Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Found 1 result for Related Articles by Review for PMID: 39536144
Filters applied. Clear filters
Book

C3 Glomerulopathy

Gashu Ayehu  1 , Mohammad Atari  2 , Mohamed Hassanein  2 , Kenar D. Jhaveri  3
In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan.
.
Affiliations
Free Books & Documents
Book

C3 Glomerulopathy

Gashu Ayehu et al.
Free Books & Documents

Excerpt

A consensus report in 2013 defined the term C3 glomerulopathy (C3G) to describe a group of glomerular disorders resulting from dysregulation of the complement system's alternative pathway. This condition is characterized by the dominant deposition of C3 in the glomerulus without or with scant immunoglobulin deposition. C3G encompasses 2 major subtypes—C3 glomerulonephritis (C3GN) and dense deposit disease (DDD)—based on different patterns of C3 deposition on electron microscopy. C3GN comprises about 66% of cases and DDD about 33%. Previously, these disease processes were often classified as types of membranoproliferative disease. Clinical manifestations of both can include features of both nephritic and nephrotic syndromes.

C3 glomerulopathy involves intricate complement system dysregulation. A solid understanding of the alternative complement pathway, how it differs from other complement-mediated diseases, and the role of genetic mutations or autoantibodies is essential for accurate diagnosis and management. The diagnosis of C3 glomerulopathy requires the use of advanced diagnostic tools, such as studies for autoantibodies to complement system components, genetic identification of essential complement proteins and regulatory proteins, and histologic analysis of kidney tissue.

PubMed Disclaimer

Conflict of interest statement

Disclosure: Gashu Ayehu declares no relevant financial relationships with ineligible companies.

Disclosure: Mohammad Atari declares no relevant financial relationships with ineligible companies.

Disclosure: Mohamed Hassanein declares no relevant financial relationships with ineligible companies.

Disclosure: Kenar Jhaveri declares no relevant financial relationships with ineligible companies.

Similar articles

See all similar articles

References

    1. Schena FP, Esposito P, Rossini M. A Narrative Review on C3 Glomerulopathy: A Rare Renal Disease. Int J Mol Sci. 2020 Jan 14;21(2) - PMC - PubMed
    1. Smith RJH, Appel GB, Blom AM, Cook HT, D'Agati VD, Fakhouri F, Fremeaux-Bacchi V, Józsi M, Kavanagh D, Lambris JD, Noris M, Pickering MC, Remuzzi G, de Córdoba SR, Sethi S, Van der Vlag J, Zipfel PF, Nester CM. C3 glomerulopathy - understanding a rare complement-driven renal disease. Nat Rev Nephrol. 2019 Mar;15(3):129-143. - PMC - PubMed
    1. Wooden B, Nester CM, Bomback AS. Update on C3 Glomerulopathy. Adv Kidney Dis Health. 2024 May;31(3):223-233. - PubMed
    1. Ponticelli C, Calatroni M, Moroni G. C3 glomerulopathies: dense deposit disease and C3 glomerulonephritis. Front Med (Lausanne) 2023;10:1289812. - PMC - PubMed
    1. Tarragon Estebanez B, Bomback AS. C3 Glomerulopathy: Novel Treatment Paradigms. Kidney Int Rep. 2024 Mar;9(3):569-579. - PMC - PubMed

Publication types

LinkOut - more resources