ArticleClinical and experimental nephrology2026
Exosomal C3a initiates the NF-κB-dependent inflammatory axis in IgA nephropathy: a three-phase pilot study integrating clinical, in vivo, and in vitro evidence.
Article in Clinical and experimental nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundIgA nephropathy (IgAN) is the most common glomerulonephritis in children. Although exosomes contribute to renal injury, their role in IgAN remains unclear. This pilot study tested whether urinary exosomal C3a normalized to creatinine (uE-C3a/Cr) reflects glomerular injury and activates NF-κB signaling.
methodsWe enrolled 70 children with IgAN, 43 with other glomerulopathies, and 30 healthy controls. After isolating exosomes, we quantified uE-C3a/Cr and assessed correlations with clinical and pathological parameters. In parallel, IgAN model rats were examined for renal exosomal C3a (rE-C3a), NF-κB phosphorylation, and inflammatory cytokines. In vitro, rat mesangial cells were exposed to patient-derived IgAN exosomes, with or without a C3aR antagonist.
resultsuE-C3a/Cr was elevated in IgAN patients, correlating with log24 h-UP (ρ = 0.480, P < 0.001) and Oxford C score (ρ = 0.565, P < 0.001). The AUC for IgAN vs. non-IgAN was 0.637. In follow-up, uE-C3a/Cr decreased in remission patients; at 12 weeks, non-remission patients in the IST group had higher levels than remission patients (P < 0.001). In IgAN rats, rE-C3a was upregulated alongside an enhanced p-p65/t-p65 ratio and elevated MCP-1 and IL-6. Exosomes from IgAN patient urine promoted rat mesangial cell proliferation and enhanced NF-κB phosphorylation and cytokines; these effects were partially reversed by C3aR antagonist.
conclusionsuE-C3a/Cr is not a disease-specific diagnostic marker for IgAN, but may serve as a non-invasive marker for monitoring disease activity and treatment response. Exosomal C3a appears to activate mesangial NF-κB through C3a/C3aR, pointing to C3aR as a therapeutic target in IgAN. Larger cohorts must validate these findings.
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