Abstract

Antineutrophil cytoplasmic autoantibody (ANCA)-associated renal vasculitis usually manifests as a rapidly progressive glomerulonephritis, with pauci-immune necrotizing, crescentic glomerulonephritis on biopsy. The current therapeutic approach for remission induction is the same as for other systemic vasculitides: cyclophosphamide with high-dose glucocorticoids, with a reported effectiveness ranging from 70% to 90% but associated with high rates of severe adverse events, including death. This has led to the use of other therapies that may be as effective and perhaps less toxic. Cyclophosphamide plus glucocorticoids has long been established as the gold standard therapy for remission induction in severe ANCA-associated vasculitis. Its use is followed by better outcomes in severe disease, including mortality rates and remission in some cases [1]. However, as in most autoimmune disorders, an important number of patients do not respond adequately to standard therapy, most likely secondary to the complex role of the immune system in triggering disease. During the past few years, several papers have shown positive results for rituximab as treatment for patients with refractory vasculitis, especially Wegener’s granulomatosis (WG). These results seem to confirm that B cells play an important role in disease pathogenesis. With this in mind, Stone et al. compared rituximab with cyclophosphamide in patients with ANCAassociated vasculitis.

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