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The understanding of the pathogenesis of diabetic nephropathy (DN) has advanced considerably in the last few years. Much has been learned about the natural history, the relative lack of significance of microalbuminuria in reflecting underlying pathological change, questionable effects of ACEs and ARBs on the progression of nephropathy, the emergence of new biomarkers such as Cystatin and the role of cytokines, inflammatory molecules and adhesion molecules. Podocytes, the cells with limited ability to replenish and to repair, play a pivotal role in glomerular filtration. In recent years these cells have become the focus for research on pathogenesis of DN as well as other nephropathies. A recent review from the NIH has identified new insights into the pathophysiology, the genetics and the role of the podocytes and some of the important new metabolic pathways such as mTOR or autophagy which may be targeting the podocyte. Knowledge is emerging about the role of podocyte as a part of immune system and about the role of growth factors and cytokines in regulation of podocyte functions. Presented in this e-book articles highlight recent advances in our understanding of the pathogenesis of kidney pathology and the role of podocytes in this process.

Diabetic nephropathies. --- Kidneys --- Podocytes --- glomeruli --- foot processes --- kidney disease --- Exosomes --- diabetes --- Proteinuria --- Diseases --- Pathogenesis. --- cytology.

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Nephrotic syndrome (NS) - characterized by heavy glomerular protein loss (proteinuria), edema, hypoalbuminemia, and hyperlipidemia - has diverse causes and frequently leads to chronic kidney disease. This E-book encompasses articles on a variety of topics in NS, including a historical perspective on understanding and treatment of NS, followed by state-of-the-art reviews of the molecular pathomechanisms, clinical outcomes, as well as current and emerging treatment strategies for NS. We hope that this comprehensive review will help to reduce the gaps between the research and the day-to-day care of patients with NS and inspire new research efforts towards updating and expanding the treatment armamentarium for the future.

edema --- podocytes --- proteinuria --- FSGS --- slit diaphragm --- minimal change disease --- APOL1 --- prednisone --- nephrotic syndrome --- calcineurin inhibitors

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The understanding of the pathogenesis of diabetic nephropathy (DN) has advanced considerably in the last few years. Much has been learned about the natural history, the relative lack of significance of microalbuminuria in reflecting underlying pathological change, questionable effects of ACEs and ARBs on the progression of nephropathy, the emergence of new biomarkers such as Cystatin and the role of cytokines, inflammatory molecules and adhesion molecules. Podocytes, the cells with limited ability to replenish and to repair, play a pivotal role in glomerular filtration. In recent years these cells have become the focus for research on pathogenesis of DN as well as other nephropathies. A recent review from the NIH has identified new insights into the pathophysiology, the genetics and the role of the podocytes and some of the important new metabolic pathways such as mTOR or autophagy which may be targeting the podocyte. Knowledge is emerging about the role of podocyte as a part of immune system and about the role of growth factors and cytokines in regulation of podocyte functions. Presented in this e-book articles highlight recent advances in our understanding of the pathogenesis of kidney pathology and the role of podocytes in this process.

Diabetic nephropathies. --- Kidneys --- Podocytes --- Diseases --- Pathogenesis. --- cytology. --- glomeruli --- foot processes --- kidney disease --- Exosomes --- diabetes --- Proteinuria

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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.

inflammation --- chronic kidney disease --- anemia --- anemia of inflammation --- ESA hyporesponsiveness --- renal tubular epithelial cells --- macrophages --- lipocalin-2 --- iron --- cilastatin --- hypoxia inducible factor-1-α --- ischemia-reperfusion injury --- acute kidney injury --- cyclophilin A --- fibrosis --- renal fibrosis --- tubular necrosis --- preeclampsia --- podocytes --- VEGF --- FSGS --- proteinuria --- endocan --- ESM-1 --- renal replacement therapy --- kidney transplantation --- biomarker --- diabetic nephropathy --- focal segmental glomerulosclerosis --- innate immunity --- membranous nephropathy --- minimal change diseases --- TLR --- NOX1 --- ML171 --- reactive oxygen species --- ERK --- T cells --- glomerulonephritis --- chemokines --- renal disease --- DJ-1 --- ND-13 --- renal inflammation --- oxidative stress --- UUO --- autophagy --- apoptosis --- trehalose --- simvastatin --- endotoxin --- tubular apoptosis --- cytochrome C --- Bcl-XL --- survivin --- hypercholesterolemia --- xanthine oxidase --- NF-κB pathway --- tertiary lymphoid organs --- B cells --- BAFF --- kidney fibrosis --- myofibroblast activation --- extracellular matrix --- Hippo pathway --- verteporfin --- IgAN --- CKD --- progression --- ACEI --- corticosteroids --- costimulation --- coinhibition --- kidney transplant --- SPR --- protein binding affinity --- adaptive immunity --- epithelial-to-mesenchymal transition --- E. cava extracts --- dieckol --- spontaneously hypertensive rats --- angiotensin II --- n/a