title: Blockade of the renin-angiotensin system and renal tissue oxygenation as measured with BOLD-MRI in patients with type 2 diabetes.
abstract: OBJECTIVE
  To assess whether blockade of the renin-angiotensin system (RAS), a recognized strategy to prevent the progression of diabetic nephropathy, affects renal tissue oxygenation in type 2 diabetes mellitus (T2DM) patients.
  
  
  METHODS
  Prospective randomized 2-way cross over study; T2DM patients with (micro)albuminuria and/or hypertension underwent blood oxygenation level-dependent magnetic resonance imaging (BOLD-MRI) at baseline, after one month of enalapril (20 mgqd), and after one month of candesartan (16 mgqd). Each BOLD-MRI was performed before and after the administration of furosemide. The mean R₂* (=1/T₂*) values in the medulla and cortex were calculated, a low R₂* indicating high tissue oxygenation.
  
  
  RESULTS
  Twelve patients (mean age: 60 ± 11 years, eGFR: 62 ± 22 ml/min/1.73 m(2)) completed the study. Neither chronic enalapril nor candesartan intake modified renal cortical or medullary R₂* levels. Furosemide significantly decreased cortical and medullary R₂* levels suggesting a transient increase in renal oxygenation. Medullary R₂* levels correlated positively with urinary sodium excretion and systemic blood pressure, suggesting lower renal oxygenation at higher dietary sodium intake and blood pressure; cortical R₂* levels correlated positively with glycemia and HbA1c.
  
  
  CONCLUSIONS
  RAS blockade does not seem to increase renal tissue oxygenation in T2DM hypertensive patients. The response to furosemide and the association with 24 h urinary sodium excretion emphasize the crucial role of renal sodium handling as one of the main determinants of renal tissue oxygenation.
authors.affiliation: Service of Nephrology, University Hospital, Lausanne, Switzerland.
authors.forename: Menno
authors.initials: M
authors.lastname: Pruijm
authors.forename: Lucie
authors.initials: L
authors.lastname: Hofmann
authors.forename: Anne
authors.initials: A
authors.lastname: Zanchi
authors.forename: Marc
authors.initials: M
authors.lastname: Maillard
authors.forename: Valentina
authors.initials: V
authors.lastname: Forni
authors.forename: Marie-Eve
authors.initials: ME
authors.lastname: Muller
authors.forename: Grégoire
authors.initials: G
authors.lastname: Wuerzner
authors.forename: Bruno
authors.initials: B
authors.lastname: Vogt
authors.forename: Matthias
authors.initials: M
authors.lastname: Stuber
authors.forename: Michel
authors.initials: M
authors.lastname: Burnier
mesh_terms: D000368:Aged; D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology; D018592:Cross-Over Studies; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism*; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008875:Middle Aged; D008962:Models, Theoretical; D011446:Prospective Studies; D012084:Renin-Angiotensin System / Q000187:drug effects*
chemical_list: D057911:Angiotensin Receptor Antagonists; D005665:Furosemide