Authors
Guido Gembillo, Chiara Casuscelli, Alberto La Spada, Ylenia Di Pietro, Giulia Cipressa, Domenico Santoro, Claudia Lo Re
Published in
Expert opinion on pharmacotherapy. Jul 29, 2026. Epub Jul 29, 2026.
Abstract
FSGS is a histological convergence point for biologically distinct conditions: primary immune-mediated, genetic, and secondary adaptive forms, each with its own pharmacological logic. ACE inhibitors and angiotensin receptor blockers have anchored its management for three decades on evidence drawn predominantly from non-FSGS populations.
Experimental and clinical literature from PubMed/MEDLINE, Embase, and Web of Science through 30 January 2026, covering angiotensin II - mediated podocyte injury, RAAS pharmacology across FSGS subtypes, and emerging strategies that extend or layer upon the RAAS backbone, including dual AT1/endothelin-A blockade, SGLT2 inhibition, and mineralocorticoid receptor antagonism, with additional podocyte-targeted and genotype-guided approaches.
The clinical benefit of RAAS blockade appears to vary across FSGS subtypes. It likely targets a key pathogenic mechanism in secondary adaptive forms, while serving mainly as supportive antiproteinuric therapy in immune-mediated and genetic disease. Nonetheless, it remains a cornerstone of care.Emerging therapies, including dual AT1/endothelin-A antagonism (sparsentan) and podocyte-targeted approaches (apecotrep), show promising proteinuria reductions but have not yet demonstrated clear benefits on hard renal outcomes. Biomarker-driven strategies (e.g. anti-nephrin antibodies, APOL1 genotyping) may enable more tailored treatment, although their clinical impact remains to be established.
PMID:
42525818
Bibliographic data and abstract were imported from PubMed on 30 Jul 2026.
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