Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome

Home

/

Specialità

/

Nefrologia

/

Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome

Editore

Springer

Anno

2016

Pagine

240

ISBN

9784431552697

I prezzi indicati possono subire variazioni poiché soggetti all'oscillazione dei cambi delle valute e/o agli aggiornamenti effettuati dagli Editori.

Dettagli Indice Recensioni (0)

Brings together all of the latest research by top researchers on molecular mechanisms in the pathogenesis of INS
Represents one putative pathogenetic molecule in each chapter and reviews its role, mechanism, and prospects as a biomaker or for new drugs
Provides valuable reading for physicians, pediatricians, nephrologists, and individuals researching nephrotic syndrome

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.

Table of contents (13 chapters)

History of Research on Pathogenesis of Idiopathic Nephrotic Syndrome

Kaneko, Kazunari

Pages 3-10
Hemopexin in Minimal Change Nephrotic Syndrome

Kobayashi, Yasuko (et al.)

Pages 13-23
Angiopoietin-Like 4 (Angptl4) in MCNS

Clément, Lionel C.

Pages 25-43
Co-stimulatory Molecule CD80 (B7.1) in MCNS

Shimada, Michiko (et al.)

Pages 45-62
Energy and Mammalian Target of Rapamycin Complex 1 (mTORC1) in Minimal Change Nephrotic Syndrome

Yan, Kunimasa

Pages 63-79

The Role of c-mip in the Pathogenesis of Minimal Change Nephrotic Syndrome

Audard, Vincent (et al.)

Pages 81-91
Regulatory T Cells and Oxidative Stress in Minimal Change Nephropathy

Bertelli, Roberta (et al.)

Pages 93-103
Cytokines as Active Factors in Minimal Change Nephrotic Syndrome

Cara-Fuentes, Gabriel M. (et al.)

Pages 105-140
Soluble Urokinase-Type Plasminogen Activator Receptor (suPAR) in Focal Segmental Glomerulosclerosis

Reiser, Jochen (et al.)

Pages 143-154
Cytokines as Active Factors in Focal Segmental Glomerulosclerosis

Cara-Fuentes, Gabriel M. (et al.)

Pages 155-178
M-type Phospholipase A2 Receptor (PLA2R) and Thrombospondin Type-1 Domain-Containing 7A (THSD7A) in Membranous Nephropathy

Beck, Laurence H. (et al.)

Pages 181-205
Cationic Bovine Serum Albumin as Cause of Membranous Nephropathy: From Mice to Men

Kemper, Markus J. (et al.)

Pages 207-217
Podocytes as a Direct Target of Drugs Used in Idiopathic Nephrotic Syndrome

Jiang, Lulu (et al.)

Pages 221-240