Time filter

Source Type

Hahn W.-H.,East West Kidney Diseases Research Institute | Suh J.-S.,East West Kidney Diseases Research Institute | Cho B.-S.,East West Kidney Diseases Research Institute | Kim S.-D.,East West Kidney Diseases Research Institute
Cytokine | Year: 2010

Background: Several experimental studies have suggested that signal transducers and activators of transcription 1 and 4 (STAT1 and STAT4) play important roles in the regulation of mesangial proliferation and renal fibrosis, and in the development of inflammation in several types of glomerulonephritis. Methods: The present study was conducted to investigate the association between single nucleotide polymorphisms (SNPs) of the STAT1 and STAT4 genes and childhood IgA nephropathy (IgAN). Results: Genotyping of 170 childhood IgAN patients and 442 controls showed no significant differences in allele frequency. However, patient subgroup analysis revealed that development of proteinuria (≤ and >4 mg/m2/h) was associated with STAT1 rs10199181 (dominant model, P = 0.035) and high serum level of IgA with STAT1 rs6718902 (dominant model, P = 0.035) and STAT1 rs2280232 (codominant model, P = 0.014; dominant model, P = 0.022). Furthermore, some SNP frequencies were significantly different between patients with pathologically mild and advanced disease; STAT1 rs6718902 (overdominant model, P = 0.030), STAT1 rs10199181 (codominant model, P = 0.023; dominant model, P = 0.012; overdominant model, P = 0.018), and STAT4 rs7561832 (dominant model, P = 0.026; overdominant model, P = 0.029). Conclusions: Our results suggest that polymorphisms of STAT1 and STAT4 are associated with increased susceptibility, pathological advancement, and development of proteinuria in childhood IgAN. Crown Copyright © 2009.

Park H.J.,Kohwang Medical Research Institute | Kim J.W.,Kohwang Medical Research Institute | Cho B.-S.,East West Kidney Diseases Research Institute | Chung J.-H.,Kohwang Medical Research Institute
Scandinavian Journal of Clinical and Laboratory Investigation | Year: 2014

Background. Apoptosis plays an important role in the mechanism regulating the development of glomerulonephritis. We investigated whether polymorphisms of apoptotic genes such as B-cell CLL/lymphoma 2 (BCL2), BH3-interacting domain death agonist (BID), and caspase 8 (CASP8) were associated with immunoglobulin A nephropathy (IgAN) and with the clinical phenotypes of IgAN patients. Methods. We genotyped promoter and coding region single nucleotide polymorphisms (SNPs) (rs2279115 and rs1801018 for BCL2; rs8190315 and rs2072392 for BID; and rs6747918 and rs1045487 for CASP8) using direct sequencing in 195 IgAN patients and 289 control subjects. Results. No SNPs were associated with IgAN. However, in analysis of clinical phenotypes, we found that rs8190315 and rs2072392 of BID were associated with proteinuria levels of IgAN patients in additive (AG vs. GG vs. AA, p = 0.0008 for rs8190315; TC vs. CC vs. TT, p = 0.0012 for rs2072392) and dominant models (AG/GG vs. AA, p = 0.0014 for rs8190315; TC/CC vs. TT, p = 0.0031 for rs2072392). In particular, the frequencies of genotypes containing minor alleles of rs8190315 (G allele) and rs2072392 (C allele) were increased in IgAN patients with higher protienuria levels (> 40 mg/m2/h). Conclusion. These results suggest that BID may play a role in severe IgAN. © 2014 Informa Healthcare.

Loading East West Kidney Diseases Research Institute collaborators
Loading East West Kidney Diseases Research Institute collaborators