ReviewFrontiers in pediatrics2018
Basement Membrane Defects in Genetic Kidney Diseases.
Review in Frontiers in pediatrics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 98 citations in OpenAlex.
- Sodium-Glucose Cotransporter-2-inhibitors in Adult Patients With Alport Syndrome.Kidney international reports · 2026Article
- Extracellular vesicle miR-93-5p cargo regulates glomerular endothelial cell damage in Alport syndrome.JCI insight · 2026Article
- Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.Clinical kidney journal · 2026Review
- Review
- A case of concurrent Alport syndrome and Nail-patella syndrome posing diagnostic challenge without genetic testing.BMC nephrology · 2025Article
- Nephrotic-range proteinuria in a 53-year-old female with thin basement membrane nephropathy: A case report with literature review.SAGE open medical case reports · 2025Article
- Article
- Trimerization profile of type IV collagen COL4A5 exon deletion in X-linked Alport syndrome.Clinical and experimental nephrology · 2024Article
- An ultrathin membrane mediates tissue-specific morphogenesis and barrier function in a human kidney chip.Science advances · 2024Article
- A NovelGenes · 2024Article
- Genetic, Clinical, and Pathologic Backgrounds of Children With X-Linked Alport Syndrome in China: A Monocenter Study.Global pediatric health · 2024Article
- Article
- Ten Years of Extracellular Matrix Proteomics: Accomplishments, Challenges, and Future Perspectives.Molecular & cellular proteomics : MCP · 2023Review
- In Vitro Models to Evaluate Molecular Permeability of the Kidney Filtration Barrier.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Proteotranscriptomic analyses reveal distinct interferon-beta signaling pathways and therapeutic targets in choroidal neovascularization.Frontiers in immunology · 2023Article
- Genetic Disorders of the Extracellular Matrix: From Cell and Gene Therapy to Future Applications in Regenerative Medicine.Annual review of genomics and human genetics · 2022Review
- Tensin 2-deficient nephropathy: mechanosensitive nephropathy, genetic susceptibility.Experimental animals · 2022Review
- Anti-glomerular basement membrane disease in children: a brief overview.Pediatric nephrology (Berlin, Germany) · 2022Review
- Advancements in nanomedicines for the detection and treatment of diabetic kidney disease.Biomaterials and biosystems · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The glomerular basement membrane (GBM) is a specialized structure with a significant role in maintaining the glomerular filtration barrier. This GBM is formed from the fusion of two basement membranes during development and its function in the filtration barrier is achieved by key extracellular matrix components including type IV collagen, laminins, nidogens, and heparan sulfate proteoglycans. The characteristics of specific matrix isoforms such as laminin-521 (α5β2γ1) and the α3α4α5 chain of type IV collagen are essential for the formation of a mature GBM and the restricted tissue distribution of these isoforms makes the GBM a unique structure. Detailed investigation of the GBM has been driven by the identification of inherited abnormalities in matrix proteins and the need to understand pathogenic mechanisms causing severe glomerular disease. A well-described hereditary GBM disease is Alport syndrome, associated with a progressive glomerular disease, hearing loss, and lens defects due to mutations in the genes
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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.