ArticleClinical and experimental medicine2024
Complement C3a/C3aR and C5a/C5aR deposits accelerate the progression of advanced IgA nephropathy to end-stage renal disease.
Article in Clinical and experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Risk Factors of Disease Progression in IgA Nephropathy: A Systematic Review and Meta-Analysis.Immunity, inflammation and disease · 2026Pooled it
- 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.Clinical and experimental nephrology · 2026Article
- Ultrasensitive Immunoassay Using a Novel Galactose-Deficient IgA1 Antibody and Its Clinical Application in the Diagnosis of IgAN.Kidney international reports · 2026Article
- Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.Frontiers in medicine · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
IgA nephropathy (IgAN) is still one of the leading causes of end-stage kidney disease (ESRD), and complement system activation is a key to the pathogenesis of IgAN. The role of complement C3a/C3aR and C5a/C5aR in late stage of IgAN remains unknown. Renal specimens of 75 IgAN patients at the stage 4 CKD were stained using immunofluorescence and immunohistochemistry. The primary outcome was a composite of end-stage renal disease (ESRD) and death. Associations of complement components with baseline clinicopathological characteristics and outcomes were assessed using multivariable Cox regression and Spearman analyses. During a median follow-up of 15.0 months, 27 patients progressed to ESRD and none died. Lower eGFR [hazards ratio (HR), 0.827, 95% confidence interval (CI), 0.732-0.935; P = 0.002] and glomerular C3 deposition (HR, 3.179, 95% CI, 1.079-9.363; P = 0.036) were predictive of time to ESRD in stage 4 CKD IgAN. Higher expression of C3a (P = 0.010), C3aR (P = 0.005), C5a (P = 0.015), and C5aR (P < 0.001) was identified in ESRD group than in non-ESRD group. Glomerular C3a/C3aR and C5a/C5aR deposits were both correlated with a lower baseline eGFR, higher baseline 24 h-urinary protein (24 h-UP) and faster decline of eGFR. Besides, C3a and C5a deposits were found in patients with high S (S1) and T (T1/2) scores, respectively. Complement C3a/C3aR and C5a/C5aR in IgAN patients with stage 4 CKD may portend a faster deterioration of kidney function.
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