Renal thrombotic microangiopathy induced by interferon‐α

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Abstract
The interferons (IFN), are a family of glycoproteins with antiviral, antitumour and immunomodulatory activities. IFN‐α is used particularly in the treatment of chronic myeloid leukaemia (CML) and other haematological malignancies, as well as in chronic hepatitis C. Various adverse effects associated with IFN‐α have been reported previously, including cardiac and renal dysfunctions. Hypotension or tachycardia, and more severe cardiac complications such as arrhythmia and congestive heart failure have been reported and are usually reversible after IFN‐α withdrawal [1]. In patients with chronic hepatitis C, IFN‐α therapy is usually not associated with renal side effects. Conversely, in patients receiving high doses of IFN‐α for malignancies, a wide range of renal side effects have been reported, including proteinuria (sometimes in nephrotic range), acute interstitial nephritis, and membranoproliferative glomerulonephritis [2–4]. In some cases, the discontinuation of treatment led to renal function resolution, but irreversible renal failure may occur [5]. Many authors have observed various renal toxicities with IFN‐α therapy, but the incidence of renal complications remains unknown, and the causal link between IFN‐α and thrombotic microangiopathy (TMA) is still underappreciated. We describe two cases of renal TMA in patients receiving IFN‐α for CML. Hypotheses regarding the potential mechanisms underlying this association are discussed.