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Relationship between expression of Pad1 homologue and multidrug resistance of idiopathic nephrotic syndrome
Author(s) -
Ma Zuxiang,
Gao Xiaojie,
Zhao Weiling,
Li Yongbai,
Li Changgang,
Li Chengrong
Publication year - 2009
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.2009.02845.x
Subject(s) - multiple drug resistance , medicine , nephrotic syndrome , messenger rna , peripheral blood mononuclear cell , real time polymerase chain reaction , gastroenterology , immunology , drug resistance , biology , gene , genetics , in vitro
Background: 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. The purpose of the present study was to investigated whether expression of Pad1 homologue ( POH1 ) plays a role in the onset of multidrug resistance of INS. Methods: Comparison was done of the mRNA level of POH1 on real‐time quantitative polymerase chain reaction in peripheral blood mononuclear cells among children with multidrug‐resistant INS, children with steroid‐sensitive INS and healthy controls. Results: The POH1 mRNA level of the onset INS group (5852.3 ± 2676.4 copies/µg) was significantly lower than that of the control group (10 877.1 ± 2386.6 copies/µg; P < 0.05). The POH1 mRNA level of the onset INS group with multidrug resistance was not significantly higher than that of the onset INS group without multidrug‐resistance before treatment (6977.1 ± 6312.3 copies/µg vs 5281.3 ± 1926.7 copies/µg; P > 0.05), but significantly higher than that of the onset INS group without multidrug resistance after treatment (436 579.6 ± 99 727.4 copies/µg vs 38 438.2 ± 16 772.5 copies/µg; P < 0.001). The POH1 mRNA level of non‐onset multidrug‐resistant INS group (337 446.4 ± 107 423.5 copies/µg) after treatment was not significantly higher than that of the onset INS group with multidrug resistance after treatment (436 579.6 ± 99 727.4 copies/µg; P > 0.05), but was significantly higher than that of the onset INS group without multidrug resistance after treatment (38 438.2 ± 16 772.5 copies/µg; P < 0.001). Conclusions: Disorder of POH1 expression is involved in the onset of INS, and confers multidrug resistance in children with INS.