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.

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.

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.

This book offers a detailed review of the pathological and imaging features, diagnosis and treatment of IgG4-Related Kidney Disease (IgG4-RKD). IgG4-related disease (IgG4-RD), which is characterized by an elevated serum IgG4 level and infiltration of systemic organs by IgG4 positive plasma cells, is a newly recognized systemic disease. Diverse renal manifestations including specific tubulointerstitial nephritis, membranous nephropathy, and tumor-like urological diseases extending to the pelvis and urinary tract in IgG4-RD have been reported and are recently attracting attention as IgG4-RKD. In this book, leading researchers in the field present the latest insights into the broad spectrum of IgG4-RKD characteristics. In addition, they provide a detailed explanation of the pathology of IgG4-RKD including comparisons between the kidney and other affected organs, such as the lacrimal, salivary glands and pancreas in the histopathological section. IgG4-Related Kidney Disease will have a major impact on future immunological and nephrological studies and offers a useful resource not only for nephrologists but also general physicians and investigators in related fields.

An algorithmic approach to interpreting renal pathology, updated in light of recent advances in understanding and new classification schemes.

In the past decade there has been a major sea change in the way disease is diagnosed and investigated due to the advent of high throughput technologies, such as microarrays, lab on a chip, proteomics, genomics, lipomics, metabolomics etc. These advances have enabled the discovery of new and novel markers of disease relating to autoimmune disorders, cancers, endocrine diseases, genetic disorders, sensory damage, intestinal diseases etc. In many instances these developments have gone hand in hand with the discovery of biomarkers elucidated via traditional or conventional methods, such as histopathology or clinical biochemistry. Together with microprocessor-based data analysis, advanced statistics and bioinformatics these markers have been used to identify individuals with active disease or pathology as well as those who are refractory or have distinguishing pathologies. New analytical methods that have been used to identify markers of disease and is suggested that there may be as many as 40 different platforms. Unfortunately techniques and methods have not been readily transferable to other disease states and sometimes diagnosis still relies on single analytes rather than a cohort of markers. There is thus a demand for a comprehensive and focused evidenced-based text and scientific literature that addresses these issues. Hence the formulation of Biomarkers in Disease. The series covers a wide number of areas including for example, nutrition, cancer, endocrinology, cardiology, addictions, immunology, birth defects, genetics, and so on. The chapters are written by national or international experts and specialists.

Tissue Repair, Contraction and the Myofibroblast summarizes the latest findings concerning the biology of the myofibroblast, a cell involved in the evolution and contraction of granulation tissue and of fibrotic changes. Coverage shows that the myofibroblast is responsible for the development of hypertrophic scars, pulmonary and renal fibrosis and bronchial asthma. Reviews the cell biology and pathology of the myofibroblast as well as mechanisms of fibrosis evolution in many organs and tissues.

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.