Renal thrombotic microangiopathy associated with interferon-alpha treatment of chronic myeloid leukemia

• Published in: American journal of kidney diseases Vol. 36; no. 1; p. E5
• Main Authors: Magee, C C, Abraham, K, Farrell, J, Dorman, T, Walshe, J J
• Format: Journal Article
• Language: English
• Published: United States 01.07.2000
• Subjects: Antiphospholipid Syndrome - complications; Female; Hemolytic-Uremic Syndrome - complications; Humans; Interferon-alpha - therapeutic use; Kidney - blood supply; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - complications; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy; Microcirculation - physiology; Middle Aged; Thrombosis - complications; Thrombosis - etiology; Thrombosis - immunology
• DOI: 10.1053/ajkd.2000.8302

Recent reports have documented the development of renal thrombotic microangiopathy in patients with chronic myeloid leukemia (CML) who have undergone treatment with interferon-alpha. The pathogenesis of the renal lesion in such cases remains unclear. We report the case of a patient with chronic myeloid leukemia who developed renal failure and nephrotic syndrome while being treated with hydroxyurea and interferon-alpha. The renal biopsy showed features of chronic thrombotic microangiopathy. The patient had serologic and functional evidence of anti-phospholipid antibody. Interferon-alpha is known to cause induction of multiple autoantibodies. We propose that in the context of CML, interferon-alpha treatment can induce pathogenic anti-phospholipid antibodies that result in renal thrombotic microangiopathy. This has important implications for patients with CML receiving immune-stimulating therapy because it suggests that prospective monitoring of such patients for anti-phospholipid antibody might identify those at risk of developing thrombotic microangiopathy. Furthermore, patients with established anti-phospholipid antibody syndrome in this context might benefit from intervention such as early anticoagulation.