ReviewClinical and experimental nephrology2025
Lupus nephritis and related renal disease: review from case series.
Review in Clinical and experimental nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Screening of diagnostic biomarkers for taurine metabolism-related genes in lupus nephritis and analysis of immune infiltration.International urology and nephrology · 2026Article
- Design of Nanocarriers for Kidney Targeted Delivery of Nucleic Acid Therapeutics.Macromolecular bioscience · 2026Review
- Two Cases of Hepatitis B Virus-associated Membranoproliferative Glomerulonephritis with Contrasting Renal and Survival Outcomes after Antiviral Therapy.Internal medicine (Tokyo, Japan) · 2026Article
- When Hepatitis B Virus-Associated Glomerulonephritis Mimics Lupus Nephritis: A Case of Adult-Onset Disease With Full-House Pattern.Kidney medicine · 2026Article
- Autoantibody repertoire in lupus nephritis: from pathogenic mechanisms to clinical integration for precision decision-making.Frontiers in immunology · 2026Review
- Distinction Between Proliferative Lupus Nephritis and Membranous Lupus Nephritis Based on Inflammation, NETosis, and Glomerular Exostosin.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal lesions due to systemic lupus erythematosus (SLE) are defined as lupus nephritis (LN), a renal disease characterized by the deposition of immunoglobulin (Ig)G-based immune complexes in the kidney and the appearance of double-stranded DNA and Smith antibodies. In particular, deposition of IgG3, which has strong complement binding properties, under the endothelium or in the mesangium activates the classical complement pathway of C1q, C4, and C3, leading to renal damage. This step is followed by migration of inflammatory cells, including neutrophils and monocytes, which induce inflammation in the glomerular capillaries and cause mesangiolysis and endothelial cell damage, resulting in endocapillary proliferative nephritis. LN is classified as class I to IV depending on the degree of inflammation or as class V in cases of subepithelial deposition of immune complexes in glomeruli. Deposition in the renal small arterioles by the same mechanism induces thrombus formation, resulting in lupus vasculopathy. Deposition in the tubular basement membrane and peritubular capillaries leads to tubulointerstitial lupus nephropathy. The appearance of antiphospholipid antibodies leads to acute and chronic forms of antiphospholipid antibody nephropathy (APSN) due to thrombus formation. This article reviews cases of the typical diverse renal lesions in LN.
Indexed as
Identifiers
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Registered trials
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.