AIM: 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. CONCLUSION: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.
RCT Entities:
AIM: 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. CONCLUSION: RAS blockade does not seem to increase renal tissue oxygenation in T2DM hypertensivepatients. 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: Pottumarthi V Prasad; Jon Thacker; Lu-Ping Li; Muhammad Haque; Wei Li; Heather Koenigs; Ying Zhou; Stuart M Sprague Journal: PLoS One Date: 2015-10-02 Impact factor: 3.240
Authors: Michael E Hall; Michael V Rocco; Timothy M Morgan; Craig A Hamilton; Matthew S Edwards; Jennifer H Jordan; Justin B Hurie; W Gregory Hundley Journal: J Cardiovasc Magn Reson Date: 2014-02-03 Impact factor: 5.364
Authors: Jeff L Zhang; Glen Morrell; Henry Rusinek; Eric E Sigmund; Hersh Chandarana; Lilach O Lerman; Pottumarthi V Prasad; David Niles; Nathan Artz; Sean Fain; Pierre-Hugues Vivier; Alfred K Cheung; Vivian S Lee Journal: Kidney Int Date: 2013-09-25 Impact factor: 10.612