Association of <it>phospholipase A2 receptor 1 </it>polymorphisms with idiopathic membranous nephropathy in Chinese patients in Taiwan

• Main Authors: Liao Wen-Ling, Lin Ying-Ju, Chen Shih-Yin, Chen Cheng-Hsu, Liu Yu-Huei, Tsai Chang-Hai, Wan Lei, Tsai Fuu-Jen
• Format: Article
• Language: English
• Published: BMC 2010-10-01
• Series: Journal of Biomedical Science
• Online Access: http://www.jbiomedsci.com/content/17/1/81
• ISSN: 1021-7770; 1423-0127

<p>Abstract</p> <p>Background</p> <p>Idiopathic membranous nephropathy (IMN) is one of the most common forms of autoimmune nephritic syndrome in adults. The purpose of this study is to evaluate whether polymorphisms of <it>PLA2R1 </it>affect the development of IMN.</p> <p>Methods</p> <p>Taiwanese-Chinese individuals (129 patients with IMN and 106 healthy controls) were enrolled in this study. The selected single nucleotide polymorphisms (SNPs) in <it>PLA2R1 </it>were genotyped by real-time polymerase chain reaction using TaqMan fluorescent probes, and were further confirmed by polymerase chain reaction-restriction fragment length polymorphism. The roles of the SNPs in disease progression were analyzed.</p> <p>Results</p> <p>Genotype distribution was significantly different between patients with IMN and controls for <it>PLA2R1 </it>SNP rs35771982 (<it>p </it>= 0.015). The frequency of <it>G </it>allele at rs35771982 was significantly higher in patients with IMN as compared with controls (<it>p </it>= 0.005). In addition, haplotypes of <it>PLA2R1 </it>may be used to predict the risk of IMN (<it>p </it>= 0.004). Haplotype H1 plays a role in an increased risk of IMN while haplotype H3 plays a protective role against this disease. None of these polymorphisms showed a significant and independent influence on the progression of IMN and the risk of end-stage renal failure and death (ESRF/death). High disease progression in patients having <it>C/T </it>genotype at rs6757188 and <it>C/G </it>genotype at rs35771982 were associated with a low rate of remission.</p> <p>Conclusions</p> <p>Our results provide new evidence that genetic polymorphisms of <it>PLA2R1 </it>may be the underlying cause of IMN, and the polymorphisms revealed by this study warrant further investigation.</p>