lupus erythematosus. Such patients can present with retinal arterial or venous occlusion to ophthalmologists, with stroke to neurologists, with thrombocytopenia to hematologists, with fetal wastage to obstetricians, or with peripheral venous thrombosis or arterial occlusive disease to general physicians. Lupus anticoagulants have also been correlated with glomerular thrombosis, infarction, and subsequent glomerular sclerosis, providing a pathogenetic mechanism for renal damage in addition to that mediated by immune-complex deposition.1 The activated partial thromboplastin time is prolonged in the presence of plasma containing lupus anticoagulants, and such prolongation is not corrected by the addition of an equal quantity of normal plasma. The prolongation of