Oxygenation Evaluated by Magnetic Resonance Imaging in Patients With Chronic Kidney Disease

Imaging of the kidney using blood oxygen level dependent (BOLD) magnetic resonance imaging (MRI) presents a major opportunity to examine differences in tissue oxygenation within the cortex and medulla applicable to human disease. The aim of this study was to evaluate BOLD signals before and after treatment with RAS inhibitors in hypertensive chronic kidney disease (CKD) patients. Ten patients with stable CKD and 5 healthy volunteers were included. Five CKD patients were subjected to BOLD MRI scan before and after chronic treatment with 300 mg/day aliskiren for at least 6 weeks. Five other CKD patients received BOLD MRI before and 1 hour after acute treatment with 50 mg captopril. A group of healthy volunteers (n=5) was scanned before and 1 hour after acute treatment with 50 mg captopril. The 10 patients had a mean age of 6117 years; eGFR of 3011 mL/min per 1.73 m 2 . Office systolic and diastolic blood pressures when on a RAS inhibito, were 13010 and 865 mmHg in CKD patients. Control subjects had normal kidney function and were not on any medication. In untreated condition, systolic and diastolic arterial blood pressure elevated, 1456 and 954 mmHg, respectively. After chronic treatment with aliskiren, arterial blood pressure decreased in all patients in this group, 1273 mmHg and 773 mmHg. After acute treatment with captopril arterial blood pressure reduced to 1254 and 718 mmHg. Tissue intensity signal (T2*) was increased in medulla after chronic treatment from 29 6t o 346 and after acute treatment with captopril from 34 9t o 3811 in CKD patients. In addition, T2* ratio between cortex and medulla decreased in CKD patients after chronic treatment and acute treatment. This ratio remained stable in healthy volunteers before and after treatment with captopril 1.620.1 and 1.650.1, respectively. This study shows for the first time that RAS inhibitors change BOLD signal in CKD patients. Importantly, in healthy volunteers, a RAS inhibitor had no such effect. Further investigation is required. J Clin Hypertens (Greenwich). 2014;16:214‐218. a2014 Wiley Periodicals, Inc. Many experimental studies have shown that kidney ischemia is the key finding in the pathogenesis and progression of chronic kidney disease (CKD) and hypertension. 1 Inhibitors of the renin-angiotensin system (RAS) are the cornerstone of the treatment of CKD patients. There are hypotheses that minor kidney damage, not affecting kidney function and therefore difficult to diagnose, might be present, resulting in “essential” hypertension and its subsequent cardiovascular complications. 1 Thus far it is a challenge to identify kidney ischemia in its early stage. Imaging of the kidney using blood oxygenation level–dependent (BOLD) magnetic resonance imaging (MRI) presents a major new opportunity to examine differences in kidney tissue oxygenation within the cortex and medulla applicable to human disease. BOLD MRI allows observation of changes in cortical and medullary concentration of deoxyhemoglobin. 2 This acquires images sensitive to local tissue oxygen concentration and quantifies changes in tissue