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.