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IgA nephropathy is the most common primary glomerulonephritis in developed countries. The primary defect lies in the abnormalities of the IgA molecule. The disease affects all ages, mainly in the young adults, and may recur in a transplanted kidney. This outstanding volume provides a comprehensive overview of the advances in this disease over the last ten years. It covers the genetics, epidemiology, clinicopathological features, pathogenesis, prognostic mechanisms, and treatment of this unique disease. Twenty-seven chapters are written by 43 experts from 13 countries; these experts have been p

IgA glomerulonephritis. --- Glomerulonephritis. --- Immune complex diseases --- Kidney glomerulus --- Berger's disease --- IgA nephropathy --- Nephropathy, IgA --- Glomerulonephritis --- Immunoglobulin A --- Diseases

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IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide and a frequent cause of kidney failure. Better understanding of the pathogenesis of IgAN and the related genetic, immunological, and cellular susceptibility factors are needed to enable the development of effective disease-specific therapy. This book brings together international experts to provide clinical and experimental studies and reviews with an emphasis on early diagnosis, prognosis, disease pathogenesis, determination of disease activity, and new strategies for treatment for IgAN.

Medicine --- obesity --- mesangial matrix expansion --- body mass index --- IgA nephropathy --- IgA Vasculitis --- IgA Nephropathy --- adults --- children --- presentation --- physiopathology --- genetics --- prognosis --- treatment --- IgA --- clinical trials --- kidney mesangium --- mouse model --- aberrantly glycosylated IgA1 --- galactose-deficient IgA1 --- glycosylation of IgA1 --- biomarker --- complement C3 --- O-glycosylation --- IgA1 --- autoantibody --- immune complex --- complement --- kidney --- nephrology --- IgA vasculitis --- nephritis --- kidney biopsy --- plasma cells --- CD38 --- renal pathology --- urinary galactose-deficient IgA1 --- KM55 --- crescents --- proteinuria --- glomerular filtration rate --- Oxford score --- obesity --- mesangial matrix expansion --- body mass index --- IgA nephropathy --- IgA Vasculitis --- IgA Nephropathy --- adults --- children --- presentation --- physiopathology --- genetics --- prognosis --- treatment --- IgA --- clinical trials --- kidney mesangium --- mouse model --- aberrantly glycosylated IgA1 --- galactose-deficient IgA1 --- glycosylation of IgA1 --- biomarker --- complement C3 --- O-glycosylation --- IgA1 --- autoantibody --- immune complex --- complement --- kidney --- nephrology --- IgA vasculitis --- nephritis --- kidney biopsy --- plasma cells --- CD38 --- renal pathology --- urinary galactose-deficient IgA1 --- KM55 --- crescents --- proteinuria --- glomerular filtration rate --- Oxford score

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IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide and a frequent cause of kidney failure. Better understanding of the pathogenesis of IgAN and the related genetic, immunological, and cellular susceptibility factors are needed to enable the development of effective disease-specific therapy. This book brings together international experts to provide clinical and experimental studies and reviews with an emphasis on early diagnosis, prognosis, disease pathogenesis, determination of disease activity, and new strategies for treatment for IgAN.

obesity --- mesangial matrix expansion --- body mass index --- IgA nephropathy --- IgA Vasculitis --- IgA Nephropathy --- adults --- children --- presentation --- physiopathology --- genetics --- prognosis --- treatment --- IgA --- clinical trials --- kidney mesangium --- mouse model --- aberrantly glycosylated IgA1 --- galactose-deficient IgA1 --- glycosylation of IgA1 --- biomarker --- complement C3 --- O-glycosylation --- IgA1 --- autoantibody --- immune complex --- complement --- kidney --- nephrology --- IgA vasculitis --- nephritis --- kidney biopsy --- plasma cells --- CD38 --- renal pathology --- urinary galactose-deficient IgA1 --- KM55 --- crescents --- proteinuria --- glomerular filtration rate --- Oxford score --- n/a

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Background: The gut microbiota is emerging as a pivotal player in the pathogenesis of many non-communicable diseases. Thus, it has been proposed as a new diagnostic and therapeutic target.Aim and scope: This Special Issue will focus on the microbiome as a potential target of new personalized therapies or diagnostic tools.History: In recent decades, the gut microbiome has been deeply investigated, and many studies have provided new information on the role of dysbiosis in many gastrointestinal and extra-gastrointestinal diseases. Recently, in addition to its phylogenetic characterization, new information has become available regarding the function of the gut microbiota, thanks to proteomic and metabolomic analyses.Cutting-edge research: The therapeutic modulation of the gut microbiota based on different strategies, including diet modification, antibiotics, prebiotics, probiotics, and, last but not least, fecal microbiota transplantation, has been tested for the treatment of various diseases. Recently, the possible applications and modalities of gut microbiota modulation have been increasingly expanding.We have collected original clinical or pre-clinical research papers and reviews focusing on the use of the microbiome for disease diagnosis, monitoring, or therapy and suggesting new possible gut microbiota-based approaches for personalized care.

Medicine --- Graves–Basedow’s diseases --- Hashimoto’s thyroiditis --- autoimmunity --- gut microbiota --- irritable bowel syndrome --- microbiota --- microbiome --- food components --- nutrients --- hematopoietic stem cell transplantation --- fecal microbiota transplantation --- aGvHD --- antibiotic-resistant bacteria --- cystic fibrosis --- rabbits --- intestinal dysbiosis --- feces microbiome --- beta-blocker --- hemodialysis --- next-generation sequencing --- propensity score matching methods --- violin plots --- random sampling --- analytical reproducibility --- fecal matter transplantation --- data disease subtypes --- personalized medicine --- maltodextrin --- dip test --- gallstone disease --- 16S rDNA gene diversity --- blood biochemical characteristics --- mesothelioma --- 16S RNA sequencing --- species --- probiotics and gut disease --- probiotics and acute diverticulitis --- probiotics and diverticular disease --- probiotics mechanism of action --- IgA Nephropathy --- rifaximin --- α1KI-CD89Tg mice --- children --- intermittent hypoxemia --- obstructive sleep apnea --- tonsil --- weight status --- oral microbiota --- rheumatology diseases --- biomarkers --- artificial intelligence --- machine learning --- rheumatoid arthritis --- Sjogren’s syndrome --- systemic lupus erythematosus --- endometrial cancer --- endometrial microbiome --- gut microbiome --- dysbiosis --- estrogen metabolism --- estrobolome --- inflammation --- antitumour treatment --- prebiotics --- probiotics --- schizophrenia --- depression --- anxiety --- functional genes --- thymoma --- genera --- driver mutation --- cardiovascular diseases --- critically ill --- intestinal permeability --- recurrent cystitis --- n/a --- Graves-Basedow's diseases --- Hashimoto's thyroiditis --- Sjogren's syndrome

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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 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.

microRNAs --- n/a --- transcription --- ischemia/reperfusion injury --- DSS-colitis --- kidney inflammation --- therapeutics targets --- CXCL13 --- glomerulus --- interleukin-6 --- rhabdomyolysis --- IgA nephropathy --- CREB Regulated Transcriptional Coactivators (CRTC) --- slit diaphragm --- injury --- xanthine oxidase --- Salt Inducible Kinase (SIK) --- acute and chronic kidney disease --- therapeutic target --- KIT-IgA score --- G-protein-coupled bile acid receptor (TGR5) --- lysophosphatidic acid --- glomerular injury --- IL-18 --- mesenchymal stem cells --- Taiwan --- acute kidney injury --- renal ischemia-reperfusion --- long non-coding RNA --- fibrosis --- acute kidney failure --- diabetic kidney diseases --- chronic kidney disease --- lncRNA --- LPS-binding protein --- endotoxemia-induced oliguric kidney injury --- dapagliflozin --- cPLA2 and COX-2 --- NLRP3 inflammasome --- CmklR1 --- haem --- chronic kidney injury --- omega-3 fatty acid --- noninvasive --- inflammation --- regulated necrosis --- GLP-1 receptor agonists --- miRNA --- AKI --- SGLT2 inhibitors --- diabetic kidney disease --- extracellular vesicles --- podocin --- type IV collagen --- epithelial cells --- nephrin --- 2-kidney-1-clip --- renal fibrosis --- papilla --- diagnostics --- necrosis --- non-coding RNAs --- podocyte --- Thy1.1 nephritis --- KIT assay --- oxidative stress --- conditioned medium --- C-reactive protein --- pericyte --- myofibroblast --- Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-?B) --- endotoxemia --- modifier gene --- polymorphism --- renal stem cells --- kidney --- polyploidization --- Class IIa Histone Deacetylases (HDAC) --- 2k1c --- molecular signaling --- proximal tubule --- arachidonic acid --- empagliflozin --- tubular injury --- signaling cascade --- signal transduction --- inflammatory maker --- niches --- biomarkers --- renal progenitors --- type V collagen --- cyclooxygenase --- focal segmental glomerulosclerosis --- inflammatory bowel disease (IBD) --- chronic kidney disease (CKD) --- allograft rejection --- renovascular hypertension --- genotype --- molecular mechanisms --- ROS --- prediction --- glomerular filtration barrier (GFB) --- alport syndrome --- scattered tubular cells --- long non-coding RNAs --- renal inflammation --- lysophosphatidic acid receptor --- cAMP Regulatory Element Binding Protein (CREB) --- Farnesiferol B --- differentiation --- mesenchymal stromal cells --- modified-MSCs --- kidney transplantation --- polyunsaturated fatty acids --- apoptosis --- type I collagen --- diabetes mellitus --- natural products --- lipoxygenase --- stem cell --- T cell-mediated rejection --- exosomes --- renal injury --- obese kidney fibrosis --- kidney injury --- cytotoxicity --- mesenchymal stem cell --- pigment nephropathy --- mesodermal stem cell --- ischemia-reperfusion --- cytochrome P450 --- renal cell carcinoma --- hematuria --- B-cell attracting chemokine --- microRNA --- chemerin --- glomerular basement membrane --- glomerular damage --- renal tubular cells --- kidney proximal tubule --- exosome --- hypertension --- diabetic nephropathy