This publication provides a synopsis of the rapid progress made in the field of renal cell biology during the last decade, progress which has resulted in a better conceptual understanding of the cellular and molecular mechanisms of fibrotic renal disease. These developments have provided new therapeutic choices and led to the discovery of gene-based therapeutic options. The topics covered in this book have been carefully selected from the immense number of aspects of the disease to provide essential information on the molecular basis of renal fibrosis. Individual chapters discuss topics such as proteinuria and tubulointerstitial injury, the roles and regulation of TGF-beta, chemokines, oxidant stress, matrix remodeling, significance of renal expression of NF-kappa, and the potential impact of cell death in renal fibrosis.Written so as to present the complex information as simply as possible, this publication will be a very useful tool for general health professionals involved in the fields of immunology and cell biology, as well as for clinicians and researchers within the fields of nephrology, pathology and matrix biology.

Scarring of the glomerular and tubulointerstitial compartments is a hallmark of progressive kidney disease. Renal fibrosis involves a complex interplay between kidney cells, leukocytes and fibroblasts in which transforming growth factor-β (TGF-β) plays a key role. This eBook provides a comprehensive update on TGF-β signalling pathways and introduces a range of cellular and molecular mechanisms involved in renal fibrosis both upstream and downstream of TGF-β. The wide variety of potential new targets described herein bodes well for the future development of effective therapies to tackle the major clinical problem of progressive renal fibrosis.

This book systemically presents the latest research on renal fibrosis, covering all the major topics in the field, including the possible mechanisms, biomarkers, and strategies for prevention and treatment of chronic kidney disease (CKD). Due to its high prevalence, CKD represents a huge global economic and social burden. Irrespective of the initial causes, CKD progresses to end stage kidney disease (ESKD) due to renal fibrosis, which is characterized by glomerulosclerosis, tubule atrophy and atresia, and the excessive accumulation of extracellular matrix (ECM) in the kidney. Unfortunately, an estimated 1%-2% of the adult population living with CKD will need renal replacement therapy at some point as a result of ESKD. As such, strategies for preventing or slowing CKD progression to ESKD are of utmost importance, and studies aiming to understand the mechanisms of renal fibrosis have been the focus of intensive research. Recently, novel insights into the pathophysiological processes have furthered our understanding of the pathogenesis of renal fibrosis, and more importantly, promoted studies on the early diagnosis and treatment of CKD. This book draws lessons from the extensive, state-of-the-art research in this field, elaborating the new theories and new techniques to offer readers a detailed and comprehensive understanding of renal fibrosis and as well as inspiration for future research directions.