Michael E Hall1, Michael V Rocco2, Timothy M Morgan3, Craig A Hamilton4, Jennifer H Jordan5, Matthew S Edwards6, John E Hall7, William G Hundley8. 1. Division of Cardiology, Department of Medicine, University of Mississippi Medical Center, Jackson, Miss, N.C., USA; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Miss, N.C., USA. 2. Division of Nephrology, Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, N.C., USA. 3. Biostatistical Sciences, Wake Forest University School of Medicine, Winston-Salem, N.C., USA. 4. Biomedical Engineering, Wake Forest University School of Medicine, Winston-Salem, N.C., USA. 5. Division of Cardiovascular Medicine, Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, N.C., USA. 6. Vascular Surgery, Wake Forest University School of Medicine, Winston-Salem, N.C., USA. 7. Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Miss, N.C., USA. 8. Division of Cardiovascular Medicine, Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, N.C., USA; Radiology, Wake Forest University School of Medicine, Winston-Salem, N.C., USA.
Abstract
BACKGROUND: Chronic renal hypoxia influences the progression of chronic kidney disease (CKD). Blood oxygen level-dependent (BOLD) magnetic resonance (MR) is a noninvasive tool for the assessment of renal oxygenation. The impact of beta-blockers on renal hemodynamics and oxygenation is not completely understood. We sought to determine the association between beta-blocker use, renal cortical and medullary oxygenation, and renal blood flow in patients suspected of renal artery stenosis. METHODS: We measured renal cortical and medullary oxygenation using BOLD MR and renal artery blood flow using MR phase contrast techniques in 38 participants suspected of renal artery stenosis. RESULTS: Chronic beta-blocker therapy was associated with improved renal cortical (p < 0.001) and medullary (p = 0.03) oxygenation, while the use of calcium channel blockers or diuretics showed no association with either cortical or medullary oxygenation. Receipt of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was associated with reduced medullary oxygenation (p = 0.01). In a multivariable model, chronic receipt of beta-blockers was the only significant predictor of renal tissue oxygenation (β = 8.4, p = 0.008). Beta-blocker therapy was not associated with significant changes in renal artery blood flow, suggesting that improved renal oxygenation may be related to reduced renal oxygen consumption. CONCLUSIONS: In addition to known benefits to reduce cardiovascular mortality in patients with renal disease, beta-blockers may reduce or prevent the progression of renal dysfunction in patients with hypertension, diabetes, and renovascular disease, partly by reducing renal oxygen consumption. These observations may have important implications for the treatment of patients with CKD.
BACKGROUND:Chronic renal hypoxia influences the progression of chronic kidney disease (CKD). Blood oxygen level-dependent (BOLD) magnetic resonance (MR) is a noninvasive tool for the assessment of renal oxygenation. The impact of beta-blockers on renal hemodynamics and oxygenation is not completely understood. We sought to determine the association between beta-blocker use, renal cortical and medullary oxygenation, and renal blood flow in patients suspected of renal artery stenosis. METHODS: We measured renal cortical and medullary oxygenation using BOLD MR and renal artery blood flow using MR phase contrast techniques in 38 participants suspected of renal artery stenosis. RESULTS: Chronic beta-blocker therapy was associated with improved renal cortical (p < 0.001) and medullary (p = 0.03) oxygenation, while the use of calcium channel blockers or diuretics showed no association with either cortical or medullary oxygenation. Receipt of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was associated with reduced medullary oxygenation (p = 0.01). In a multivariable model, chronic receipt of beta-blockers was the only significant predictor of renal tissue oxygenation (β = 8.4, p = 0.008). Beta-blocker therapy was not associated with significant changes in renal artery blood flow, suggesting that improved renal oxygenation may be related to reduced renal oxygen consumption. CONCLUSIONS: In addition to known benefits to reduce cardiovascular mortality in patients with renal disease, beta-blockers may reduce or prevent the progression of renal dysfunction in patients with hypertension, diabetes, and renovascular disease, partly by reducing renal oxygen consumption. These observations may have important implications for the treatment of patients with CKD.
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