Issues in renovascular disease and ischemic nephropathy: beyond ASTRAL

被引:14
|
作者
Textor, Stephen C. [1 ]
机构
[1] Mayo Clin, Div Nephrol & Hypertens, Rochester, MN 55905 USA
关键词
BOLD MR; hypertension; ischemic nephropathy; oxygen; renal artery stenosis; RENAL-ARTERY STENOSIS; KIDNEY; REVASCULARIZATION; OXYGENATION; HYPERTENSION; ANGIOGRAPHY; MECHANISMS; TRIALS;
D O I
10.1097/MNH.0b013e328342bb35
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Purpose Whereas atherosclerotic renal artery stenosis is recognized to accelerate hypertension and threaten kidney function, recent trials indicate that many patients can be managed primarily with antihypertensive drug therapy without renal revascularization. These trials have been criticized for many reasons, including inclusion of large groups with only minor vascular occlusive disease. Recent findings Although moderate stenosis is associated with preserved oxygenation within both cortex and medulla, severe disease is demonstrably associated with reduced oxygenation that can be identified using blood oxygen level-dependent magnetic resonance. Fewer clinical procedures to revascularize stenotic kidneys likely will be followed by advanced occlusion with loss of function. Experimental studies confirm that poststenotic microvascular injury is magnified in the presence of atherosclerosis, activating local inflammatory and fibrogenic pathways in the kidney. Even without restoring renal blood flow, experimental studies with endothelial progenitor cells indicate that recovery of renal vascular structures and function may be possible. Summary The short-term prospective trials to date remain at odds with observational studies indicating improved blood pressure, stabilization of renal function, and improved management of some patients with congestive heart failure. Nephrologists will need to balance optimizing medical therapy for complex patients with renovascular disease and identifying those most likely to benefit from renal revascularization on an individualized basis.
引用
收藏
页码:139 / 145
页数:7
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