ArticleJournal of the American Society of Nephrology : JASN2017
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Genetic and environmental factors associated with alteration of filtration slit proteins and their functions: a scoping review.Frontiers in nephrology · 2025Pooled it
- Extended motif recognition tunes WW domain affinity in MAGI-IQSEC complexes.The FEBS journal · 2026Article
- Gene-disease relationships for glomerular phenotypes: expert recommendations from ClinGen.Nature reviews. Nephrology · 2026Review
- Article
- Integrating machine learning and GWAS for variant prioritization in the INCIPE cohort highlights ABC transporter genes in chronic kidney disease.Frontiers in genetics · 2026Article
- Emerging genetic mechanisms of glomerular proteinuria: a podocyte-centered multi-layer network perspective.Frontiers in genetics · 2026Review
- A case of Frasier syndrome achieved complete remission by cyclosporine A for steroid-resistant nephrotic syndrome.CEN case reports · 2025Article
- Review
- The differential expression of MAGI2 in glomerulopathies and its application as a molecular discriminator of podocytopathies.Journal of translational medicine · 2025Article
- Mechanisms of podocyte injury in genetic kidney disease.Pediatric nephrology (Berlin, Germany) · 2025Review
- Celastrol protects against diabetic nephropathy by modulating immune-related pathways: a bioinformatics and experimental validation.American journal of translational research · 2025Article
- High Rate of Mutations of Adhesion Molecules and Extracellular Matrix Glycoproteins in Patients with Adult-Onset Focal and Segmental Glomerulosclerosis.Biomedicines · 2023Article
- Phosphorylation-dependent recognition of diverse protein targets by the cryptic GK domain of MAGI MAGUKs.Science advances · 2023Article
- Mapping of the podocin proximity-dependent proteome reveals novel components of the kidney podocyte foot process.Frontiers in cell and developmental biology · 2023Article
- Podocyte-specific Transcription Factors: Could MafB Become a Therapeutic Target for Kidney Disease?Internal medicine (Tokyo, Japan) · 2023Review
- Exploring the relevance of NUP93 variants in steroid-resistant nephrotic syndrome using next generation sequencing and a fly kidney model.Pediatric nephrology (Berlin, Germany) · 2022Article
- A critical re-analysis of cases of post-transplantation recurrence in genetic nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2021Article
- Influence of Genetic Polymorphisms on Clinical Outcomes of Glatiramer Acetate in Multiple Sclerosis Patients.Journal of personalized medicine · 2021Review
- Genetic variants of SDCCAG8 and MAGI2 in mitosis-related pathway genes are independent predictors of cutaneous melanoma-specific survival.Cancer science · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
Steroid-resistant nephrotic syndrome (SRNS), a heterogeneous disorder of the renal glomerular filtration barrier, results in impairment of glomerular permselectivity. Inheritance of genetic SRNS may be autosomal dominant or recessive, with a subset of autosomal recessive SRNS presenting as congenital nephrotic syndrome (CNS). Mutations in 53 genes are associated with human SRNS, but these mutations explain ≤30% of patients with hereditary cases and only 20% of patients with sporadic cases. The proteins encoded by these genes are expressed in podocytes, and malfunction of these proteins leads to a universal end point of podocyte injury, glomerular filtration barrier disruption, and SRNS. Here, we identified novel disease-causing mutations in
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.