Suppr超能文献

脑死亡供体肾脏具有免疫活性:干预是否合理?

Brain dead donor kidneys are immunologically active: is intervention justified?

作者信息

Vergoulas G, Boura P, Efstathiadis G

机构信息

Organ Transplant Unit, Hippokratio General Hospital, Thessaloniki, Greece.

出版信息

Hippokratia. 2009 Oct;13(4):205-10.

Abstract

The improvement in the field of kidney transplantation, during the last decades, has brought kindey transplantation to the top of patient preference as the best kidney replacement therapy. The use of marginal kidney grafts, which are highly immunogenic has become common practice because of lack of kidney donors. Inflammatory activity in the kidneys after brain death is an ongoing phenomenon. The inappropriate treatment of brain dead donor may result to primary non function (PNF) of the graft, delayed graft function (DGF) or to long term graft dysfunction and shortened graft survival. Therefore correct handling of the brain dead donor is of paramount importance. The impact of various pharmacologic agents (catecholamines, glucocorticoids, carbamylated recombinant human erythropoietin, recombinant soluble P-selectin glycoprotein ligant, heme oxygenase-1, carbon monoxide, and mycophenolate mofetil) on the immunogenicity of brain dead donor kidneys is discussed.

摘要

在过去几十年中,肾移植领域的进步已使肾移植成为患者首选的最佳肾脏替代疗法。由于缺乏肾供体,使用具有高度免疫原性的边缘性肾移植物已成为常见做法。脑死亡后肾脏中的炎症活动是一种持续存在的现象。对脑死亡供体的不当处理可能导致移植物原发性无功能(PNF)、移植肾功能延迟恢复(DGF)或长期移植物功能障碍以及缩短移植物存活时间。因此,正确处理脑死亡供体至关重要。本文讨论了各种药物制剂(儿茶酚胺、糖皮质激素、氨甲酰化重组人促红细胞生成素、重组可溶性P-选择素糖蛋白配体、血红素加氧酶-1、一氧化碳和霉酚酸酯)对脑死亡供体肾脏免疫原性的影响。

相似文献

3
Improvements in early behavior of rat kidney allografts after treatment of the brain-dead donor.
Ann Surg. 2001 Dec;234(6):732-40. doi: 10.1097/00000658-200112000-00004.
8
Effects of brain death on stress and inflammatory response in the human donor kidney.
Transplant Proc. 2005 Jan-Feb;37(1):367-9. doi: 10.1016/j.transproceed.2004.12.262.
10
Effect of brain death on gene expression and tissue activation in human donor kidneys.
Transplantation. 2004 Oct 15;78(7):978-86. doi: 10.1097/01.tp.0000135565.49535.60.

引用本文的文献

1
Cascading renal injury after brain death: Unveiling glycocalyx alteration and the potential protective role of tacrolimus.
Front Cell Dev Biol. 2024 Aug 6;12:1449209. doi: 10.3389/fcell.2024.1449209. eCollection 2024.
2
Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond.
EBioMedicine. 2018 Feb;28:31-42. doi: 10.1016/j.ebiom.2018.01.025. Epub 2018 Feb 2.
3
The role of innate immunity in donor organ procurement.
Semin Immunopathol. 2011 Mar;33(2):169-84. doi: 10.1007/s00281-011-0254-z. Epub 2011 Mar 23.

本文引用的文献

1
Signal transduction pathways involved in brain death-induced renal injury.
Am J Transplant. 2009 May;9(5):989-97. doi: 10.1111/j.1600-6143.2009.02587.x.
2
Epithelial-to-mesenchymal transition in early transplant tubulointerstitial damage.
J Am Soc Nephrol. 2008 Aug;19(8):1571-83. doi: 10.1681/ASN.2007050580. Epub 2008 May 14.
3
Early events in kidney donation: progression of endothelial activation, oxidative stress and tubular injury after brain death.
Am J Transplant. 2008 May;8(5):933-41. doi: 10.1111/j.1600-6143.2008.02166.x. Epub 2008 Mar 2.
4
Cytoprotective doses of erythropoietin or carbamylated erythropoietin have markedly different procoagulant and vasoactive activities.
Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5965-70. doi: 10.1073/pnas.0601377103. Epub 2006 Apr 3.
5
Improved long-term graft survival after HO-1 induction in brain-dead donors.
Am J Transplant. 2006 Mar;6(3):477-86. doi: 10.1111/j.1600-6143.2005.01208.x.
6
Low-dose carbon monoxide inhalation prevents development of chronic allograft nephropathy.
Am J Physiol Renal Physiol. 2006 Feb;290(2):F324-34. doi: 10.1152/ajprenal.00026.2005. Epub 2005 Aug 30.
7
Cyclosporine A-induced renal fibrosis: a role for epithelial-mesenchymal transition.
Am J Pathol. 2005 Aug;167(2):395-407. doi: 10.1016/S0002-9440(10)62984-7.
8
Cyclosporine A induced epithelial-mesenchymal transition in human renal proximal tubular epithelial cells.
Nephrol Dial Transplant. 2005 Oct;20(10):2215-25. doi: 10.1093/ndt/gfh967. Epub 2005 Jul 19.
9
Autophagy and intracellular surveillance: Modulating MHC class II antigen presentation with stress.
Proc Natl Acad Sci U S A. 2005 May 31;102(22):7779-80. doi: 10.1073/pnas.0503088102. Epub 2005 May 23.
10
Autophagy promotes MHC class II presentation of peptides from intracellular source proteins.
Proc Natl Acad Sci U S A. 2005 May 31;102(22):7922-7. doi: 10.1073/pnas.0501190102. Epub 2005 May 13.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验