Remission of refractory minimal change nephrotic syndrome after basiliximab therapy
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BRIEF REPORT
Remission of refractory minimal change nephrotic syndrome after basiliximab therapy Sung-Shin Park & Won-Ho Hahn & Sung-Do Kim & Byoung-Soo Cho
Received: 21 October 2008 / Revised: 2 February 2009 / Accepted: 3 February 2009 / Published online: 26 February 2009 # IPNA 2009
Abstract Minimal change nephrotic syndrome has been proposed to be a disorder of T cell dysfunction. It is hypothesized that a circulating factor(s) from activated T cells might alter glomerular permeability to protein. Some studies have provided evidence that up-regulation of interleukin-2 may be involved, not only in the pathophysiology of minimal change nephrotic syndrome, but also in steroid resistance. Basiliximab, an anti-interleukin-2 receptor antibody, is indicated for the prophylaxis of acute organ rejection in adults and children with kidney transplants. Clinical trials have shown that basiliximab is effective and well tolerated. We describe here a pediatric patient who continuously had massive proteinuria and hypoalbuminemia for 5 years, despite pulse therapy with methylprednisolone and cyclophosphamide and prolonged oral treatment with cyclosporine and mizoribine. He had experienced several disease- and treatment-associated complications, such as bacterial infections, indirect inguinal hernias, and cataracts. After he had been given a single dose of basiliximab, he achieved complete remission of proteinuria and then discontinued all immunosuppressant treatment. Keywords Anti-interleukin-2 receptor antibody . Basiliximab . Cyclosporine-resistant nephrotic syndrome . Minimal change nephrotic syndrome . Steroid-resistant nephrotic syndrome S.-S. Park : W.-H. Hahn : S.-D. Kim : B.-S. Cho (*) Department of Pediatrics, East West Kidney Diseases Research Institute, Kyung-Hee University, Hoegi-dong, Dongdaemun-gu, Seoul 130-702, Korea e-mail: [email protected]
Introduction Minimal change nephrotic syndrome (MCNS) is the most common cause of nephrotic syndrome in children. MCNS accounts for 85% of all cases of childhood nephrotic syndrome [1]. The pathophysiologic process of MCNS remains poorly understood; however, experimental and clinical data suggest that this nephropathy is the consequence of an immune disorder, especially T cell dysfunction, in which a circulating factor(s) causes effacement of the epithelial foot processes and subsequent proteinuria [2–5]. To date, the circulating factor(s) remains unidentified; however, the implication of several cytokines has been suggested. Some studies have provided evidence that upregulation of interleukin (IL)-2 may be involved, not only in the pathophysiology of MCNS, but also in steroid resistance [6–10]. Children with the onset of nephrotic syndrome between 1 year and 8 years of age are likely to have steroid-sensitive MCNS; ≥ 95% of children with MCNS respond to corticosteroid therapy [1]. MCNS accounts for 20% of children with steroid-resistant nephrotic syndrome [1]. High-dose pulses of methylprednisolone, cyclosporine or tacrolimus, cyclophosphamide, and mycophenolate are use
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