ArticleScientific reports2025
Serum IgA/C3 ratio as a diagnostic and prognostic biomarker for IgA nephropathy.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- IgA Nephropathy: Mechanisms, Risk Stratification, and Precision Therapy.Diagnostics (Basel, Switzerland) · 2026Review
- Complement biomarkers in IgA nephropathy: current insights and clinical relevance.Frontiers in nephrology · 2026Review
- From immune dysregulation to renal injury: mechanistic insights and translational opportunities in immune-mediated nephropathies.Frontiers in cell and developmental biology · 2026Review
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12 authors.
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Abstract
IgA nephropathy (IgAN) is a common glomerular disease in adults with a smoldering course and high risk of progression to end-stage kidney disease (ESKD) in South Asians. We investigated serum IgA/C3 ratio as a potential biomarker for IgAN. We measured serum levels of IgA and C3 in 258 patients with IgAN and 90 controls with non-IgAN primary glomerular disease and examined if serum IgA/C3 ratio differentiates IgAN from other glomerular diseases and if it predicts renal survival in IgAN. The primary outcome was lack of renal survival, defined as irreversible decline in eGFR > 50% from baseline or progression to ESKD. Median serum IgA/C3 ratio was higher in IgAN patients compared to controls (2.4, IQR: 1.9-3.0 vs. 1.8, IQR: 1.3-2.5, p < 0.001). The AUC for the receiver operating curve of IgA/C3 ratio was 0.6760 (95% CI: 0.6074-0.7446). The sensitivity and specificity of IgA/C3 ratio > 2.0 were 70.5% and 62.2% respectively, for differentiating IgAN from other non-IgAN glomerular diseases. With a median duration of follow-up of 35.0(IQR 16-56.8) months, 26.7% patients reached the primary outcome. Compared to patients with a low IgA/C3 ratio(≤ 2.0), those with a high ratio(> 2.0) were significantly older [median age 34 vs. 29 years, p = 0.003], more likely to have hypertension (70.6% vs. 50.5%, p = 0.001), had lower median eGFR [47.7 mL/min/1.73 m² vs. 77.7 mL/min/1.73 m², p < 0.001], lower urine protein creatinine ratio [2.0 g/g vs. 2.5 g/g, p = 0.015] and a significantly higher proportion of segmental glomerulosclerosis (S1 lesions) (80.4% vs. 62.1%, p = 0.005). Renal disease progression was comparable (26.3% vs. 27.0%, p = 0.906) between the low and high IgA/C3 ratio groups respectively. High IgA/C3 ratio (> 2.0) was not a significant predictor of primary outcome (HR = 1.32 95% CI: 0.80-2.2, p = 0.278). Serum IgA/C3 ratio is elevated in IgAN compared to other glomerular diseases but has limited diagnostic and prognostic utility in our patients.
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