[Molecular mechanisms of idiopathic nephrotic syndrome].
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.
Deschênes
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G
Service de néphrologie pédiatrique, hôpital Armand-Trousseau, 26, avenue du Docteur-Arnold-Netter, 75571 Paris, France.
Martinat
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L
D003599:Cytoskeleton / Q000473:pathology; D004487:Edema / Q000473:pathology; D004727:Endothelium / Q000502:physiology*; D018793:Interleukin-13 / Q000494:pharmacology; D009404:Nephrotic Syndrome / Q000235:genetics / Q000276:immunology / Q000503:physiopathology*; D010539:Permeability; D011507:Proteinuria / Q000503:physiopathology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013601:T-Lymphocytes / Q000502:physiology
D018793:Interleukin-13; D000254:Sodium-Potassium-Exchanging ATPase