Michela Amatruda, Nicolina Stefania Carucci, Roberto Chimenz, Giovanni Conti
{"title":"Immunoglobulin A vasculitis nephritis: Current understanding of pathogenesis and treatment.","authors":"Michela Amatruda, Nicolina Stefania Carucci, Roberto Chimenz, Giovanni Conti","doi":"10.5527/wjn.v12.i4.82","DOIUrl":null,"url":null,"abstract":"<p><p>The clinical spectrum of immunoglobulin A vasculitis nephritis (IgAVN) ranges from the relatively common transitory microscopic hematuria and/or low-grade proteinuria to nephritic or nephrotic syndrome, rapidly progressive glomerulonephritis, or even renal failure. Clinical and experimental studies have shown a multifactor pathogenesis: Infection triggers, impaired glycosylation of IgA1, complement activation, Toll-like-receptor activation and B cell proliferation. This knowledge can identify IgAVN patients at a greater risk for adverse outcome and increase the evidence for treatment recommendations.</p>","PeriodicalId":94272,"journal":{"name":"World journal of nephrology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/79/5f/WJN-12-82.PMC10520755.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"World journal of nephrology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5527/wjn.v12.i4.82","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The clinical spectrum of immunoglobulin A vasculitis nephritis (IgAVN) ranges from the relatively common transitory microscopic hematuria and/or low-grade proteinuria to nephritic or nephrotic syndrome, rapidly progressive glomerulonephritis, or even renal failure. Clinical and experimental studies have shown a multifactor pathogenesis: Infection triggers, impaired glycosylation of IgA1, complement activation, Toll-like-receptor activation and B cell proliferation. This knowledge can identify IgAVN patients at a greater risk for adverse outcome and increase the evidence for treatment recommendations.