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利妥昔单抗未能改善复发性局灶节段性肾小球硬化的肾移植患者的肾病综合征。

Rituximab failed to improve nephrotic syndrome in renal transplant patients with recurrent focal segmental glomerulosclerosis.

作者信息

Yabu J M, Ho B, Scandling J D, Vincenti F

机构信息

Department of Medicine, University of California, San Francisco, CA, USA.

出版信息

Am J Transplant. 2008 Jan;8(1):222-7. doi: 10.1111/j.1600-6143.2007.02021.x. Epub 2007 Nov 2.

DOI:10.1111/j.1600-6143.2007.02021.x
PMID:17979998
Abstract

Focal segmental glomerulosclerosis (FSGS) recurs in 30% of patients with FSGS receiving a first renal transplant and in over 80% of patients receiving a second transplant after a recurrence. Recurrence often leads to graft failure. The pathogenesis remains unknown and may involve a circulating permeability factor that initiates injury to the glomerular capillary. There are anecdotal reports of pediatric patients with posttransplant lymphoproliferative disorder (PTLD) and recurrent FSGS who have had remission of proteinuria after treatment with rituximab. These observations have prompted speculation that B cells may play a role in the pathogenesis of recurrent FSGS. We report four consecutive adult patients with early recurrent FSGS refractory or dependent on plasmapheresis who received rituximab (total dose 2000-4200 mg). None of the patients treated with rituximab achieved remission in proteinuria, and one patient experienced early graft loss. In these four adult renal transplant patients with recurrent FSGS, rituximab failed to diminish proteinuria.

摘要

局灶节段性肾小球硬化(FSGS)在接受首次肾移植的FSGS患者中有30%会复发,而在复发后接受第二次移植的患者中,复发率超过80%。复发常导致移植肾失功。其发病机制尚不清楚,可能涉及一种循环通透因子,该因子引发肾小球毛细血管损伤。有个案报道称,患有移植后淋巴细胞增生性疾病(PTLD)和复发性FSGS的儿科患者在接受利妥昔单抗治疗后蛋白尿缓解。这些观察结果促使人们推测B细胞可能在复发性FSGS的发病机制中起作用。我们报告了4例连续的成年患者,他们患有早期复发性FSGS,难治或依赖血浆置换,接受了利妥昔单抗治疗(总剂量2000 - 4200毫克)。接受利妥昔单抗治疗的患者均未实现蛋白尿缓解,且1例患者早期移植肾失功。在这4例复发性FSGS的成年肾移植患者中,利妥昔单抗未能减少蛋白尿。

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