Document Detail


Molecular basis of steroid-resistant nephrotic syndrome.
MedLine Citation:
PMID:  16050398     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The identification of the underlying gene defect in some cases of steroid resistant nephrotic syndrome (SRNS) has recently led to a critical breakthrough in the understanding of the pathogenesis of nephrotic syndromes. The more severe form of hereditary nephrotic syndromes is the congenital nephrotic syndrome of the Finnish type (CNF). The causative gene, NPHS1, encodes a novel protein, nephrin which is a transmembrane protein belonging to the immunoglobulin superfamily specifically expressed in the podocyte at the slit diaphragm. Using a positional cloning approach, our group identified a gene, NPHS2, involved in a specific entity of familial SRNS characterized by early onset, complete steroid-resistance, rapid progression to ESRD and no recurrence after renal transplantation. NPHS2 encodes a novel membrane protein named podocin localized at the cytoplasmic part of the slit diaphragm. Familial autosomal dominant cases of primary FSGS have been described in adulthood. Two corresponding genes have been mapped to date, one to 19q13 and the second to 11q21-22. The former has been identified as ACTN4, the gene encoding the actin-binding protein, a-actinin 4. Other genes involved in the slit-diaphragm or the nephrotic syndrome are CD2-associated protein (CD2AP), FAT1, WT1, LMX1B, SMARCAL1. Altogether, these data demonstrate the pivotal role of the podocyte in the development and the maintenance of the glomerular filtration barrier and the crucial role of the genetic factors in the development of SRNS.
Authors:
C Antignac
Related Documents :
10884998 - Nephrotic syndrome secondary to amyloidosis.
3819048 - Hyperbiliverdinemia in the bronze baby syndrome.
2805458 - The role of soluble immune response suppressor lymphokine in the prediction of steroid ...
17469738 - Congenital nephrotic syndrome-a treatable cause.
12108508 - Novel cause of spurious mode switching in dual-chamber pacemakers: atrioventricular des...
20195738 - Punishment and sympathy judgments: is the quality of mercy strained in asperger's syndr...
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Nefrología : publicación oficial de la Sociedad Española Nefrologia     Volume:  25 Suppl 2     ISSN:  0211-6995     ISO Abbreviation:  Nefrologia     Publication Date:  2005  
Date Detail:
Created Date:  2005-07-29     Completed Date:  2005-10-07     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8301215     Medline TA:  Nefrologia     Country:  Spain    
Other Details:
Languages:  eng     Pagination:  25-8     Citation Subset:  IM    
Affiliation:
Inserm U574 and Department of Genetics, Necker Hospital, Paris 5 University, Paris, France.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Actinin
Adaptor Proteins, Signal Transducing
Adult
Child
Cytoskeletal Proteins
Disease Progression
Drug Resistance
Humans
Intracellular Signaling Peptides and Proteins
Kidney Failure, Chronic / etiology
Kidney Transplantation
Membrane Proteins* / genetics
Microfilament Proteins
Mutation
Nephrotic Syndrome / complications,  congenital,  drug therapy,  etiology,  genetics*
Proteins / genetics
Steroids / therapeutic use
Chemical
Reg. No./Substance:
0/ACTN4 protein, human; 0/Adaptor Proteins, Signal Transducing; 0/CD2-associated protein; 0/Cytoskeletal Proteins; 0/Intracellular Signaling Peptides and Proteins; 0/Membrane Proteins; 0/Microfilament Proteins; 0/NPHS2 protein; 0/Proteins; 0/Steroids; 0/nephrin; 11003-00-2/Actinin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  From adequate to optimal dialysis long 3 x 8 hr dialysis: a reasonable compromise.
Next Document:  Collagen IV (alpha3-alpha4) nephropathy