ArticlePediatric nephrology (Berlin, Germany)1996
Mechanism underlying early anaemia in children with familial juvenile nephronophthisis.
Article in Pediatric nephrology (Berlin, Germany), 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 42 citations in OpenAlex.
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Case report of a child with nephronophthisis from South Africa.BMC pediatrics · 2024Article
- TheBiomedicines · 2024Review
- Association of Nephronophthisis 4 genetic variation with cardiorenal syndrome and cardiovascular events in Japanese general population: the Yamagata (Takahata) study.Heart and vessels · 2022Article
- Nephronophthisis-Pathobiology and Molecular Pathogenesis of a Rare Kidney Genetic Disease.Genes · 2021Review
- Endothelial marker-expressing stromal cells are critical for kidney formation.American journal of physiology. Renal physiology · 2017Article
- Ciliopathies.Cold Spring Harbor perspectives in biology · 2017Review
- Nephronophthisis and related syndromes.Current opinion in pediatrics · 2015Review
- Cystic kidney diseases: many ways to form a cyst.Pediatric nephrology (Berlin, Germany) · 2013Review
- Nephronophthisis: a genetically diverse ciliopathy.International journal of nephrology · 2011Article
- Nephronophthisis: disease mechanisms of a ciliopathy.Journal of the American Society of Nephrology : JASN · 2009Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Familial juvenile nephronophthisis (NPH) is a hereditary form of chronic tubulointerstitial nephritis with onset in childhood. About one-third of patients develop anaemia before renal insufficiency. We investigated the pathogenetic mechanisms leading to anaemia by comparing 6 patients with NPH and 12 reference patients with other renal diseases. We studied their iron metabolism and measured transferrin receptor-ferritin ratios. There was no evidence for iron deficiency or haemolysis. The serum erythropoietin concentrations of the patients with NPH (12 +/- 2.3 U/I) were low compared with the 12 reference patients (25 +/- 18.9 U/I). In the 2 patients with NPH who were fully investigated, the pharmacokinetics of recombinant human erythropoietin appeared normal. Thus, anaemia in patients with NPH does not result from iron deficiency or correlate with impaired iron status. The mechanism underlying the anaemia of NPH appears to affect the function or regulation of the cells producing erythropoietin.
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