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Nephrol Dial Transplant (2003) 18: 245-248
© 2003 European Renal Association-European Dialysis and Transplant Association

Editorial Comment

Recent approaches to the pathogenesis of minimal-change nephrotic syndrome

Philippe Grimbert, Vincent Audard, Philippe Remy, Philippe Lang and Djillali Sahali

INSERM U99 and Service de Néphrologie, Hôpital Henri Mondor, Créteil, France

Keywords: c-maf; minimal-change nephrotic syndrome; NF{kappa}B; pathogenesis; Proteasome; T cells

The first 150 words of the full text of this article appear below.

Introduction

Minimal-change nephrotic syndrome (MCNS) is a clinical and pathological entity defined by selective proteinuria and hypoalbuminaemia that occurs in the absence of cellular glomerular infiltrates or immunoglobulin deposits. The only detectable abnormalities involve the epithelial visceral cells with effacement of foot processes. These morphological alterations are typical of the nephrotic syndrome but not specific of the MCNS disease [1].

Whereas recent genetic approaches to familial idiopathic nephrotic syndromes have been determining factors in elucidating several molecular aspects of focal glomerular sclerosis [2–4], our knowledge about the pathogenesis of MCNS is inchoate, despite arguments suggesting a disorder of the immune function. In support of this view, occurrence of the disease in the context of immune challenge initiated by infectious or allergic stimuli, as well as relapse sensitivity to drugs known to inhibit the immune system (glucocorticoids, cyclosporin and cyclophosphamide) are particularly relevant [5]. . . . [Full Text of this Article]

T cells in MCNS

Transcription factors and proteasome activity in MCNS

Alteration of other immune cell subsets in MCNS

Contribution of subtractive and differential cloning to study of MCNS pathogenesis

Perspectives

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