title: A candidate gene approach to genetic contributors to the development of IgA nephropathy.
abstract: BACKGROUND
  Genetic factors contributing to the development of IgA nephropathy remain to be elucidated.
  
  
  METHODS
  The present multicenter cross-sectional case-control study measured genotype frequencies of 65 atherosclerotic disease-related gene polymorphisms in 230 Japanese patients with IgA nephropathy and 262 apparently healthy volunteers with estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m(2) and negative or trace proteinuria and hematuria by dipstick test [non-chronic kidney disease (CKD) participants]. Clinical characteristics at kidney biopsy of patients with IgA nephropathy and those at the study recruitment of non-CKD participants were included as covariates in multivariate logistic regression models.
  
  
  RESULTS
  Among 31 gene polymorphisms with ≥5% of minor genotype in non-CKD participants, methionine synthase MTR A2756G (D919G) was significantly associated with IgA nephropathy using χ(2) test even after controlling for family-wise error rate by the method of Bonferroni (P = 0.044). A multivariate nonconditional logistic regression model identified MTR A2756G as a significant contributor of IgA nephropathy [2756AG and GG versus AA, odds ratio 0.42 (95% confidence interval 0.25-0.69) and 0.21 (95% confidence interval 0.06-0.68), P(trend) < 0.001]. After each patient with IgA nephropathy was randomly matched to a non-CKD participant on age (±5 years), gender, mean arterial pressure (±5 mmHg) and eGFR (±5 mL/min/1.73 m(2)), a multivariate conditional logistic regression model also verified their significant association [odds ratio 0.42 (95% confidence interval 0.18-1.00) and odds ratio 0.09 (95% confidence interval 0.01-0.73), P(trend) = 0.004]. MTR A2756G was not associated with slope of eGFR (mL/min/1.73 m(2)/year) in 230 patients with IgA nephropathy.
  
  
  CONCLUSIONS
  MTR A2756G was associated with the development, but not progression, of IgA nephropathy.
authors: Department of Geriatric Medicine and Nephrology, Osaka University Graduate School of Medicine, Suita, Japan.
authors: Ryohei
authors: R
authors: Yamamoto
authors: Yasuyuki
authors: Y
authors: Nagasawa
authors: Tatsuya
authors: T
authors: Shoji
authors: Naoto
authors: N
authors: Katakami
authors: Kentaro
authors: K
authors: Ohtoshi
authors: Rieko
authors: R
authors: Hayaishi-Okano
authors: Yoshimitsu
authors: Y
authors: Yamasaki
authors: Atsushi
authors: A
authors: Yamauchi
authors: Yoshiharu
authors: Y
authors: Tsubakihara
authors: Enyu
authors: E
authors: Imai
authors: Hiromi
authors: H
authors: Rakugi
authors: Yoshitaka
authors: Y
authors: Isaka
mesh_terms: D000328:Adult; D044466:Asian People / Q000235:genetics; D050197:Atherosclerosis / Q000150:complications / Q000235:genetics; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D018450:Disease Progression; D005260:Female; D005819:Genetic Markers / Q000235:genetics*; D005838:Genotype; D005919:Glomerular Filtration Rate; D005922:Glomerulonephritis, IGA / Q000209:etiology* / Q000473:pathology*; D006801:Humans; D007676:Kidney Failure, Chronic; D008297:Male; D011110:Polymorphism, Genetic / Q000235:genetics*; D011379:Prognosis; D011507:Proteinuria / Q000235:genetics* / Q000473:pathology
chemical_list: D005819:Genetic Markers