Suppr超能文献

原发性局灶节段性肾小球硬化与可溶性因子尿激酶型纤溶酶原激活物受体

Primary focal and segmental glomerulosclerosis and soluble factor urokinase-type plasminogen activator receptor.

作者信息

Trimarchi Hernán

机构信息

Hernán Trimarchi, Servicio de Nefrología, Hospital Británico de Buenos Aires, Buenos Aires 1280, Argentina.

出版信息

World J Nephrol. 2013 Nov 6;2(4):103-10. doi: 10.5527/wjn.v2.i4.103.

Abstract

Primary focal and segmental glomerulosclerosis (FSGS) may be due to genetic or acquired etiologies and is a common cause of nephrotic syndrome with high morbidity that often leads to end-stage renal failure. The different available therapeutic approaches are unsuccessful, in part due to partially deciphered heterogeneous and complex pathophysiological mechanisms. Moreover, the term FSGS, even in its primary form, comprises a histological description shared by a number of different causes with completely different molecular pathways of disease. This review focuses on the latest developments regarding the pathophysiology of primary acquired FSGS caused by soluble factor urokinase type plasminogen activator receptor, a circulating permeability factor involved in proteinuria and edema formation, and describes recent advances with potential success in therapy.

摘要

原发性局灶节段性肾小球硬化(FSGS)可能由遗传或后天病因引起,是肾病综合征的常见病因,发病率高,常导致终末期肾衰竭。现有的不同治疗方法均未成功,部分原因是其异质性和复杂的病理生理机制尚未完全阐明。此外,FSGS这一术语,即使是其原发性形式,也包含了多种不同病因共有的组织学描述,而这些病因具有完全不同的疾病分子途径。本综述聚焦于由可溶性因子尿激酶型纤溶酶原激活物受体引起的原发性获得性FSGS的病理生理学最新进展,该受体是一种参与蛋白尿和水肿形成的循环通透性因子,并描述了在治疗方面可能取得成功的最新进展。

相似文献

2
Molecular Mechanisms of Proteinuria in Focal Segmental Glomerulosclerosis.
Front Med (Lausanne). 2018 Apr 16;5:98. doi: 10.3389/fmed.2018.00098. eCollection 2018.
3
A circulating permeability factor in focal segmental glomerulosclerosis: the hunt continues.
Clin Kidney J. 2015 Dec;8(6):708-15. doi: 10.1093/ckj/sfv090. Epub 2015 Sep 15.
6
Soluble Urokinase Receptors in Focal Segmental Glomerulosclerosis: A Review on the Scientific Point of View.
J Immunol Res. 2016;2016:2068691. doi: 10.1155/2016/2068691. Epub 2016 Jul 18.
7
Circulating Permeability Factors in Primary Focal Segmental Glomerulosclerosis: A Review of Proposed Candidates.
Biomed Res Int. 2016;2016:3765608. doi: 10.1155/2016/3765608. Epub 2016 Apr 21.

引用本文的文献

1
Roles of Immune Cells in Hereditary Angioedema.
Clin Rev Allergy Immunol. 2021 Jun;60(3):369-382. doi: 10.1007/s12016-021-08842-9. Epub 2021 May 29.
2
Mechanisms of Podocyte Detachment, Podocyturia, and Risk of Progression of Glomerulopathies.
Kidney Dis (Basel). 2020 Sep;6(5):324-329. doi: 10.1159/000507997. Epub 2020 May 27.
5
New therapeutic perspectives for IgA nephropathy in children.
Pediatr Nephrol. 2021 Mar;36(3):497-506. doi: 10.1007/s00467-020-04475-w. Epub 2020 Feb 10.
6
Soluble CD40 ligand directly alters glomerular permeability and may act as a circulating permeability factor in FSGS.
PLoS One. 2017 Nov 20;12(11):e0188045. doi: 10.1371/journal.pone.0188045. eCollection 2017.
7
Podocyturia: Potential applications and current limitations.
World J Nephrol. 2017 Sep 6;6(5):221-228. doi: 10.5527/wjn.v6.i5.221.
8
Podocyturia: What is in a name?
J Transl Int Med. 2015 Apr-Jun;3(2):51-56. doi: 10.1515/jtim-2015-0003. Epub 2015 Jun 30.
9
Copious Podocyturia without Proteinuria and with Normal Renal Function in a Young Adult with Fabry Disease.
Case Rep Nephrol. 2015;2015:257628. doi: 10.1155/2015/257628. Epub 2015 May 21.
10
Podocyte directed therapy of nephrotic syndrome-can we bring the inside out?
Pediatr Nephrol. 2016 Mar;31(3):393-405. doi: 10.1007/s00467-015-3116-4. Epub 2015 May 5.

本文引用的文献

1
suPAR and FSGS: the gap between bench and bedside.
Transplantation. 2013 Aug 27;96(4):368-9. doi: 10.1097/TP.0b013e31829e6d40.
3
Serum suPAR in patients with FSGS: trash or treasure?
Pediatr Nephrol. 2013 Jul;28(7):1041-8. doi: 10.1007/s00467-013-2452-5. Epub 2013 Mar 21.
4
Remission of nephrotic syndrome diminishes urinary plasmin content and abolishes activation of ENaC.
Pediatr Nephrol. 2013 Aug;28(8):1227-34. doi: 10.1007/s00467-013-2439-2. Epub 2013 Mar 16.
5
Circulating suPAR in two cohorts of primary FSGS.
J Am Soc Nephrol. 2012 Dec;23(12):2051-9. doi: 10.1681/ASN.2012030302. Epub 2012 Nov 8.
6
Urinary plasmin inhibits TRPV5 in nephrotic-range proteinuria.
J Am Soc Nephrol. 2012 Nov;23(11):1824-34. doi: 10.1681/ASN.2011111126. Epub 2012 Sep 27.
7
Therapeutic apheresis rescue mission: recurrent focal segmental glomerulosclerosis in renal allografts.
Semin Dial. 2012 Mar-Apr;25(2):190-2. doi: 10.1111/j.1525-139X.2011.01031.x. Epub 2011 Dec 16.
8
Amiloride off-target effect inhibits podocyte urokinase receptor expression and reduces proteinuria.
Nephrol Dial Transplant. 2012 May;27(5):1746-55. doi: 10.1093/ndt/gfr612. Epub 2011 Nov 9.
9
The podocyte cytoskeleton--key to a functioning glomerulus in health and disease.
Nat Rev Nephrol. 2011 Oct 25;8(1):14-21. doi: 10.1038/nrneph.2011.151.
10
A suPAR circulating factor causes kidney disease.
Nat Med. 2011 Aug 4;17(8):926-7. doi: 10.1038/nm.2443.

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