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Pathogenesis of Henoch-Schönlein purpura nephritis

The severity of renal involvement is the major factor determining the long-term outcome of children with Henoch-Schönlein purpura (HSP) nephritis (HSPN). Approximately 40% children with HSP develop nephritis, usually within 4 to 6 weeks after the initial onset of the typical purpuric rashes. Althoug...

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Detalles Bibliográficos
Autores principales: Lau, Keith K., Suzuki, Hitoshi, Novak, Jan, Wyatt, Robert J.
Formato: Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778786/
https://www.ncbi.nlm.nih.gov/pubmed/19526254
http://dx.doi.org/10.1007/s00467-009-1230-x
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author Lau, Keith K.
Suzuki, Hitoshi
Novak, Jan
Wyatt, Robert J.
author_facet Lau, Keith K.
Suzuki, Hitoshi
Novak, Jan
Wyatt, Robert J.
author_sort Lau, Keith K.
collection PubMed
description The severity of renal involvement is the major factor determining the long-term outcome of children with Henoch-Schönlein purpura (HSP) nephritis (HSPN). Approximately 40% children with HSP develop nephritis, usually within 4 to 6 weeks after the initial onset of the typical purpuric rashes. Although the pathogenetic mechanisms are still not fully delineated, several studies suggest that galactose-deficient IgA1 (Gd-IgA1) is recognized by anti-glycan antibodies, leading to the formation of the circulating immune complexes and their mesangial deposition that induce renal injury in HSPN.
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spelling pubmed-27787862009-11-20 Pathogenesis of Henoch-Schönlein purpura nephritis Lau, Keith K. Suzuki, Hitoshi Novak, Jan Wyatt, Robert J. Pediatr Nephrol Review The severity of renal involvement is the major factor determining the long-term outcome of children with Henoch-Schönlein purpura (HSP) nephritis (HSPN). Approximately 40% children with HSP develop nephritis, usually within 4 to 6 weeks after the initial onset of the typical purpuric rashes. Although the pathogenetic mechanisms are still not fully delineated, several studies suggest that galactose-deficient IgA1 (Gd-IgA1) is recognized by anti-glycan antibodies, leading to the formation of the circulating immune complexes and their mesangial deposition that induce renal injury in HSPN. Springer Berlin Heidelberg 2010-01-01 2010 /pmc/articles/PMC2778786/ /pubmed/19526254 http://dx.doi.org/10.1007/s00467-009-1230-x Text en © The Author(s) 2009 https://creativecommons.org/licenses/by-nc/2.0/Open AccessThis is an open access article distributed under the terms of the Creative Commons Attribution Noncommercial License (https://creativecommons.org/licenses/by-nc/2.0 (https://creativecommons.org/licenses/by-nc/2.0/) ), which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Review
Lau, Keith K.
Suzuki, Hitoshi
Novak, Jan
Wyatt, Robert J.
Pathogenesis of Henoch-Schönlein purpura nephritis
title Pathogenesis of Henoch-Schönlein purpura nephritis
title_full Pathogenesis of Henoch-Schönlein purpura nephritis
title_fullStr Pathogenesis of Henoch-Schönlein purpura nephritis
title_full_unstemmed Pathogenesis of Henoch-Schönlein purpura nephritis
title_short Pathogenesis of Henoch-Schönlein purpura nephritis
title_sort pathogenesis of henoch-schönlein purpura nephritis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778786/
https://www.ncbi.nlm.nih.gov/pubmed/19526254
http://dx.doi.org/10.1007/s00467-009-1230-x
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