Japanese Researchers Identify CFHR1 as Critical Biomarker for Diagnosing and Tracking IgA Nephropathy

Fujita Health University researchers discover that CFHR1 levels in immune complexes can diagnose IgA nephropathy and track treatment success.

By: AXL Media

Published: Mar 30, 2026, 10:34 AM EDT

Source: Information for this report was sourced from Fujita Health University

Unraveling the Molecular Drivers of Glomerular Injury

Immunoglobulin A (IgA) nephropathy remains a leading cause of chronic kidney disease worldwide, characterized by the buildup of IgA-containing immune complexes (IgA-ICs) in the kidney's filters. Despite its prevalence, the specific molecular components that drive inflammation and eventual organ failure have remained partially obscured. To address this, Professor Kazuo Takahashi and his team at Fujita Health University conducted a comprehensive proteome study. By analyzing kidney tissues and isolated immune complexes, the researchers sought to identify actionable therapeutic targets that could provide a safer alternative to systemic corticosteroid therapy, which often carries significant side effects.

The Role of the Complement Pathway in Kidney Inflammation

The study’s findings highlight a significant overexpression of complement pathway proteins in the glomeruli of IgAN patients. Specifically, the researchers identified a cluster of proteins—including CFHR1, CFHR2, CFHR3, and CFHR5—that were present at much higher levels than in healthy kidney segments. These proteins are part of the body's innate immune system, and their presence suggests that the "alternative" complement pathway is being triggered prematurely. Professor Takahashi speculates that exposure to mucosal microbial antigens may cause these proteins to bind to IgA, catalyzing the formation of the destructive immune complexes that lodge in the kidney.

CFHR1 as a Dynamic Marker for Treatment Response

One of the study's most significant longitudinal findings is the behavior of CFHR1 during treatment. While total serum levels of the protein remained relatively stable, the concentration of CFHR1 specifically within circulating IgA immune complexes dropped significantly after two years of immunosuppressive therapy. Conversely, patients receiving only supportive care showed no such change. This distinction suggests that CFHR1 is not just a static marker for the presence of the disease, but a dynamic indicator that reflects whether a specific treatment is successfully disrupting the underlying autoimmune process.