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Updated: Jul 29, 2026

Measurement of Tissue Oxygenation Using Near-Infrared Spectroscopy in Patients Undergoing Hemodialysis
Published on: October 2, 2020
Blood oxygen level-dependent measurement of acute intra-renal ischemia
Laurent Juillard1, Lilach O Lerman, David G Kruger
1Department of Physiology, Mayo Clinic, Rochester, Minnesota 55905, USA.
Background:
Ischemic nephropathy is a common cause of end-stage renal disease. Exploration of the mechanisms of deterioration of renal function is limited due to lack of noninvasive techniques available to study the single kidney. The Blood Oxygen Level-Dependent (BOLD) MRI method can measure deoxyhemoglobin and therefore indirectly estimates renal oxygen content, but has never been evaluated in renal artery stenosis (RAS). This study was therefore designed to test if BOLD can detect the characteristic of renal hypoxia induced by RAS.
Methods:
RAS was induced in 8 pigs using an occluder placed around the right renal artery. Renal blood flow (RBF) was measured continuously with an ultrasound probe. BOLD signal was measured bilaterally in the cortex and medulla (as the slope of the logarithm of MR signal) at baseline and at the lower limit of RBF autoregulation. The measurements were then repeated during six sequential graded decreases in RBF (80 to 0% of baseline) and during recovery.
Results:
During the control period, BOLD signals were not significantly different between the right and the left kidneys. In the occluded kidney, BOLD signal of the cortex (19.3 +/- 1.9/s) and the medulla (17.3 +/- 2.0/s) increased during occlusion gradually and significantly (P < 0.0001) to a maximum (at total occlusion) of 33.8 +/- 2.0/s (+79%) and 29.8 +/- 2.3/s (+78%), respectively, and returned to baseline values during recovery.
Conclusion:
This study shows that the BOLD technique can noninvasively detect change in intra-renal oxygenation during an acute reduction of RBF. This study provides a strong rationale for developing the BOLD method for the detection and evaluation of renal hypoxia induced by RAS, which may be potentially applicable in humans.
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