In IgA nephropathy (IgAN), kidney biopsy remains necessary for diagnosis, while proteinuria and hematuria continue to provide important—but imperfect—information about disease activity and progression. Proteinuria is an established prognostic marker and treatment endpoint, but it is nonspecific and cannot reliably distinguish active inflammation from chronic damage. Hematuria is also limited by day-to-day variability and a lack of standardized measurement. These limitations underscore why current monitoring often requires integrating clinical, laboratory, and histologic information rather than relying on any single marker.
Growing clinical research is now evaluating biomarkers tied more directly to IgAN pathophysiology, including galactose-deficient IgA1, disease-specific autoantibodies and immune complexes, complement components, BAFF and APRIL, urinary soluble CD163, and markers of kidney inflammation and fibrosis. These candidates could eventually help improve diagnosis and prognosis, refine risk stratification, guide treatment selection, and monitor treatment response. However, none of these novel biomarkers is currently validated and standardized for routine clinical practice. Further research is needed to determine how they should be incorporated into patient care.
Reference: Jain K, Rizk DV. The expanding role of biomarkers in the management of IgA nephropathy. Kidney Int Suppl (2011). 2026 Aug;15(1):37-46. doi: 10.1016/j.kisu.2026.01.004.
