Review article

BioMedicine

, 4:9

First online:

Open Access This content is freely available online to anyone, anywhere at any time.

Genetic susceptibility to idiopathic membranous nephropathy in high-prevalence Area, Taiwan

  • Shih-Yin ChenAffiliated withGenetics Center, Department of Medical Research, China Medical University HospitalGraduate Institute of Chinese Medical Science, China Medical UniversityDepartment of Biotechnology and Bioinformatics, Asia University
  • , Cheng-Hsu ChenAffiliated withDivision of Nephrology, Department of Internal Medicine, Taichung Veterans General Hospital
  • , Yu-Chuen HuangAffiliated withGenetics Center, Department of Medical Research, China Medical University HospitalGraduate Institute of Chinese Medical Science, China Medical University
  • , Chia-Jung ChanAffiliated withGenetics Center, Department of Medical Research, China Medical University Hospital
  • , Da-Chung ChenAffiliated withTaiwan LandSeed HospitalDepartment of Chemical and Materials Engineering, National Central University
  • , Fuu-Jen TsaiAffiliated withDepartment of Pediatrics, China Medical University HospitalDepartment of Medical Genetics, China Medical University HospitalDepartment of Biotechnology and Bioinformatics, Asia University Email author 

Abstract

Idiopathic membranous nephropathy (MN) is one common cause of idiopathic nephrotic syndrome in adults; 25% of MN patients proceed to end-stage renal disease. In adults, membranous nephropathy is a lead cause of nephrotic syndrome, with about 75% of the cases idiopathic. Secondary causes include autoimmune disease, infection, drugs and malignancy. Three hypotheses about pathogenesis have surfaced: preformed immune complex, in situ immune complex formation, and auto-antibody against podocyte membrane antigen. Pathogenesis does involve immune complex formation with later deposition in sub-epithelial sites, but definite mechanism is still unknown. Several genes were recently proven associated with primary membranous nephropathy in Taiwan: IL-6, NPHS1, TLR-4, TLR-9, STAT4, and MYH9 . These may provide a useful tool for diagnosis and prognosis. This article reviews epidemiology and lends new information on KIRREL2 (rs443186 and rs447707) polymorphisms as underlying causes of MN; polymorphisms revealed by this study warrant further investigation.

Keywords:

Membranous glomerulonephritis (MN) Single nucleotide polymorphisms (SNPs) Haplotype