ReviewAdvances in chronic kidney disease2014
Familial FSGS.
Review in Advances in chronic kidney disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02455908 (Use of IL-2 for Pediatric, Multi Drug Resistant, Idiopathic Nephrotic Syndrome), which is not on this map. Cited by 37 papers, 2 of them syntheses that pooled it.
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.
Use of IL-2 for Pediatric, Multi Drug Resistant, Idiopathic Nephrotic Syndrome
Who cites it
37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.
- KDIGO Clinical Practice Guideline on the Evaluation and Care of Living Kidney Donors.Transplantation · 2017Guideline
- Association of kidney structure-related gene variants with type 2 diabetes-attributed end-stage kidney disease in African Americans.Human genetics · 2016Pooled 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
- INF2-Related Charcot-Marie-Tooth Disease in a Japanese Cohort: Genetic and Clinical Insights.Annals of clinical and translational neurology · 2026Article
- Review
- Cellular and Molecular Resolution of Focal Segmental Glomerulosclerosis Recurrence in Human Allografts.bioRxiv : the preprint server for biology · 2025Article
- Advances in focal segmental glomerulosclerosis research: genetic causes to non-coding RNAs.Molecular biology reports · 2025Review
- Clinical implications of apolipoprotein L1 testing in patients with focal segmental glomerulosclerosis: a review of diagnostic and prognostic implications.Annals of medicine and surgery (2012) · 2025Review
- Pathogenesis of Focal Segmental Glomerulosclerosis and Related Disorders.Annual review of pathology · 2025Review
- INF2 mutations cause kidney disease through a gain-of-function mechanism.Science advances · 2024Article
- INF2 formin variants linked to human inherited kidney disease reprogram the transcriptome, causing mitotic chaos and cell death.Cellular and molecular life sciences : CMLS · 2024Article
- A Review of Focal Segmental Glomerulosclerosis Classification With a Focus on Genetic Associations.Kidney medicine · 2024Article
- Clinical and Pathological Heterogeneity in FSGS due toKidney international reports · 2022Article
- Biochemical composition of the glomerular extracellular matrix in patients with diabetic kidney disease.World journal of diabetes · 2022Review
- Integrated genomic, transcriptomic and metabolomic analysis reveals MDH2 mutation-induced metabolic disorder in recurrent focal segmental glomerulosclerosis.Frontiers in immunology · 2022Article
- Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.Kidney diseases (Basel, Switzerland) · 2021Review
- Case Report: Renal Failure due to Focal Segmental Glomerulosclerosis in a Patient with Murine Typhus.The American journal of tropical medicine and hygiene · 2020Article
- Autosomal Dominant Tubulointerstitial Kidney Disease-Uromodulin Misclassified as Focal Segmental Glomerulosclerosis or Hereditary Glomerular Disease.Kidney international reports · 2020Article
- Familial Focal Segmental Glomerulosclerosis With Late-Onset Presentation and R229Q/R291W Podocin Mutations.Frontiers in genetics · 2020Article
- Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Focal segmental glomerulosclerosis (FSGS) and nephrotic syndrome can be caused by rare highly penetrant mutations in number of genes. FSGS can follow both recessive and dominant inheritance patterns. In general, recessive forms present early, whereas the autosomal dominant forms present in adolescence or adulthood. Many of the genes found to be mutated in FSGS and nephrotic syndrome patients encode proteins essential for normal podocyte structure and/or function. An exception appears to be APOL1, which harbors common variants responsible for the high rate of FSGS and other nephropathies in people of recent African ancestry. Familial FSGS should be regarded as part of a spectrum of inherited glomerulopathies where the precise histologic presentation may depend on the age of onset, function of the responsible gene and gene products, and other factors.
Indexed as
Identifiers
What OpenQuestion holds
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.