Conversations in Nephrology: Treating FSGS: From Steroids to Dual Endothelin Angiotensin Receptor Antagonists and What Comes Next

Travere and KDIGO Podcast Collaboration
Conversations in Nephrology: The Podocyte Problem: Understanding FSGS
Episode Summary
In this Travere-sponsored episode of KDIGO Conversations in Nephrology, Dr. Kirk Campbell is joined by Dr. Alessia Fornoni for an in-depth discussion on focal segmental glomerulosclerosis (FSGS), from its etiological classifications to a more precise clinical and molecular understanding.
The conversation covers the definition and pathogenesis of FSGS, its evolving understanding as a podocytopathy driven by podocyte injury, as well as clinical management and the future of treatment.
The episode also explores the role of endothelin-1 (ET-1) and angiotensin II (Ang II) signaling in disease progression, alongside insights into how targeted therapies may help preserve podocyte function and slow disease progression.
Dr. Alessia Fornoni, MD, PhD University of Miami
Dr. Kirk Campbell, MD (host) – University of Pennsylvania
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Key Takeaways
“Working in tandem with endothelin-1, angiotensin II can even induce endothelin-1 and amplify the effect of endothelin-1, which is one of the reasons why targeting both pathway is biologically current, and it’s plausible.” (7:10)
“So really early recognition matters, because once we lose the podocyte, once we lose the threshold, the sclerosis is irreversible, and the damage continues to accelerate no matter what we do. And this gives us a sense of therapeutic urgency, the need to identify patients early, the need to have the patient on lifelong treatment strategies to reduce the progression of the kidney disease.” (9:37)
- The KDIGO classification enables more precise identification of FSGS etiology, categorizing it as primary, genetic, secondary, or undetermined
- Regardless of etiology, FSGS is a podocytopathy driven by podocyte injury, resulting in increased proteinuria and loss of estimated glomerular filtration rate (eGFR)
- ET-1 and Ang II are key disease mediators and drivers of podocyte injury in FSGS, whose cross-talk creates a self-perpetuating loop of podocyte–endothelial–podocyte signaling, ultimately leading to progressive and irreversible injury
- Early intervention is key to reducing proteinuria and preserving podocyte number, underscoring the urgent need for early identification and lifelong treatment strategies to slow disease progression
- Given the limitations of historical therapies in addressing the underlying podocyte injury in FSGS, emerging treatments targeting the ET-1 and Ang II pathways represent a step forward in disease management
MA-SP-26-0101
Disclaimer: This episode of Conversations in Nephrology was supported by Travere Therapeutics and developed by Kidney Disease: Improving Global Outcomes. The opinions presented are those of the individual speakers and not those of Travere Therapeutics. This podcast episode was published on May 27, 2026. Please always consult updated sources for the latest information, as information discussed may have changed since the recording date.
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