title: Genotypes of renin-angiotensin system and plasma adiponectin concentration in kidney transplant patients.
abstract: BACKGROUND
  Low plasma adiponectin concentration was recently recognized as a novel risk factor for new-onset diabetes after transplantation. Pharmacological modulation of the renin-angiotensin system activity and genetic predisposition were shown to have an influence on plasma adiponectin level. Therefore the aim of this study is to analyze the association between angiotensin-converting enzyme (ACE) I/D, angiotensin II type 1 receptor (AT1R) A1166C and angiotensinogen (AGT) M235T genotypes and plasma adiponectin concentration as well as insulin resistance in a cohort of kidney transplant patients.
  
  
  METHODS
  AGT M235T, ACE I/D and AT1R A1166C genotyping and plasma adiponectin and insulin concentrations assessment were performed in 372 patients with functioning kidney allograft (eGFR >20 ml/min/1.73 m2) from 2 transplant centres.
  
  
  RESULTS
  Females with II ACE I/D genotype had a significantly higher plasma adiponectin concentration than the ID+DD subgroup, which could partially be explained by a lower BMI in the II subgroup. Males with TT genotype of the AGT M235T gene polymorphism (and higher BMI) had higher plasma concentration of insulin and HOMAIR values than those in the MT+MM subgroup. A multiple regression analysis revealed that only female sex (b=0.239), BMI (b=–0.208) and ACE II genotype (b=0.129) were significantly associated with plasma adiponectin concentration variability. A similar analysis for HOMA-IR showed that its variability was associated with BMI (b=0.333), eGFR (b=–0.115) and plasma adiponectin concentration (b=–0.064) irrespective of any of the analyzed genotypes.
  
  
  CONCLUSIONS
  Plasma adiponectin concentration, but not insulin resistance, seems to be modulated only by ACE I/D polymorphism in kidney transplant patients. Polymorphisms of the other renin-angiotensin system components do not influence plasma adiponectin concentration or insulin resistance in these patients.
authors.affiliation: Department of Nephrology, Endocrinology and Metabolic Diseases, Medical University of Silesia in Katowice, Katowice, Poland and Department of Pathophysiology, Medical University of Silesia in Katowice, Katowice, Poland.
authors.forename: Jerzy
authors.initials: J
authors.lastname: Chudek
authors.forename: Magdalena
authors.initials: M
authors.lastname: Szotowska
authors.forename: Henryk
authors.initials: H
authors.lastname: Karkoszka
authors.forename: Francis
authors.initials: F
authors.lastname: Verbeke
authors.forename: Wanda
authors.initials: W
authors.lastname: Trautsolt
authors.forename: Janusz
authors.initials: J
authors.lastname: Gumprecht
authors.forename: Raymond
authors.initials: R
authors.lastname: Vanholder
authors.forename: Andrzej
authors.initials: A
authors.lastname: Wiecek
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D000808:Angiotensinogen / Q000235:genetics; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D012084:Renin-Angiotensin System / Q000235:genetics*
chemical_list: D052242:Adiponectin; D044140:Receptor, Angiotensin, Type 1; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A