Steroid-sensitive idiopathic nephrotic syndrome is a T-cell disorder associated with a functional renal impairment. The molecular mechanisms leading from the stimulation of the immune system to the clinical expression of the renal disease can be analyzed according to five biological events: 1) a Th2 activation of T-cells by interleukin-13; 2) a yet unidentified glomerular permeability factor from immune origin; 3) a molecular disorientation of slit diaphragms or glomerular basement membrane responsible for proteinuria; 4) a podocyte cytoskeleton rearrangement responsible for foot process effacement; 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.