Textor Stephen C, Glockner James F, Lerman Lilach O, Misra Sanjay, McKusick Michael A, Riederer Stephen J, Grande Joseph P, Gomez S Ivan, Romero J Carlos
Division of Nephrology and Hypertension, Departments of Physiology and Pathology, Center for Magnetic Imaging Research and Department of Radiology, Mayo Clinic, W19, Rochester, MN 55905, USA.
J Am Soc Nephrol. 2008 Apr;19(4):780-8. doi: 10.1681/ASN.2007040420. Epub 2008 Feb 20.
Vascular occlusive disease poses a threat to kidney viability, but whether the events leading to injury and eventual fibrosis actually entail reduced oxygenation and regional tissue ischemia is unknown. Answering this question has been difficult because of the lack of an adequate method to assess tissue oxygenation in humans. BOLD (blood oxygen-level-dependent) magnetic resonance imaging detects changes in tissue deoxyhemoglobin during maneuvers that affect oxygen consumption, therefore this technique was used to image and analyze cortical and medullary segments of 50 kidneys in 25 subjects undergoing magnetic resonance (MR) angiography to diagnose renal artery stenosis (RAS). Magnetic rate of relaxation (R2*) positively correlates with deoxyhemoglobin levels and was therefore used as a surrogate measure of tissue oxygenation. Furosemide was administered to examine the effect of inhibiting energy-dependent electrolyte transport on tissue oxygenation in subjects with renovascular disease. In 21 kidneys with normal nephrograms, administration of furosemide led to a 20% decrease in medullary R2* (P < 0.01) and an 11.2% decrease in cortical R2*. In normal-size kidneys downstream of high-grade renal arterial stenoses, R2* was elevated at baseline, but fell after furosemide. In contrast, atrophic kidneys beyond totally occluded renal arteries demonstrated low levels of R2* that did not change after furosemide. In kidneys with multiple arteries, localized renal artery stenoses produced focal elevations of R2*, suggesting areas of deoxyhemoglobin accumulation. These results suggest that BOLD MR coupled with a method to suppress tubular oxygen consumption can be used to evaluate regional tissue oxygenation in the human kidney affected by vascular occlusive disease.
血管闭塞性疾病对肾脏的存活构成威胁,但导致损伤及最终纤维化的过程是否真的会导致氧合降低和局部组织缺血尚不清楚。由于缺乏评估人体组织氧合的适当方法,回答这个问题一直很困难。血氧水平依赖性功能磁共振成像(BOLD)在影响氧消耗的操作过程中检测组织脱氧血红蛋白的变化,因此该技术被用于对25名接受磁共振(MR)血管造影以诊断肾动脉狭窄(RAS)的受试者的50个肾脏的皮质和髓质节段进行成像和分析。磁弛豫率(R2*)与脱氧血红蛋白水平呈正相关,因此被用作组织氧合的替代指标。给予呋塞米以检查抑制能量依赖性电解质转运对肾血管疾病患者组织氧合的影响。在21个肾图正常的肾脏中,给予呋塞米导致髓质R2降低20%(P<0.01),皮质R2降低11.2%。在严重肾动脉狭窄下游的正常大小肾脏中,R2在基线时升高,但在给予呋塞米后下降。相反,完全闭塞肾动脉后的萎缩肾脏显示R2水平较低,给予呋塞米后无变化。在有多条动脉的肾脏中,局部肾动脉狭窄导致R2*局部升高,提示有脱氧血红蛋白积聚区域。这些结果表明,BOLD磁共振成像结合一种抑制肾小管氧消耗的方法可用于评估受血管闭塞性疾病影响的人肾局部组织氧合。