Abstract
Pathogenesis of idiopathic nephrotic syndrome in children: molecular mechanisms and therapeutic implications
Highlights
The conventional paradigm on the pathogenesis of nephrotic syndrome revolves around the concept of a glomerular disorder which is characterized by massive proteinuria with consequent hypoalbuminemia, generalized edema and hyperlipidemia [1]
In a nut-shell, idiopathic nephrotic syndrome has been defined as a T-cell disorder associated with a functional renal impairment in which 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: a Th 2 activation of T cells by interleukin-13; a yet unresolved glomerular permeability factor of immune origin; a molecular disorientation of slit diaphragms or glomerular basement membrane responsible for proteinuria; a podocyte cytoskeleton rearrangement responsible for foot process effacement; and renal avidity for sodium and edema formation resulting from a primary stimulation of tubular sodium, K+-ATPase and an increase of endothelial permeability [7]
The molecular mechanisms involved in the pathogenesis of idiopathic nephrotic syndrome are complex and depend on all the components of the glomerular filtration barrier
Summary
The conventional paradigm on the pathogenesis of nephrotic syndrome revolves around the concept of a glomerular disorder which is characterized by massive proteinuria with consequent hypoalbuminemia, generalized edema and hyperlipidemia [1]. This effacement suggests a key role for the podocytes in the pathogenesis of idiopathic nephrotic syndrome, either as a target of a glomerular permeability factor or as the site of alteration of a structural component of the foot processes [2].
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