Molecular basis of idiopathic nephrotic syndrome

Citation
G. Deschenes et L. Martinat, Molecular basis of idiopathic nephrotic syndrome, ARCH PED, 7(12), 2000, pp. 1318-1329
Citations number
81
Categorie Soggetti
Pediatrics
Journal title
ARCHIVES DE PEDIATRIE
ISSN journal
0929693X → ACNP
Volume
7
Issue
12
Year of publication
2000
Pages
1318 - 1329
Database
ISI
SICI code
0929-693X(200012)7:12<1318:MBOINS>2.0.ZU;2-V
Abstract
Steroid-sensitive idiopathic nephrotic syndrome is a T-cell disorder associ ated with a functional renal impairment. The molecular mechanisms leading f rom the stimulation of the immune system to the clinical expression of the renal disease can be analyzed according to five biological events: I) a Th2 activation of T-cells by interleukin-13; 2) a yet unidentified glomerular permeability factor from immune origin; 3) a molecular disorientation of sl it diaphragms or glomerular basement membrane responsible for proteinuria; 4) a podocyte cytoskeleton rearrangement responsible for foot process effac ement; and 5) renal avidity for sodium and edema formation resulting from a primary stimulation of tubular Na, K-ATPase and an increase of endothelial permeability. (C) 2000 Editions scientifiques et medicales Elsevier SAS.