[Molecular mechanisms of idiopathic nephrotic syndrome]

Arch Pediatr. 2000 Dec;7(12):1318-29. doi: 10.1016/s0929-693x(00)00151-2.
[Article in French]

Abstract

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.

Publication types

  • Review

MeSH terms

  • Cytoskeleton / pathology
  • Edema / pathology
  • Endothelium / physiology*
  • Interleukin-13 / pharmacology
  • Nephrotic Syndrome / genetics
  • Nephrotic Syndrome / immunology
  • Nephrotic Syndrome / physiopathology*
  • Permeability
  • Proteinuria / physiopathology
  • Sodium-Potassium-Exchanging ATPase / metabolism
  • T-Lymphocytes / physiology

Substances

  • Interleukin-13
  • Sodium-Potassium-Exchanging ATPase