ReviewPediatric nephrology (Berlin, Germany)2022
An updated view of the pathogenesis of steroid-sensitive nephrotic syndrome.
Review in Pediatric nephrology (Berlin, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- The efficacy and safety of rituximab monotherapy in the new onset pediatric idiopathic nephrotic syndrome: a randomized controlled clinical trial.Renal failure · 2025Trial
- The first randomized controlled trial in pediatric nephrology: the history of the International Study of Kidney Disease in Children (ISKDC).Pediatric nephrology (Berlin, Germany) · 2023Trial
- Urinary leukotriene E4 for predicting steroid sensitivity in children with nephrotic syndrome: an observational cohort study.Pediatric nephrology (Berlin, Germany) · 2026Observational
- Polygenic risk scores and HLA class II variants are biomarkers of corticosteroid response in childhood nephrotic syndrome.Kidney international · 2026Article
- Identification of monogenic variants in steroid-resistant and steroid-sensitive nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2026Article
- [Effect of rituximab combined with short-course glucocorticoid therapy on cellular immunity and cytokines in children with new-onset nephrotic syndrome].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- [Clinical study on low-dose rituximab maintenance therapy in children with primary nephrotic syndrome].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- Polygenic Risk Scores and HLA Class II Variants are Biomarkers of Corticosteroid Response in Childhood Nephrotic Syndrome.medRxiv : the preprint server for health sciences · 2025Article
- Genetic aspects of pediatric nephrotic syndrome and anti-nephrin antibodies.Clinical and experimental nephrology · 2025Review
- Amino acid variants in the HLA-DQA1 and HLA-DQB1 molecules explain the major association of variants with relapse status in pediatric patients with steroid-sensitive nephrotic syndrome.Italian journal of pediatrics · 2025Article
- Article
- Clinico-demographic and biochemical correlation of inflammatory gene expression in pediatric nephrotic syndrome.Molecular biology reports · 2024Article
- The association between dental caries and steroid-sensitive nephrotic syndrome in children.Pediatric nephrology (Berlin, Germany) · 2024Article
- Enzyme-activatable kidney-targeted dendrimer-drug conjugate for efficient childhood nephrotic syndrome therapy.Theranostics · 2024Article
- Idiopathic Nephrotic Syndrome in Children in Chad: Epidemiology and Clinical Outcomes.Journal of clinical medicine · 2023Article
- Correlation between Toll-like Receptor Gene Polymorphisms and Idiopathic Nephrotic Syndrome in Chinese Children.Current medical science · 2023Article
- [Distribution of memory B cell subsets in peripheral blood of children with frequently relapsing nephrotic syndrome].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Article
- Genetic risk variants for childhood nephrotic syndrome and corticosteroid response.Frontiers in pediatrics · 2023Article
- Intrinsic Kidney Pathology in Children and Adolescents Following COVID-19 Vaccination: A Systematic Review.Children (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic nephrotic syndrome is the most common childhood glomerular disease. Most forms of this syndrome respond to corticosteroids at standard doses and are, therefore, defined as steroid-sensitive nephrotic syndrome (SSNS). Immunological mechanisms and subsequent podocyte disorders play a pivotal role in SSNS and have been studied for years; however, the precise pathogenesis remains unclear. With recent advances in genetic techniques, an exhaustive hypothesis-free approach called a genome-wide association study (GWAS) has been conducted in various populations. GWASs in pediatric SSNS peaked in the human leukocyte antigen class II region in various populations. Additionally, an association of immune-related CALHM6/FAM26F, PARM1, BTNL2, and TNFSF15 genes, as well as NPHS1, which encodes nephrin expressed in podocytes, has been identified as a locus that achieves genome-wide significance in pediatric SSNS. However, the specific mechanism of SSNS development requires elucidation. This review describes an updated view of SSNS pathogenesis from immunological and genetic aspects, including interactions with infections or allergies, production of circulating factors, and an autoantibody hypothesis.
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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.