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. (C) 2000 Editions scientifiques et medicales Elsevier SAS.
CITATION STYLE
Zhang, S.-Y., Audard, V., Lang, P., & Sahali, D. (2010). Mécanismes moléculaires du syndrome néphrotique idiopathique à rechutes. Médecine/Sciences, 26(6–7), 592–596. https://doi.org/10.1051/medsci/2010266-7592
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