title: [Individual renal hemodynamic response to chronic angiotensin II receptor blockade and the influence on the renin-angiotensin system gene polymorphisms].
abstract: BACKGROUND
  Our study was aimed at determining whether the polymorphism of genes for different components of the renin-angiotensin-aldosterone system could influence the renal hemodynamic response to losartan treatment.
  
  
  METHODS
  The study included 35 patients with type I diabetes mellitus and persistent albuminuria, genotyped for the 1166 A/C polymorphism gene for the angiotensin II type 1 receptor and I/D polymorphism of the angiotensin-converting enzyme gene. The participants were divided into groups according to the combinations of A or C allele: AA, AC, CC; and according to the combinations of I or D allele: II, ID and DD genotype. The patients received losartan therapy for 12 weeks. The renal hemodynamic measurements were determined at baseline and after the examination period.
  
  
  RESULTS
  Losartan therapy significantly reduced the filtration fraction from the baseline by 0.018 +/- 0.024 (p = 0.012) only in the AC genotype. The glomerular filtration rate remained unchanged in all genotype groups. A significant increase in the effective renal plasma flow was obtained only in AC genotype (544 +/- 88 vs 575 +/- 90 ml/min; p = 0.02), while significant reductions in the renal vascular resistance were found in AA group (115 +/- 25 vs 95 +/- 21 mmHg x l(-1) x min(-1), p = 0.001) and in AC group (118 +/- 30 vs 101 +/- 28 mmHg x l(-1) x min(-1); p = 0.001). A significant reduction of the glomerular filtration rate by 8 +/- 10 ml/min was obtained only in the DD genotype (p = 0.016), and only the DD genotype achieved a significant reduction of the filtration fraction by 0.019 +/- 0,022 (p = 0.008). The most pronounced increase of the effective renal plasma flow was found only in the ID genotype (536 +/- 75 vs 591 +/- 63 ml/min; p = 0.01). The reduction of the renal vascular resistance was independent of ACE gene polymorphism.
  
  
  CONCLUSIONS
  Our study shows that individual renal vascular response to losartan treatment in diabetic patients with persistent albuminuria, could be influenced by genetic polymorphisms.
authors: Klinika za endokrinologiju, Vojnomedicinska akademija, Beograd. drtamara@nadlanu.com
authors: Tamara
authors: T
authors: Dragović
authors: Boris
authors: B
authors: Ajdinović
authors: Vesna
authors: V
authors: Ilić
authors: Zvonko
authors: Z
authors: Magić
authors: Zoran
authors: Z
authors: Andelković
authors: Nikola
authors: N
authors: Kocev
mesh_terms: D000328:Adult; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000235:genetics*; D003928:Diabetic Nephropathies / Q000188:drug therapy / Q000235:genetics / Q000503:physiopathology*; D005260:Female; D005838:Genotype; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D019808:Losartan / Q000627:therapeutic use*; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics* / Q000627:therapeutic use*; D012079:Renal Circulation / Q000187:drug effects*; D017596:Renal Plasma Flow, Effective / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000235:genetics*
chemical_list: D044140:Receptor, Angiotensin, Type 1; D007703:Peptidyl-Dipeptidase A; D019808:Losartan