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Published on: July 8, 2020
Hypercomplementemia in adult patients with IgA nephropathy.
Kisara Onda1, Hiroyuki Ohi, Mariko Tamano
1Division of Nephrology, Department of Internal Medicine, School of Medicine, Juntendo University, Tokyo, Japan.
IgA nephropathy (IgAN) shows elevated complement levels and regulatory proteins. C4 binding protein levels can predict IgAN disease prognosis, indicating its role in pathogenesis.
Area of Science:
- Nephrology
- Immunology
- Complement System
Background:
- IgA nephropathy (IgAN) is the leading cause of chronic glomerulonephritis.
- Serological evidence of complement activation in IgAN remains inconclusive.
- The relationship between complement system proteins and IgAN pathogenesis requires further investigation.
Purpose of the Study:
- To investigate serum levels of complement components and regulatory proteins in IgAN patients.
- To explore correlations between complement factors and IgAN clinical gradings.
- To determine the prognostic value of complement C4 binding protein in IgAN.
Main Methods:
- Serum samples from 50 IgAN patients and 50 healthy controls were analyzed.
- Complement components (C5, C1 inhibitor, factor B, C4 binding protein, factor H, factor I, MBL, P) were quantified using single radial immunodiffusion and ELISA.
- Correlations between complement levels and IgAN prognosis groups were evaluated.
Main Results:
- IgAN patients exhibited significantly higher levels of CH50, C4, factor B, properdin, factor I, and factor H compared to controls.
- Significant correlations were observed between C5 and C4 binding protein, C3 and C5, and C4 and factor B in IgAN patients.
- Elevated C4 binding protein levels were notably higher in the poor prognosis group of IgAN patients.
Conclusions:
- Hypercomplementemia is present in IgA nephropathy and linked to increased complement regulatory proteins.
- Complement C4 binding protein serves as a potential biomarker for predicting IgAN disease progression.
- These findings highlight the involvement of the complement system in IgAN pathogenesis and prognosis.
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