ArticleClinical kidney journal2018
Clinical and pathological phenotype of genetic causes of focal segmental glomerulosclerosis in adults.
Article in Clinical kidney journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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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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.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Efficacy of extracorporeal plasma therapy for adult native kidney patients with Primary FSGS: a Systematic review.Renal failure · 2023Pooled it
- Pathogenic variants in COL4A3, COL4A4, JAG1, and NPHS2 genes in focal segmental glomerulosclerosis: Insights from targeted gene panel sequencing.Molecular genetics and metabolism reports · 2026Article
- Genetic insights into congenital and infantile nephrotic syndrome: predicting severity and informing care.Pediatric nephrology (Berlin, Germany) · 2026Article
- Broadening the Phenotypic Spectrum ofGenes · 2026Article
- Patient-specific hiPSC-Podocytes as an in vitro model of genetic FSGS.Scientific reports · 2025Article
- Advances in focal segmental glomerulosclerosis research: genetic causes to non-coding RNAs.Molecular biology reports · 2025Review
- Pathogenesis of Focal Segmental Glomerulosclerosis and Related Disorders.Annual review of pathology · 2025Review
- Advances in Focal Segmental Glomerulosclerosis Treatment From the Perspective of the Newest Mechanisms of Podocyte Injury.Drug design, development and therapy · 2025Review
- Novel Pathogenic Mutation of P209L in TRPC6 Gene Causes Adult Focal Segmental Glomerulosclerosis.Biochemical genetics · 2024Article
- Regulation of formin INF2 and its alteration in INF2-linked inherited disorders.Cellular and molecular life sciences : CMLS · 2024Review
- A Review of Focal Segmental Glomerulosclerosis Classification With a Focus on Genetic Associations.Kidney medicine · 2024Article
- A Prospective Study on Complement Activation Distinguishes Focal Segmental Glomerulosclerosis from Minimal Change Disease.Kidney international reports · 2024Article
- Article
- The epidemiology of primary FSGS including cluster analysis over a 20-year period.BMC nephrology · 2023Observational
- Focal Segmental Glomerulosclerosis: Assessing the Risk of Relapse.Kidney international reports · 2023Article
- [Diagnosis and treatment of focal-segmental glomerulosclerosis-2023].Wiener klinische Wochenschrift · 2023Article
- High Rate of Mutations of Adhesion Molecules and Extracellular Matrix Glycoproteins in Patients with Adult-Onset Focal and Segmental Glomerulosclerosis.Biomedicines · 2023Article
- Modeling ofKidney international reports · 2023Article
- The most common founder pathogenic variant c.868G > A (p.Val290Met) in theFrontiers in medicine · 2023Article
- Current understanding of the molecular mechanisms of circulating permeability factor in focal segmental glomerulosclerosis.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal segmental glomerulosclerosis (FSGS) is a histologic lesion resulting from a variety of pathogenic processes that cause injury to the podocytes. Recently, mutations in more than 50 genes expressed in podocyte or glomerular basement membrane were identified as causing genetic forms of FSGS, the majority of which are characterized by onset in childhood. The prevalence of adult-onset genetic FSGS is likely to be underestimated and its clinical and histological features have not been clearly described. A small number of studies of adult-onset genetic FSGS showed that there is heterogeneity in clinical and histological findings, with a presentation ranging from sub-nephrotic proteinuria to full nephrotic syndrome. A careful evaluation of adult-onset FSGS that do not have typical features of primary or secondary FSGS (familial cases, resistance to immunosuppression and absence of evident cause of secondary FSGS) should include a genetic evaluation. Indeed, recognizing genetic forms of adult-onset FSGS is of the utmost importance, given that this diagnosis will have major implications on treatment strategies, selecting of living-related kidney donor and renal transplantation success.
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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.