New insights into the pathophysiology of idiopathic nephrotic syndrome

被引:17
作者
Bruneau, Sarah
Dantal, Jacques [1 ]
机构
[1] CHU Hotel Dieu, ITERT, INSERM, U643, F-44093 Nantes 1, France
关键词
Idiopathic nephrotic syndrome; Transplantation; Recurrence; Immune origin; Rituximab; FOCAL SEGMENTAL GLOMERULOSCLEROSIS; MEASLES-VIRUS INFECTION; OF-THE-LITERATURE; RENAL-TRANSPLANTATION; RITUXIMAB TREATMENT; GLOMERULAR-PERMEABILITY; KIDNEY-TRANSPLANTATION; PROTEIN EXCRETION; LUPUS NEPHRITIS; IN-VITRO;
D O I
10.1016/j.clim.2009.03.532
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Corticoresistant idiopathic nephrotic syndrome (INS) is a glomerulopathy of unknown etiology whose original aspect is its recurrence after kidney transplantation in 30 to 50% of patients with end-stage renal disease. This suggests the involvement of circulating factors that would alter the glomerular filtration barrier, but whose nature remains elusive. Although a T cell. immune origin has been suggested, the actual role of these cells in INS recurrence is still unclear. Here we present an 8-year-old patient with corticoresistant INS who developed a recurrence of her initial disease after kidney transplantation. Rituximab therapy was proposed 11 months after transplantation; although no immediate effect was induced, a slow but persistent decrease in proteinuria began a few months after Rituximab infusions despite cessation of plasma exchanges and steroid therapy. The pathophysiology of INS and the putative mechanisms of action of Rituximab are discussed. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:13 / 21
页数:9
相关论文
共 80 条
[1]  
ALI AA, 1994, TRANSPLANTATION, V58, P849
[2]   A case of unfulfilled expectations. Cytokines in idiopathic minimal lesion nephrotic syndrome [J].
Araya, CE ;
Wasserfall, CH ;
Brusko, TM ;
Mu, W ;
Segal, MS ;
Johnson, RJ ;
Garin, EH .
PEDIATRIC NEPHROLOGY, 2006, 21 (05) :603-610
[3]   PLASMAPHERESIS REDUCES PROTEINURIA AND SERUM CAPACITY TO INJURE GLOMERULI IN PATIENTS WITH RECURRENT FOCAL GLOMERULOSCLEROSIS [J].
ARTERO, ML ;
SHARMA, R ;
SAVIN, VJ ;
VINCENTI, F .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1994, 23 (04) :574-581
[4]   Measles virus infection of thymic epithelium in the SCID-hu mouse leads to thymocyte apoptosis [J].
Auwaerter, PG ;
Kaneshima, H ;
McCune, JM ;
Wiegand, G ;
Griffin, DE .
JOURNAL OF VIROLOGY, 1996, 70 (06) :3734-3740
[5]   Rituximab in patients with the steroid-resistant nephrotic syndrome [J].
Bagga, Arvind ;
Sinha, Aditi ;
Moudgil, Asha .
NEW ENGLAND JOURNAL OF MEDICINE, 2007, 356 (26) :2751-2752
[6]   Rituximab for post-transplant recurrences of FSGS [J].
Bayrakci, Umut Selda ;
Baskin, Esra ;
Sakalli, Hale ;
Karakayali, Hamdi ;
Haberal, Mehmet .
PEDIATRIC TRANSPLANTATION, 2009, 13 (02) :240-243
[7]  
BURSTEIN DM, 1993, J AM SOC NEPHROL, V4, P1288
[8]   Serum glomerular permeability activity in patients with podocin mutations (NPHS2) and steroid-resistant nephrotic syndrome [J].
Carraro, M ;
Caridi, G ;
Bruschi, M ;
Artero, M ;
Bertelli, R ;
Zennaro, C ;
Musante, L ;
Candiano, G ;
Perfumo, F ;
Ghiggeri, GM .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2002, 13 (07) :1946-1952
[9]   Atopy, serum IgE, and interleukin-13 in steroid-responsive nephrotic syndrome [J].
Cheung, W ;
Wei, CL ;
Seah, CC ;
Jordan, SC ;
Yap, HK .
PEDIATRIC NEPHROLOGY, 2004, 19 (06) :627-632
[10]   Nephrotic plasma alters slit diaphragm-dependent signaling and translocates nephrin, podocin, and CD2 associated protein in cultured human podocytes [J].
Coward, RJM ;
Foster, RR ;
Patton, D ;
Ni, L ;
Lennon, R ;
Bates, DO ;
Harper, SJ ;
Mathieson, PW ;
Saleem, MA .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2005, 16 (03) :629-637