IgA nephropathy: the lectin pathway and implications for targeted therapy
Language English Country United States Media print-electronic
Document type Journal Article, Review
PubMed
37263354
DOI
10.1016/j.kint.2023.04.029
PII: S0085-2538(23)00395-2
Knihovny.cz E-resources
- Keywords
- IgA nephropathy, complement, glomerulonephritis,
- MeSH
- Kidney Glomerulus pathology MeSH
- Glomerulonephritis, IGA * pathology MeSH
- Immunoglobulin A metabolism MeSH
- Kidney pathology MeSH
- Lectins metabolism MeSH
- Humans MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Immunoglobulin A MeSH
- Lectins MeSH
Many patients with immunoglobulin A nephropathy (IgAN) progress to kidney failure even with optimal supportive care. An improved understanding of the pathophysiology of IgAN in recent years has led to the investigation of targeted therapies with acceptable tolerability that may address the underlying causes of IgAN or the pathogenesis of kidney injury. The complement system-particularly the lectin and alternative pathways of complement-has emerged as a key mediator of kidney injury in IgAN and a possible target for investigational therapy. This review will focus on the lectin pathway. The examination of kidney biopsies has consistently shown glomerular deposition of mannan-binding lectin (1 of 6 pattern-recognition molecules that activate the lectin pathway) together with IgA1 in up to 50% of patients with IgAN. Glomerular deposition of pattern-recognition molecules for the lectin pathway is associated with more severe glomerular damage and more severe proteinuria and hematuria. Emerging research suggests that the lectin pathway may also contribute to tubulointerstitial fibrosis in IgAN and that collectin-11 is a key mediator of this association. This review summarizes the growing scientific and clinical evidence supporting the role of the lectin pathway in IgAN and examines the possible therapeutic role of lectin pathway inhibition for these patients.
Department of Cardiovascular Sciences University of Leicester Leicester UK
Department of Medicine Division of Nephrology Stanford Health Care Stanford California USA
Department of Medicine Division of Renal Medicine Emory University Atlanta Georgia USA
Department of Nephrology and Rheumatology RWTH Aachen University Hospital Aachen Germany
References provided by Crossref.org
The role of BAFF and APRIL in IgA nephropathy: pathogenic mechanisms and targeted therapies
