ReviewCurrent opinion in nephrology and hypertension2020
The glomerular crescent: triggers, evolution, resolution, and implications for therapy.
Review in Current opinion in nephrology and hypertension, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 90 citations in OpenAlex.
- Clinical value of repeat kidney biopsy in pediatric IgA vasculitis nephritis.Pediatric nephrology (Berlin, Germany) · 2026Article
- The Src-Family Kinases Hck, Fgr and Lyn Drive Immune Complex-Mediated Glomerulonephritis Through the Syk Tyrosine Kinase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Decoding Lupus Diagnosis, Pathogenesis and Therapy: From Systemic Autoimmunity to Renal Damage.Diagnostics (Basel, Switzerland) · 2026Review
- Outcomes and Validation of Histopathological Scores in Pediatric ANCA-vasculitis.Kidney international reports · 2026Article
- Exploring Deep Learning Models for Small Histopathology Datasets: Segmentation and Classification of Glomerular Crescent Lesions with Ablation, Interpretability, and Calibration Analyses.Interdisciplinary sciences, computational life sciences · 2026Article
- Mucosal-associated invariant T cells and the gut-kidney axis: a review.Clinical kidney journal · 2026Review
- How to Cure Autoimmune GN and Podocytopathies.Journal of the American Society of Nephrology : JASN · 2026Review
- The Assessment of Disease Activity and Renal Prognosis in AAV - The Contribution of Urinary Biomarkers and Renal Biopsy.Current rheumatology reports · 2026Review
- Glomerular Crescents in Adult Lupus Nephritis: Clinical and Pathological Insights From Saudi Arabia.TheScientificWorldJournal · 2026Article
- Neutrophils in Kidney Disease: Linking Neutrophil Function and Microenvironment to Therapeutic Targets.Journal of inflammation research · 2026Review
- Unveiling the role of oxidative stress in ANCA-associated glomerulonephritis through integrated machine learning and bioinformatics analyses.Renal failure · 2025Article
- Rare and rapidly progressive crescentic proliferative glomerulonephritis with monoclonal immunoglobulin deposits: a case series study.Renal failure · 2025Article
- Histopathological spectrum and short-term outcome of rapidly progressive glomerulonephritis in children: a retrospective analysis from a tertiary care center.BMC nephrology · 2025Article
- IgG-Secreting Lymphoplasmacytic Lymphoma Presenting With Massive Kidney Infiltration.Clinical case reports · 2025Article
- Patterns of Glomerular Injury: Histopathological Classification and Clinical Correlation.Cureus · 2025Review
- The Evolution of Crescents in Lupus Nephritis.Kidney international reports · 2025Article
- Molecular mechanisms and therapeutic interventions in acute kidney injury: a literature review.BMC nephrology · 2025Review
- Kidney Failure in Pauci-immune Crescentic Glomerulonephritis: Rationale for Immunosuppression to Improve Kidney Outcome.Current rheumatology reports · 2024Review
- [Renal involvement in systemic diseases].Pathologie (Heidelberg, Germany) · 2024Review
- Glomerular crescents are associated with the risk of type 2 diabetic kidney disease progression: a retrospective cohort study.BMC nephrology · 2024Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewCrescents are classical histopathological lesions found in severe forms of rapidly progressive glomerulonephritis, also referred to as crescentic glomerulonephritis (CGN). Crescent formation is a consequence of diverse upstream pathomechanisms and unraveling these mechanisms is of great interest for improving the management of patients affected by CGN. Thus, in this review, we provide an update on the latest insight into the understanding on how crescents develop and how they resolve. RECENT
findingsCellular crescents develop from activated parietal epithelial cells (PECs) residing along Bowman's capsule and their formation has as a consequence the decline in glomerular filtration rate (GFR). Cellular crescents can be reversible, but when multilevel growth of PECs associate with an epithelial--mesenchymal transition-like change in cell phenotype, fibrous crescents form, and crescents become irreversible also in terms of GFR recovery. Different molecular pathways trigger the activation of PECs and are a prime therapeutics target in CGN. First, crescent formation requires also vascular injury causing ruptures in the glomerular basement membrane that trigger plasmatic coagulation within Bowman's space. This vascular necrosis can be triggered by different upstream mechanisms, such as small vessel vasculitides, immune complex glomerulonephritis, anti-GBM disease, and C3 glomerulonephritis, that all share complement activation but involve diverse upstream immune mechanisms outside the kidney accessible for therapeutic intervention. SUMMARY: Knowing the upstream mechanisms that triggered crescent formation provides a tool for the development of therapeutic interventions for CGN.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.