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Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome

Kaneko Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome

ISBN: 978-4-431-55269-7

Erscheinungsdatum: November 2015

Einband: Hardcover

Seitenzahl: 200 p.

Illustrationen: 100 ill.

Verlag: Springer

Lieferzeit: 2 - 15 Tage

Beschreibung

 

  • Brings together all of the latest research on molecular mechanisms in the pathogenesis of INS  
  • Each chapter represents one putative pathgenetic molecule and reviews its roleplay, mechanism, and its prospect for the biomarker or new drugs     
  • Valuable reading for physicians, pediatricians, nephrologists, and individuals researching nephrotic syndrome
This comprehensive book reviews our current state of knowledge on 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 adjective 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.