الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Idiopathic nephrotic syndrome is the most frequent glomerular disease in children. The mechanisms underlying its pathophysiology have been investigated by genetic, cellular and molecular approaches (Zhang et al., 2011).
The response to corticosteroids distinguishes steroid-sensitive nephrotic syndrome (SSINS), by far the most frequent (90% of cases), from steroid-resistant nephrotic syndrome (SRINS). The steroid resistance of nephrotic syndrome is defined by the absence of remission after a full dose of oral corticosteroid therapy for 1 month followed by 3 pulses of intravenous methylprednisolone (Chemli and Harbi, 2009). Multidrug resistance is an occasionally seen phenomenon in children with idiopathic nephrotic syndrome (INS), but the mechanism of multidrug resistance is not clear as yet (Ma et al., 2009).
Funaki et al., (2008) investigated the role of multiple drug-resistant gene 1 (MDR1) mRNA expression in the steroid response in children with nephrotic syndrome. They found that MDR1 mRNA levels before completes remission (CR) were variable in each patient, but there was an apparent decrease in the MDR1 gene expression after CR in SSNS.