ANCA-associated vasculitis: a phase-oriented therapeutic framework from immunopathology to precision treatment.

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides are rare, severe autoimmune diseases characterized by necrotizing small-vessel inflammation, heterogeneous organ involvement, and a substantial burden of relapse, damage, and treatment-related toxicity. Although their management has traditionally been framed around the dichotomy between remission induction and maintenance, this model does not fully capture the dynamic immunopathological transitions that occur across the disease course. In this review, we propose a phase-oriented therapeutic framework that integrates disease stage, dominant pathogenic mechanisms, organ-specific risk, and unmet clinical needs to support a more precise and clinically actionable approach to treatment. Within this model, the induction phase is focused on rapid control of active inflammation and prevention of irreversible organ damage, with treatment intensity increasingly informed by clinical severity, renal histopathology, complement activation, ANCA specificity, and patient-level vulnerability to toxicity. The consolidation phase represents a biologically active post-induction window in which clinical remission must be stabilized, residual autoreactive immune circuits further suppressed, and glucocorticoids tapered. Rituximab-based strategies exemplify this concept by sustaining B-cell depletion after remission induction rather than replacing the pathogenic target with non-specific immunosuppression. The maintenance phase is then reframed as a period of individualized surveillance, relapse prevention, toxicity minimization, and selective de-escalation. For eosinophilic granulomatosis with polyangiitis, a purely phase-based model is insufficient, and treatment should also account for the relative contribution of eosinophilic inflammation and autoimmune vasculitis, although it should not be reduced to ANCA status alone. Overall, this framework shifts AAV management from a rigid induction-maintenance sequence toward a mechanism-based strategy aimed at matching therapeutic ambition to immunopathology, evidence strength, and patient-specific risk.