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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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Formato: | Texto |
Lenguaje: | English |
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Springer Berlin Heidelberg
2010
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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. |
format | Text |
id | pubmed-2778786 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
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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