Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome

  • Kazunari Kaneko

Table of contents

  1. Front Matter
    Pages i-viii
  2. Introduction

    1. Front Matter
      Pages 1-1
  3. Minimal-Change Nephrotic Syndrome (MCNS)

    1. Front Matter
      Pages 11-11
    2. Yasuko Kobayashi, Moin A. Saleem
      Pages 13-23
    3. Lionel C. Clément
      Pages 25-43
    4. Michiko Shimada, Takuji Ishimoto, Richard J. Johnson
      Pages 45-62
    5. Vincent Audard, André Pawlak, Dil Sahali
      Pages 81-91
    6. Roberta Bertelli, Armando Di Donato, Alice Bonanni, Roberta Rossi, Pietro Ravani, Gian Marco Ghiggeri
      Pages 93-103
    7. Gabriel M. Cara-Fuentes, Richard J. Johnson, Eduardo H. Garin
      Pages 105-140
  4. Focal Segmental Glomerulosclerosis (FSGS)

    1. Front Matter
      Pages 141-141
    2. Gabriel M. Cara-Fuentes, Richard J. Johnson, Eduardo H. Garin
      Pages 155-178
  5. Idiopathic Membranous Nephropathy (IMN)

  6. Treatment in Idiopathic Nephrotic Syndrome

    1. Front Matter
      Pages 219-219
    2. Lulu Jiang, Peter W. Mathieson, Gavin I. Welsh
      Pages 221-240

About this book


This comprehensive book reviews our current state of knowledge about the pathogenesis of idiopathic nephrotic syndrome (INS), which comprises a heterogeneous group of diseases with distinct histological characteristics, such as minimal-change nephrotic syndrome (MCNS), focal segmental glomerulosclerosis (FSGS), and idiopathic membranous nephropathy (IMN). As the word “idiopathic” indicates, the pathogenesis of INS remains unclear. Historically, T-cell dysfunction has been thought to play an important part in the pathogenesis of MCNS, while circulating vascular permeabilities have been believed to induce proteinuria in FSGS. The book further describes recent advances in molecular biology, which have allowed us to speculate on the interactions between visceral glomerular epithelial cells (podocytes) and the relative significance of several molecules in the pathogenesis of INS, such as reactive oxygen species, nuclear factor-kappa B, CD80, angiopoietin-like 4, cardiotrophin-like cytokine-1, and M-type phospholipase A2 receptor. The normally rapid pace of scientific progress occasionally devolves into a state of chaos, and the pathogenetic research on INS is one such case. This volume will help researchers and scientists to collaborate, share resources, and expedite the design of protocols to evaluate the putative factors.


CD80 angiopoietin-like 4 focal segmental glomerulosclerosis (FSGS) idiopathic membranous nephropathy (IMN) minimal-change nephrotic syndrome (MCNS) podocytes

Editors and affiliations

  • Kazunari Kaneko
    • 1
  1. 1.Department of PediatricsKansai Medical UniversityHirakata, OsakaJapan

Bibliographic information