Educational Symposium
Anti-CD38 Therapies for IgAN: Is Durable Remission Possible?
October 24, 2026 | 12:45 PM - 01:45 PM
Location: TBD Room, Hyatt Regency Denver
Session Description
IgAN remains the most common primary glomerulonephritis worldwide. Disease pathogenesis is driven by overproduction of galactose-deficient IgA1 (Gd-IgA1) and formation of pathogenic immune complexes, leading to mesangial inflammation and progressive kidney fibrosis. Emerging data identify CD38+ plasma cells as key upstream contributors to this process through production of Gd-IgA1 and anti-Gd-IgA1 antibodies. CD38, highly expressed on long-lived plasma cells, has a central role in B-cell activation, differentiation, and antibody secretion. Early clinical experience with anti-CD38 monoclonal antibodies has demonstrated rapid and durable reductions in Gd-IgA1 levels and proteinuria, supporting the potential of plasma cell-directed strategies as disease-modifying approaches in IgAN.
Important questions remain, however, regarding the mechanistic role of CD38 in IgAN and how CD38-targeted therapies differ from and may complement existing approaches such as corticosteroids, endothelin inhibition, complement blockade, and APRIL and BAFF inhibition. As the therapeutic landscape expands, clarifying the biologic rationale for targeting CD38 and interpreting the emerging clinical evidence supporting this pathway in the context of other available and investigational therapies become increasingly important. This symposium provides a focused overview of CD38 biology in IgAN, highlights ongoing clinical trials of anti-CD38 agents, and examines how plasma cell-directed therapies may fit within the evolving treatment paradigm as these agents advance toward clinical availability.
Seating is limited and available on a first-come, first-served basis to fully paid Annual Meeting participants. Doors open approximately 15 minutes prior to each symposium. When a room reaches capacity, ASN will shut down access to the room. No other participants will be allowed to enter the room, regardless of the number of participants who exit the room during the activity.
Support is provided by an educational grant from Takeda Pharmaceuticals U.S.A., Inc.
Learning Objective(s)
- Describe the pathophysiologic role of CD38+ plasma cells in IgAN, including their contribution to Gd-IgA1 production and to pathogenic immune complex formation
- Compare CD38-directed therapies with existing and investigational treatments for IgAN in terms of mechanism of action, depth of immunologic control, and potential clinical positioning
- Discuss emerging clinical data on anti-CD38 therapies for IgAN, including effects on Gd-IgA1 levels, proteinuria, and potential disease modification
Learning Pathway(s)
- Glomerular Diseases
- Kidney Biology and Physiology
Moderator
Presentations
- Introduction
12:45 PM - 12:55 PM
- CD38 and Plasma Cells in IgAN: Pathogenesis to Therapeutic Target
12:55 PM - 01:15 PM
- Clinical Rationale, Emerging Data, and Clinical Context for CD38-Directed Therapy in the Evolving Landscape of IgAN Therapies
01:15 PM - 01:35 PM
- Q&A
01:35 PM - 01:45 PM