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An Efficient Sieving Method to Isolate Intact Glomeruli from Adult Rat Kidney
Published on: November 1, 2018
Update on crescentic glomerulonephritis
Carole Hénique1, Christina Papista, Léa Guyonnet
1Paris Cardiovascular Centre - PARCC, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France.
Insights
Extracapillary glomerulonephritis involves immune complex deposits and inflammation. Recent advances focus on immune cell interactions and mediators driving crescent formation in kidney diseases.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Extracapillary glomerulonephritis results from diverse immunological disorders.
- Pathological mechanisms include immune complex deposition, microvascular injury, and inflammation.
- Key mediators involve proinflammatory cytokines, neutrophil extracellular traps (NETs), and cell adhesion molecules.
Purpose of the Study:
- To review recent advancements in understanding crescentic glomerulonephritis.
- To focus on the interplay of local immune cells and mediators in crescent formation.
- To highlight mechanisms particularly relevant to anti-glomerular basement membrane (anti-GBM) antibody disease.
Main Methods:
- Literature review of recent scientific publications.
- Synthesis of findings on immune cell interactions and mediator roles.
- Focus on pathomechanisms in crescentic glomerulonephritis.
Main Results:
- Progress has been made in understanding the immunological underpinnings of extracapillary glomerulonephritis.
- Local immune cells and mediators significantly contribute to the formation of glomerular crescents.
- Insights into anti-GBM antibody disease pathogenesis are highlighted.
Conclusions:
- Recent research has elucidated key pathways in crescentic glomerulonephritis.
- Understanding these pathways is crucial for developing targeted therapies.
- The review provides a foundation for broader applications in various glomerulonephritis causes.
Abstract:
The recent years have seen a number of major progresses in the field of extracapillary glomerulonephritis. This entity is the final damage caused by unrelated immunological disorders such as immune complexes glomerular deposits or microvascular injury caused by proinflammatory cytokines, neutrophil extracellular traps (NET), and cell adhesion molecules in the context of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). This review provides a summary of recent advances in the understanding of crescentic glomerulonephritis, focusing on interplays of local immune cells and on local mediators participating to crescent formation especially in anti-glomerular basement membrane (anti-GBM) antibody disease. The recent advances about AAV and lupus nephritis are covered by other chapters of this issue. Nevertheless, these considerations may apply to the general case of crescentic glomerulonephritis of all causes.
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