IgA nephropathy (IgAN) is increasingly understood as a B-cell–driven disease in which class-switched B cells, plasmablasts, and plasma cells contribute to production of galactose-deficient IgA1 and the immune complexes that ultimately damage the glomeruli. As therapies targeting immune pathways expand, clinicians may need a stronger understanding of this biology. However, IgAN-specific biomarkers that could guide precision treatment are still lacking, leaving clinicians to base treatment decisions on biopsy findings, proteinuria, hematuria, eGFR, and individual patient factors. Treatment sequencing generally aims to address both immunologic inflammation and kidney protection, although evidence for combination strategies remains limited.
Earlier recognition remains a major opportunity to improve IgAN care. Samir Parikh, MD, emphasized that hematuria—particularly glomerular hematuria—should not be dismissed and advocated for greater use of routine urinalysis and evaluation of potentially secondary causes of hypertension, especially in younger patients. Because IgAN may remain asymptomatic for years, delayed diagnosis can mean patients first reach specialty care at chronic kidney disease stage 3 or 4, after substantial irreversible kidney damage has occurred. Greater awareness among primary care and other frontline clinicians could help identify patients sooner and create opportunities for earlier evaluation and treatment.
Reference: Parikh S. Understanding the B-Cell Pathway in IgA Nephropathy, With Samir Parikh, MD. HCP Live. Published August 17, 2026. Accessed August 20, 2026. https://www.hcplive.com/view/understanding-the-b-cell-pathway-in-iga-nephropathy-with-samir-parikh-md
