Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of subsequent chronic kidney disease. Although the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function is urgently needed. The Special Issue covers research articles that investigated the molecular mechanisms of inflammation and injury during different renal pathologies, renal regeneration, diagnostics using new biomarkers, and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models. The Special Issue contains important reviews that consider the current knowledge of cell death and regeneration, inflammation, and the molecular mechanisms of kidney diseases. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells or their derivates is summarized. This edition is complemented by reviews that deal with the current data situation on other specific topics like diabetes and diabetic nephropathy or new therapeutic targets.

Based on the Oxford Textbook of Clinical Nephrology and companion to the Oxford Handbook of Dialysis, this handbook provides clear information and practical advice about the day-to-day management of patients with renal disease.

Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of chronic kidney disease in the sequel. Whereas the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function-in both the short- and long-term-is urgently needed. This Special Issue includes papers investigating the pathological mechanisms of renal inflammation and AKI and diagnostics using new biomarkers. Furthermore, experimental in vitro and in vivo studies examining potential new approaches to attenuate kidney dysfunction are included, as well as review articles.

Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a highly prevalent hereditary renal disorder in which fluid-filled cysts are appeared in both kidneys. Main causative genes of ADPKD are PKD1 and PKD2, encoding for polycystin-1 (PC1) and polycystin-2 (PC2) respectively. Those proteins are localized on primary cilia and function as mechanosensor in response to the fluid flow, translating mechanistic stimuli into calcium signaling. With mutations either of PKD1 or PKD2, hyper-activated renal tubular epithelial cell proliferation is observed, followed by disrupted calcium homeostasis and aberrant intracellular cyclic AMP (cAMP) accumulation. Increased cell proliferation with fluid secretion leads to the development of thousands of epithelial-lined, fluid-filled cysts in kidneys. It is also accompanied by interstitial inflammation, fibrosis, and finally reaching end-stage renal disease (ESRD). In human ADPKD, the age at which renal failure typically occurs is later in life, however no specific targeted medications are available to cure ADPKD. Recently, potential therapeutic targets or surrogate diagnostic biomarkers for ADPKD are proposed with the advances in the understanding of ADPKD pathogenesis, and some of them were attempted for clinical trials. Herein, we will summarize genetic and epi-genetic molecular mechanisms in ADPKD progression, and overview the currently available biomarkers or potential therapeutic reagents suggested.

This book presents up-to-date information on the clinical-pathophysiological features of acute renal injury and discusses the KDIGO diagnostic criteria, as well as novel experimental findings, including in the area of regenerative medicine. It also highlights the clinical-pathophysiological importance of AKI in clinical settings, including differential diagnoses and management of AKI. In the past, the pathology associated with sudden renal impairment was characterized as acute renal failure (ARF). However, in the 2000s, the joint efforts of specialists in fields including nephrology, intensive care medicine, and cardiovascular medicine led to the introduction of a novel concept known as acute kidney injury (AKI). As medical care progressed, patients such as high-risk elderly subjects who were not deemed to be candidates for invasive therapy came to be treated in intensive care units (ICUs). As a result, kidney injury as a subset of multiple organ failure was re-considered as AKI, especially in intensive care medicine. AKI was then proposed as a novel disease concept to emphasize the importance of early diagnosis and early intervention to improve prognosis.Presenting novel features, such as the definition of AKI, risk factors and management; biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL) and L-type fatty acid-binding protein (L-FABP); long-term outcomes of AKI; as well as renal regeneration using iPS cell, manipulation of embryonic genes, and Xenotransplanted embryonic kidney, this book is of interest to all physicians and researchers in this field around the globe.

Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of subsequent chronic kidney disease. Although the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function is urgently needed. The Special Issue covers research articles that investigated the molecular mechanisms of inflammation and injury during different renal pathologies, renal regeneration, diagnostics using new biomarkers, and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models. The Special Issue contains important reviews that consider the current knowledge of cell death and regeneration, inflammation, and the molecular mechanisms of kidney diseases. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells or their derivates is summarized. This edition is complemented by reviews that deal with the current data situation on other specific topics like diabetes and diabetic nephropathy or new therapeutic targets.

The podocyte is a key cell that forms the last barrier of the kidney filtration unit. One of the most exciting developments in the field of nephrology in the last decade has been the elucidation of its biology and its role in the pathophysiology of inherited and acquired glomerular disease, termed podocytopathy. In this publication, world-renowned experts summarize the most recent findings and advances in the field: they describe the unique biological features and injury mechanisms of the podocyte, novel techniques used in their study, and diagnosis and potential therapeutic approaches to glomerular diseases. Due to its broad scope, this publication is of great value not only for clinical nephrologists and researchers, but also for students, residents, fellows, and postdocs.

Progression of chronic diseases in general and chronic kidney disease in particular has been traditionally viewed in the light of various contributors to development of glomerulosclerosis and tubulointerstitial scarring culminating in renal fibrosis. Indeed, this dogma prevailed for decades underscoring experimental attempts to halt fibrotic processes. Breakthrough investigations of the past few years on stem/progenitor cell involvement in organ regeneration caused a conceptual shift in tackling the mechanisms of nephrosclerosis. It has become clear that the rate of progression of chronic kidney disease is the net sum of the opposing trends: degenerative fibrotic processes and regenerative repair mechanisms. The latter part of this equation has been by and large ignored for years and only recently attracted investigative attention. This book revisits the problem of kidney disease by focusing on regenerative mechanisms in renal repair and on the ways these regenerative processes can become subverted by an intrinsic disease process eventuating in its progression. Cutting-edge investigations are summarized by the most experienced international team of experts. - Presents a comprehensive, translational source for all aspects of renal stem cells, tissue regeneration, and stem cell therapies for renal diseases in one reference work. This will ultimately result in time savings for academic, medical and pharma researchers - Experts in the renal stem cell system in kidney repair and regeneration take readers from the bench research to new therapeutic approaches, providing a common language for nephrology researchers, fellows and other stem cell researchers. This enables the discussion of development of stem cells and their use in the repair and regeneration of the kidney

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

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.