ArticlePediatric nephrology (Berlin, Germany)2008
NPHS3: new clues for understanding idiopathic nephrotic syndrome.
Article in Pediatric nephrology (Berlin, Germany), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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
6 citing papers in PubMed, 18 citations in OpenAlex.
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Diagnostic and Management Challenges in Congenital Nephrotic Syndrome.Pediatric health, medicine and therapeutics · 2019Review
- Parental attitudes to genetic testing differ by ethnicity and immigration in childhood nephrotic syndrome: a cross-sectional study.Canadian journal of kidney health and disease · 2016Article
- Late steroid resistance in childhood nephrotic syndrome: do we now know more than 40 years ago?Pediatric nephrology (Berlin, Germany) · 2013Article
- Familial forms of nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2010Review
- Genetic forms of nephrotic syndrome: a single-center experience in Brussels.Pediatric nephrology (Berlin, Germany) · 2009Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary forms of childhood nephrotic syndrome (H-CHNS) have long been counted as rare variants of steroid-resistant nephrotic syndrome (SRNS). This concept must be specified by two new findings: First, a study on nephrotic syndrome manifesting in the first year of life documents that H-CHNS are actually the predominant cause of nephrotic syndrome in infants. Second, the recent identification of autosomal recessive nephrotic syndrome type 3 (NPHS3) caused by mutations in the phospholipase PLCE1 gene has, for the first time, shown steroid responsiveness in H-CHNS. NPHS3 is a severe form of isolated nephrotic syndrome with rapid progression to terminal renal failure. NPHS3 is caused by a developmental rather than structural podocyte dysfunction and is a major cause of diffuse mesangial sclerosis. Therapy response in NPHS3 is documented and could open insights into direct genomic and nongenomic effects of glucocorticoids on podocytes. The findings on NPHS3 support the idea that both clinical course and histology in H-CHNS are subject to genotypic variability and that mutational analysis is the most reliable diagnostic tool. Future studies are needed to determine the clinical implications of NPHS3. Identification of further variants of H-CHNS can be anticipated and may include steroid-responsive hereditary diseases.
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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.