| Microvascularmanifestations |
| Renal (aPL nephropathy) |
| Acute—thrombotic microangiopathy |
| Chronic (ie, fibrous intimal hyperplasia, focal cortical atrophy, tubular thyroidization, glomerular ischemia, interstitial fibrosis, tubular atrophy, organized thrombi with or without recanalization) |
| Pulmonary (diffuse alveolar hemorrhage) |
| Cardiac (microvascular disease) |
| Dermatologic (livedo with/without skin ulcers) |
| Nonthromboticmanifestations |
| Thrombocytopenia |
| Immune mediated |
| Thrombotic microangiopathy related |
| Hemolytic anemia |
| Immune mediated |
| With schistocytes and thrombotic microangiopathy |
| Cardiac valve vegetations or thickening |
| Neurologic* |
| Cognitive dysfunction in the absence of stroke |
| Subcortical white matter changes |
| Microvascularmanifestations |
| Renal (aPL nephropathy) |
| Acute—thrombotic microangiopathy |
| Chronic (ie, fibrous intimal hyperplasia, focal cortical atrophy, tubular thyroidization, glomerular ischemia, interstitial fibrosis, tubular atrophy, organized thrombi with or without recanalization) |
| Pulmonary (diffuse alveolar hemorrhage) |
| Cardiac (microvascular disease) |
| Dermatologic (livedo with/without skin ulcers) |
| Nonthromboticmanifestations |
| Thrombocytopenia |
| Immune mediated |
| Thrombotic microangiopathy related |
| Hemolytic anemia |
| Immune mediated |
| With schistocytes and thrombotic microangiopathy |
| Cardiac valve vegetations or thickening |
| Neurologic* |
| Cognitive dysfunction in the absence of stroke |
| Subcortical white matter changes |
Due to multiple mechanisms, including small vessel ischemic events and the direct pathogenic role of aPL.