title: Impact of renin-angiotensin system polymorphisms on renal haemodynamic responsiveness to acute angiotensin-converting enzyme inhibition in type 2 diabetes mellitus.
abstract: BACKGROUND
  The aim of this study was to document the impact of renin-angiotensin system (RAS) polymorphisms on renal haemodynamics and renal hormones in type 2 diabetes mellitus.
  
  
  METHODS
  Fifty-nine adult patients were studied. Renal haemodynamics were evaluated using 99mTc-MAG3 clearance (MAG3( Cle)) using Bubeck's method and captopril renogram. RAS hormones and angiotensin-converting enzyme (ACE) levels were measured before and after captopril.ACE, angiotensin II type 1 receptor and angiotensinogen gene polymorphisms were analysed.
  
  
  RESULTS
  Post-captopril MAG3(Cle) values were significantly lower in patients with microalbuminuria compared to nonproteinuric patients. Statistically significant negative correlation was found between clearance percentage change values and HbA(1c) levels (r: -0.42, p=0.009). MAG3(Cle) was relatively lower following captopril administration in DD patients, while a relative increment was observed in I allele carriers (p=0.02).TheAC-CC group had significantly higher mean post-captopril clearance value compared to the AA genotype (480.9+/-56.1 ml/min/1.73 m(2) vs. 428.4+/-74.8 ml/min/1.73 m(2), p=0.022).
  
  
  CONCLUSIONS
  Our data indicate that the heterogeneity of patients' response to ACE inhibition is, at least partly, genetically determined, and the genetic polymorphisms in RAS might predict the acute responsiveness to ACE inhibitors.
authors.affiliation: Department of Nuclear Medicine, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
authors.forename: Bilge
authors.initials: B
authors.lastname: Volkan-Salanci
authors.forename: Selcuk
authors.initials: S
authors.lastname: Dagdelen
authors.forename: Mehmet
authors.initials: M
authors.lastname: Alikasifoglu
authors.forename: Tomris
authors.initials: T
authors.lastname: Erbas
authors.forename: Mutlu
authors.initials: M
authors.lastname: Hayran
authors.forename: Belkis
authors.initials: B
authors.lastname: Erbas
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology*; D005260:Female; D005838:Genotype; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011110:Polymorphism, Genetic; D011866:Radioisotope Renography; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000235:genetics*; D017263:Technetium Tc 99m Mertiatide
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D044140:Receptor, Angiotensin, Type 1; D017263:Technetium Tc 99m Mertiatide; D002216:Captopril; D007703:Peptidyl-Dipeptidase A