Wenrong Cheng1, Xujie Zhou, Li Zhu, Sufang Shi, Jicheng Lv, Lijun Liu, Hong Zhang. 1. Renal Division, Peking University First Hospital, Peking University Institute of Nephrology, and Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, People's Republic of China.
Abstract
BACKGROUND: IgA nephropathy (IgAN) is the leading cause of end-stage renal disease (ESRD) in China considering different compositions of ESRD causes in different ethnicities. A recent genome-wide association study (GWAS) indicated that the MYH9 gene was significantly associated with non-diabetic ESRD in African-Americans and also influenced kidney function in Europeans. Thus, in the present study, we aim to clarify whether MYH9 confers a shared mechanism among different causes of ESRD and to seek possible further insight into our understanding of IgAN by applying GWAS data from ESRD to IgAN. METHODS: One thousand one hundred and sixteen Chinese, including 527 patients with renal biopsy-proven IgAN and 589 healthy controls, were enrolled in the present study. Four single neucleotide polymorphisms (SNPs) (rs3752462, rs4821480, rs11089788 and rs2413396) reported to be associated with ESRD with the most significance were genotyped by TaqMan assay or a restriction fragment length polymorphism assay for a further case-control study. RESULTS: None of the four SNPs was associated with the susceptibility to IgAN or clinical and pathological characters at the time of renal biopsy. However, estimated glomerular filtration rate decline rate was associated with rs11089788 in the dominant model (P = 0.021). Cox regression showed that rs11089788 (hazard ratio, 3.95; 95% confidence interval, 1.23-12.63; P = 2.1 × 10(-2)) was an independent predictive factor for renal survival. CONCLUSIONS: Based on a large Chinese IgAN cohort, we found an association between rs11089788 and prognosis of IgAN, adding to the mounting evidence of MYH9 as an important gene in IgAN to ESRD.
BACKGROUND:IgA nephropathy (IgAN) is the leading cause of end-stage renal disease (ESRD) in China considering different compositions of ESRD causes in different ethnicities. A recent genome-wide association study (GWAS) indicated that the MYH9 gene was significantly associated with non-diabetic ESRD in African-Americans and also influenced kidney function in Europeans. Thus, in the present study, we aim to clarify whether MYH9 confers a shared mechanism among different causes of ESRD and to seek possible further insight into our understanding of IgAN by applying GWAS data from ESRD to IgAN. METHODS: One thousand one hundred and sixteen Chinese, including 527 patients with renal biopsy-proven IgAN and 589 healthy controls, were enrolled in the present study. Four single neucleotide polymorphisms (SNPs) (rs3752462, rs4821480, rs11089788 and rs2413396) reported to be associated with ESRD with the most significance were genotyped by TaqMan assay or a restriction fragment length polymorphism assay for a further case-control study. RESULTS: None of the four SNPs was associated with the susceptibility to IgAN or clinical and pathological characters at the time of renal biopsy. However, estimated glomerular filtration rate decline rate was associated with rs11089788 in the dominant model (P = 0.021). Cox regression showed that rs11089788 (hazard ratio, 3.95; 95% confidence interval, 1.23-12.63; P = 2.1 × 10(-2)) was an independent predictive factor for renal survival. CONCLUSIONS: Based on a large Chinese IgAN cohort, we found an association between rs11089788 and prognosis of IgAN, adding to the mounting evidence of MYH9 as an important gene in IgAN to ESRD.
Authors: Gregory A Hawkins; David J Friedman; Lingyi Lu; David R McWilliams; Jeff W Chou; Satria Sajuthi; Jasmin Divers; Rulan S Parekh; Man Li; Giulio Genovese; Martin R Pollack; Pamela J Hicks; Donald W Bowden; Lijun Ma; Barry I Freedman; Carl D Langefeld Journal: Am J Nephrol Date: 2015-09-08 Impact factor: 3.754
Authors: Mathias Gorski; Adrienne Tin; Maija Garnaas; Gearoid M McMahon; Audrey Y Chu; Bamidele O Tayo; Cristian Pattaro; Alexander Teumer; Daniel I Chasman; John Chalmers; Pavel Hamet; Johanne Tremblay; Marc Woodward; Thor Aspelund; Gudny Eiriksdottir; Vilmundur Gudnason; Tamara B Harris; Lenore J Launer; Albert V Smith; Braxton D Mitchell; Jeffrey R O'Connell; Alan R Shuldiner; Josef Coresh; Man Li; Paul Freudenberger; Edith Hofer; Helena Schmidt; Reinhold Schmidt; Elizabeth G Holliday; Paul Mitchell; Jie Jin Wang; Ian H de Boer; Guo Li; David S Siscovick; Zoltan Kutalik; Tanguy Corre; Peter Vollenweider; Gérard Waeber; Jayanta Gupta; Peter A Kanetsky; Shih-Jen Hwang; Matthias Olden; Qiong Yang; Mariza de Andrade; Elizabeth J Atkinson; Sharon L R Kardia; Stephen T Turner; Jeanette M Stafford; Jingzhong Ding; Yongmei Liu; Cristina Barlassina; Daniele Cusi; Erika Salvi; Jan A Staessen; Paul M Ridker; Harald Grallert; Christa Meisinger; Martina Müller-Nurasyid; Bernhard K Krämer; Holly Kramer; Sylvia E Rosas; Ilja M Nolte; Brenda W Penninx; Harold Snieder; M Fabiola Del Greco; Andre Franke; Ute Nöthlings; Wolfgang Lieb; Stephan J L Bakker; Ron T Gansevoort; Pim van der Harst; Abbas Dehghan; Oscar H Franco; Albert Hofman; Fernando Rivadeneira; Sanaz Sedaghat; André G Uitterlinden; Stefan Coassin; Margot Haun; Barbara Kollerits; Florian Kronenberg; Bernhard Paulweber; Nicole Aumann; Karlhans Endlich; Mike Pietzner; Uwe Völker; Rainer Rettig; Vincent Chouraki; Catherine Helmer; Jean-Charles Lambert; Marie Metzger; Benedicte Stengel; Terho Lehtimäki; Leo-Pekka Lyytikäinen; Olli Raitakari; Andrew Johnson; Afshin Parsa; Murielle Bochud; Iris M Heid; Wolfram Goessling; Anna Köttgen; W H Linda Kao; Caroline S Fox; Carsten A Böger Journal: Kidney Int Date: 2014-12-10 Impact factor: 10.612