ArticlePediatric nephrology (Berlin, Germany)2003
Glomerular structural factors in progression of congenital nephrotic syndrome.
Article in Pediatric nephrology (Berlin, Germany), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 10 citations in OpenAlex.
- The proximal tubule is the primary target of injury and progression of kidney disease: role of the glomerulotubular junction.American journal of physiology. Renal physiology · 2016Review
- Formation of atubular glomeruli in the developing kidney following chronic urinary tract obstruction.Pediatric nephrology (Berlin, Germany) · 2011Review
- Induction of podocyte VEGF164 overexpression at different stages of development causes congenital nephrosis or steroid-resistant nephrotic syndrome.The American journal of pathology · 2010Article
- Genetics of idiopathic nephrotic syndrome.Indian journal of pediatrics · 2005Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The glomerular structural factors associated with progression of congenital nephrotic syndrome of Finnish type (CNF) are incompletely understood. We studied glomerular volume and the proportion of various glomerular subtypes in seven CNF patients (aged 4 months to 3 years). Glomerular tubular connections (GTC) were analyzed in two patients early and late in the disease spectrum (creatinine 0.2 and 2.8 mg/dl, respectively). The proportions of "normal" glomeruli decreased (r=-0.91, P=0.003) and microcystic glomeruli increased (r=0.85, P=0.015), while the fetal and sclerosed glomeruli remained stable (r=0.073 and 0.08 respectively, P=NS for both) with age. The "normal" glomeruli were larger in CNF than in six age-matched minimal change nephrotic patients (P=0.009). GTC analyses in the mild disease showed that 75% of the 12 "normal" glomeruli had normal tubules, and 25% were atubular or were attached to atrophic tubules, while 88% of the 12 fetal glomeruli were either atubular or were attached to atrophic tubules. In the advanced disease, 67% of 12 "normal" glomeruli had normal tubules, and 33% were atubular or atrophic, while none of the fetal or microcystic glomeruli had "normal tubules". Thus atubular glomeruli may play an important role in disease progression in CNF, as it is associated with a progressive decrease in hypertrophied "normal" glomeruli and an increase in largely atubular microcystic glomeruli.
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