New Therapies in IgA Nephropathy
Brad Rovin, MD, outlines the use of complement inhibitors as an alternative to systemic glucocorticoids for the treatment of IgAN.
EP: 1.Disease Progression of IgA Nephropathy
EP: 2.Foundational Therapies in IgA Nephropathy
EP: 3.Interrupting Disease Progression of IgA Nephropathy
EP: 4.New Therapies in IgA Nephropathy
EP: 5.Dual Inhibition of BlyS and APRIL in IgA Nephropathy
EP: 6.Clinical Trial Results From Emerging Therapies in IgA Nephropathy
EP: 7.Use of Povetacicept in Treatment of IgA Nephropathy
EP: 8.The Future of IgA Nephropathy Treatment
This is a video synopsis/summary of a panel discussion involving Jonathan Barratt, PhD, FRCP, and Brad Rovin, MD.
In this discussion between Jonathan Barratt, PhD, FRCP, and Brad Rovin, MD, the focus shifts to the emerging therapeutic options for IgA nephropathy (IgAN). Dr Barratt highlights the excitement around a new class of anti-inflammatory drugs targeting various proteins within the cascade, including small molecules, biologics, and renin-angiotensin-aldosterone system (RAAS) interfering therapies. However, it's emphasized that these drugs are not yet approved but have shown promising data in clinical trials.
Dr Rovin provides insights into the decision-making process for incorporating complement inhibitors into the treatment regimen for IgAN patients. He discusses scenarios where, despite using renin-angiotensin-aldosterone system inhibition and other therapies to control IgA, a patient presents with a fairly inflammatory kidney picture. In such cases, where inflammation is significant, the current approach involves a defined and short-term use of systemic glucocorticoids. However, Dr Rovin expresses optimism about complement inhibitors, citing early-phase trials that demonstrate favorable effects, such as rapid reductions in proteinuria with minimal side effects.
The complement inhibitors offer a more targeted approach to inflammation, potentially eliminating the need for prolonged systemic glucocorticoid use. Dr Rovin emphasizes the importance of developing complement-associated biomarkers to identify patients with high complement activation, providing a more personalized and precise treatment approach.
The conversation shifts to the need to address the root cause of IgAN, focusing on the production of pathogenic IgA. Traditional B cell depletion therapies like rituximab showed little efficacy in targeting pathogenic IgA production in previous trials. However, Dr Barratt notes that new classes of drugs have transformed the landscape, offering renewed hope for managing IgAN more effectively.
The discussion anticipates a future where a combination of complement inhibitors and therapies targeting pathogenic IgA production could provide a comprehensive and personalized treatment strategy for IgAN patients.
Video synopsis is AI-generated and reviewed by HCPLive editorial staff.
