title: Gene polymorphisms contributing to hypertension in immunoglobulin A nephropathy.
abstract: BACKGROUND
  Hypertension, which is affected by genetic and environmental factors, is one of the major risk factors for chronic kidney disease. Identification of the genetic factor contributing to hypertension in patients with chronic kidney disease may potentially refine a therapeutic strategy.
  
  
  METHODS
  In the present multicenter cross-sectional study, 240 patients were eligible (aged 15-50 years with urinary protein ≥0.25 g/day) out of 429 patients who were diagnosed as having immunoglobulin (Ig) A nephropathy (IgAN) by renal biopsy between 1990 and 2005 and enrolled in our previous study, PREDICT-IgAN. The outcome was hypertension defined as ≥140 and/or ≥90 mmHg of systolic and diastolic blood pressure and/or use of antihypertensives at renal biopsy. We assessed associations between hypertension and 28 polymorphisms with the frequency of minor genotype ≥10% among 100 atherosclerosis-related polymorphisms using the Chi-squared test in dominant and recessive models. We identified polymorphisms associated with hypertension in multivariate logistic regression models.
  
  
  RESULTS
  Baseline characteristics: hypertension 36.3%. Among 28 polymorphisms, the Chi-squared test revealed that CD14 (-159CC vs CT/TT, P = 0.03) and ACE (DD vs DI/II, P = 0.03) were significantly associated with hypertension after Bonferroni correction. Multivariate logistic regression models revealed that CD14 -159CC [vs CT/TT, odds ratio (OR) 3.58 (95% confidence interval (CI) 1.66-7.63)] and ACE DD [vs DI/II, OR 4.41 (95% CI 1.80-10.8), P = 0.001] were independently associated with hypertension.
  
  
  CONCLUSIONS
  CD14 C-159T and ACE I/D contributed to hypertension in patients with IgAN.
authors.affiliation: Department of Geriatric Medicine and Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
authors.forename: Maki
authors.initials: M
authors.lastname: Shinzawa
authors.forename: Ryohei
authors.initials: R
authors.lastname: Yamamoto
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Nagasawa
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Shoji
authors.forename: Yoshitsugu
authors.initials: Y
authors.lastname: Obi
authors.forename: Tomoko
authors.initials: T
authors.lastname: Namba
authors.forename: Harumi
authors.initials: H
authors.lastname: Kitamura
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Kaneko
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Okada
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Iwatani
authors.forename: Atsushi
authors.initials: A
authors.lastname: Yamauchi
authors.forename: Yoshiharu
authors.initials: Y
authors.lastname: Tsubakihara
authors.forename: Enyu
authors.initials: E
authors.lastname: Imai
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Isaka
authors.forename: Hiromi
authors.initials: H
authors.lastname: Rakugi
mesh_terms: D000293:Adolescent; D000328:Adult; D000959:Antihypertensive Agents; D001794:Blood Pressure; D003430:Cross-Sectional Studies; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D005922:Glomerulonephritis, IGA / Q000150:complications / Q000235:genetics*; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000235:genetics*; D007676:Kidney Failure, Chronic / Q000235:genetics*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012307:Risk Factors; D055815:Young Adult
chemical_list: D000959:Antihypertensive Agents
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