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Treatments have historically relied on optimized supportive care aimed at controlling blood pressure and reducing proteinuria through blockading of the renin-angiotensin system and inhibition of the sodium glucose cotransporter 2. Growing insights into immune dysregulation, mucosal immunity, complement activation, and maladaptive hemodynamic responses have facilitated the development of multiple disease-targeting therapies for IgAN. These include agents that modulate mucosal immune responses, inhibit APRIL (a proliferation-inducing ligand) and BAFF (B-cell activating factor) signaling, block complement activation, or target endothelin-mediated pathways. Several of these therapies have shown promising antiproteinuric and kidney-protective effects in clinical trials. 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