Digital Ischemia as a Rare Manifestation of C3 Glomerulopathy Associated With Monoclonal Gammopathy

Abstract

C3 glomerulopathy (C3GP) is a group of rare glomerular diseases histologically characterized by isolated or predominant C3 deposits within glomeruli associated with glomerular inflammation. Dysregulation of complement alternative pathway was shown to be the cornerstone of their pathogenesis. Patients usually display either rare and pathogenic variants in complement genes implicated in alternative pathway regulation or, more often, autoantibodies interacting with components of this pathway. Some of these antibodies stabilize the activity of C3 or C5 convertase – C3 and C5 nephritic factors (C3NeF and C5NeF) –, while others inhibit regulatory proteins such as complement factor H (CFH).

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BibTeX

@article{baber2026digital,
  title = {{Digital Ischemia as a Rare Manifestation of C3 Glomerulopathy Associated With Monoclonal Gammopathy}},
  author = {Alistair Baber and Paul Legendre and Sophie Chauvet and Alexandre Karras and Samuel Deshayes and Antoine Huart and Marguerite Vignon and Kathleen Dessaix and Baptiste Hervier and Bruno Legallicier and Nicolas Martin Silva and Véronique Frémeaux-Bacchi and Benjamin Terrier},
  journal = {Kidney International Reports},
  year = {2026},
  month = sep,
  doi = {10.1016/j.ekir.2023.12.001},
  url = {https://hal.science/hal-05750610v1},
  note = {CC BY-NC-ND},
}

RIS

TY  - JOUR
TI  - Digital Ischemia as a Rare Manifestation of C3 Glomerulopathy Associated With Monoclonal Gammopathy
AU  - Alistair Baber
AU  - Paul Legendre
AU  - Sophie Chauvet
AU  - Alexandre Karras
AU  - Samuel Deshayes
AU  - Antoine Huart
AU  - Marguerite Vignon
AU  - Kathleen Dessaix
AU  - Baptiste Hervier
AU  - Bruno Legallicier
AU  - Nicolas Martin Silva
AU  - Véronique Frémeaux-Bacchi
AU  - Benjamin Terrier
PY  - 2026
DA  - 2026/09/15
JO  - Kidney International Reports
DO  - 10.1016/j.ekir.2023.12.001
UR  - https://hal.science/hal-05750610v1
AB  - C3 glomerulopathy (C3GP) is a group of rare glomerular diseases histologically characterized by isolated or predominant C3 deposits within glomeruli associated with glomerular inflammation. Dysregulation of complement alternative pathway was shown to be the cornerstone of their pathogenesis. Patients usually display either rare and pathogenic variants in complement genes implicated in alternative pathway regulation or, more often, autoantibodies interacting with components of this pathway. Some of these antibodies stabilize the activity of C3 or C5 convertase – C3 and C5 nephritic factors (C3NeF and C5NeF) –, while others inhibit regulatory proteins such as complement factor H (CFH).
SN  - 2468-0249
ER  -

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