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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 --- n/a

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The Special Issue entitled “Pediatric and adolescent nephrology facing the future: diagnostic advances and prognostic biomarkers in everyday practice” contains articles written in the era when COVID-19 had not yet been a major clinical problem in children. Now that we know its multifaceted clinical course, complications concerning the kidneys, and childhood-specific post-COVID pediatric inflammatory multisystem syndrome (PIMS), the value of diagnostic and prognostic biomarkers in the pediatric area should be appreciated, and their importance ought to increase.

Medicine --- Clinical & internal medicine --- chronic kidney disease --- cytokines --- solitary functioning kidney --- tumor necrosis factor-like weak inducer of apoptosis --- netrin-1 --- renal tubular damage --- premature newborns --- overactive bladder --- urinary microbiome --- children --- adolescents --- cystatin C --- galectin-3 --- periostin --- primary hypertension --- arterial damage --- blood pressure --- neurogenic bladder --- myelomeningocele --- markers --- furosemide stress test --- hyperfiltration --- [IGFBP-7] × [TIMP-2] --- NGAL --- renal angina index --- renal functional reserve --- tubular damage --- tubuloglomerular feedback --- neurotrophins --- transcutaneous electrical nerve stimulation --- hemopexin --- nephrotic syndrome --- HNF1B --- hyperuricemia --- PTH --- renal function --- uric acid --- FEUA --- sclerostin --- obesity --- childhood --- dental caries --- gingivitis --- kidney injury --- glomerulopathy --- glomerular injury --- alpha-1 acid glycoprotein --- urinary mRNA expression of podocyte-associated proteins --- cathepsin B --- premature neonates --- immaturity --- NT-proBNP --- cardiovascular disease --- common carotid artery intima-media thickness --- bone morphogenetic protein (BMP)-2 --- bone morphogenetic protein (BMP)-6 --- extracellular matrix metalloproteinases inducer (EMMPRIN) --- macrophage migration inhibitory factor (MIF) --- tubular functional reserve --- cytokeratin-18 --- endoglin --- transforming growth factor-β1 --- renal fibrosis --- congenital obstructive nephropathy --- diabetic kidney disease --- vascular endothelial markers --- eGFR --- adenine nucleotide metabolites --- chronic renal failure --- antibiotic resistance --- Escherichia coli --- inflammatory markers --- urinary tract infection --- B2M --- cancer --- CCS --- CKD --- nephropathies --- renal toxicity --- voiding cystography --- infection --- urinary tract --- IgA nephropathy --- IgA vasculitis with nephritis --- vanin-1 --- biomarker --- urinary tract infections --- artificial intelligence --- machine learning --- medical decision support system --- n/a