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Multi-Parametric Evaluation of Chronic Kidney Disease by MRI: A Preliminary Cross-Sectional Study.

Prasad PV, Thacker J, Li LP, Haque M, Li W, Koenigs H, Zhou Y, Sprague SM - PLoS ONE (2015)

Bottom Line: All three parameters showed significant correlation with estimated glomerular filtration rate (eGFR).The difference in cortical R2* between these subjects compared to the rest were highly significant and had a large effect size (Cohen's d = 3.5).Diffusion MRI showed no differences between CKD and healthy controls.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiology, NorthShore University HealthSystem, Evanston, Illinois, United States of America.

ABSTRACT

Background: The current clinical classification of chronic kidney disease (CKD) is not perfect and may be overestimating both the prevalence and the risk for progressive disease. Novel markers are being sought to identify those at risk of progression. This preliminary study evaluates the feasibility of magnetic resonance imaging based markers to identify early changes in CKD.

Methods: Fifty-nine subjects (22 healthy, 7 anemics with no renal disease, 30 subjects with CKD) participated. Data using 3D volume imaging, blood oxygenation level dependent (BOLD) and Diffusion MRI was acquired. BOLD MRI acquisition was repeated after 20 mg of iv furosemide.

Results: Compared to healthy subjects, those with CKD have lower renal parenchymal volumes (329.6±66.4 vs. 257.1±87.0 ml, p<0.005), higher cortical R2* values (19.7±3.2 vs. 23.2±6.3 s(-1), p = 0.013) (suggesting higher levels of hypoxia) and lower response to furosemide on medullary R2* (6.9±3.3 vs. 3.1±7.5 s(-1), p = 0.02). All three parameters showed significant correlation with estimated glomerular filtration rate (eGFR). When the groups were matched for age and sex, cortical R2* and kidney volume still showed significant differences between CKD and healthy controls. The most interesting observation is that a small number of subjects (8 of 29) contributed to the increase in mean value observed in CKD. The difference in cortical R2* between these subjects compared to the rest were highly significant and had a large effect size (Cohen's d = 3.5). While highly suggestive, future studies may be necessary to verify if such higher levels of hypoxia are indicative of progressive disease. Diffusion MRI showed no differences between CKD and healthy controls.

Conclusions: These data demonstrate that BOLD MRI can be used to identify enhanced hypoxia associated with CKD and the preliminary observations are consistent with the chronic hypoxia model for disease progression in CKD. Longitudinal studies are warranted to further verify these findings and assess their predictive value.

No MeSH data available.


Related in: MedlinePlus

illustrates anatomic MRI and R2* maps from a representative subject from control, CKD_Low and CKD_High R2* groups.The R2* maps of the kidneys are overlaid on the anatomic image and the color bar indicates high levels of hypoxia in red and progressively lower values with orange, yellow, green and blue. Note R2* values are low in the cortex of both the control and subject with CKD even though the eGFR values are significantly different, while the subject with CKD_High clearly shows higher R2* values, even though his/her eGFR values are high and comparable to the control subject. We have also included R2* values for muscle to rule out any systematic bias in R2* values in CKD_High.
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pone.0139661.g002: illustrates anatomic MRI and R2* maps from a representative subject from control, CKD_Low and CKD_High R2* groups.The R2* maps of the kidneys are overlaid on the anatomic image and the color bar indicates high levels of hypoxia in red and progressively lower values with orange, yellow, green and blue. Note R2* values are low in the cortex of both the control and subject with CKD even though the eGFR values are significantly different, while the subject with CKD_High clearly shows higher R2* values, even though his/her eGFR values are high and comparable to the control subject. We have also included R2* values for muscle to rule out any systematic bias in R2* values in CKD_High.

Mentions: Fig 1 summarizes the cortical R2* data in subjects with CKD and healthy controls in the form of box-and-whisker plots. The plot for the CKD_All group suggests that fewer subjects contributed to the higher half of the distribution. Using a threshold of 27s-1 (> max value in the control group), we found that the CKD group can be subdivided in to two distinct distributions (CKD_Low (n = 21) and CKD_High (n = 8)) as shown in Fig 1. The CKD_Low group appears very similar to the control group while the CKD_High group has values distinctly higher than either the control or the CKD_Low groups. Fig 2 shows representative images (anatomic and R2* maps) at baseline for each group of subjects for illustrative purposes. Note the similarity of the R2* map in the healthy control and a subject in the CKD_Low group (similar in age and sex) even though the eGFR was substantially different. On the other hand the subject in the CKD_High group with similar age and eGFR as the control subject has much higher cortical R2* values. To rule out any systemic artifactual increase in R2* in the CKD_High group, we have also included ROIs in the muscle, which appears to be comparable in all three subjects. Table 4 summarizes differences between the CKD_Low and CKD_High groups in terms of all the parameters. Except for cortical and medullary R2*, none of the other observed parameters showed significant differences.


Multi-Parametric Evaluation of Chronic Kidney Disease by MRI: A Preliminary Cross-Sectional Study.

Prasad PV, Thacker J, Li LP, Haque M, Li W, Koenigs H, Zhou Y, Sprague SM - PLoS ONE (2015)

illustrates anatomic MRI and R2* maps from a representative subject from control, CKD_Low and CKD_High R2* groups.The R2* maps of the kidneys are overlaid on the anatomic image and the color bar indicates high levels of hypoxia in red and progressively lower values with orange, yellow, green and blue. Note R2* values are low in the cortex of both the control and subject with CKD even though the eGFR values are significantly different, while the subject with CKD_High clearly shows higher R2* values, even though his/her eGFR values are high and comparable to the control subject. We have also included R2* values for muscle to rule out any systematic bias in R2* values in CKD_High.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4591972&req=5

pone.0139661.g002: illustrates anatomic MRI and R2* maps from a representative subject from control, CKD_Low and CKD_High R2* groups.The R2* maps of the kidneys are overlaid on the anatomic image and the color bar indicates high levels of hypoxia in red and progressively lower values with orange, yellow, green and blue. Note R2* values are low in the cortex of both the control and subject with CKD even though the eGFR values are significantly different, while the subject with CKD_High clearly shows higher R2* values, even though his/her eGFR values are high and comparable to the control subject. We have also included R2* values for muscle to rule out any systematic bias in R2* values in CKD_High.
Mentions: Fig 1 summarizes the cortical R2* data in subjects with CKD and healthy controls in the form of box-and-whisker plots. The plot for the CKD_All group suggests that fewer subjects contributed to the higher half of the distribution. Using a threshold of 27s-1 (> max value in the control group), we found that the CKD group can be subdivided in to two distinct distributions (CKD_Low (n = 21) and CKD_High (n = 8)) as shown in Fig 1. The CKD_Low group appears very similar to the control group while the CKD_High group has values distinctly higher than either the control or the CKD_Low groups. Fig 2 shows representative images (anatomic and R2* maps) at baseline for each group of subjects for illustrative purposes. Note the similarity of the R2* map in the healthy control and a subject in the CKD_Low group (similar in age and sex) even though the eGFR was substantially different. On the other hand the subject in the CKD_High group with similar age and eGFR as the control subject has much higher cortical R2* values. To rule out any systemic artifactual increase in R2* in the CKD_High group, we have also included ROIs in the muscle, which appears to be comparable in all three subjects. Table 4 summarizes differences between the CKD_Low and CKD_High groups in terms of all the parameters. Except for cortical and medullary R2*, none of the other observed parameters showed significant differences.

Bottom Line: All three parameters showed significant correlation with estimated glomerular filtration rate (eGFR).The difference in cortical R2* between these subjects compared to the rest were highly significant and had a large effect size (Cohen's d = 3.5).Diffusion MRI showed no differences between CKD and healthy controls.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiology, NorthShore University HealthSystem, Evanston, Illinois, United States of America.

ABSTRACT

Background: The current clinical classification of chronic kidney disease (CKD) is not perfect and may be overestimating both the prevalence and the risk for progressive disease. Novel markers are being sought to identify those at risk of progression. This preliminary study evaluates the feasibility of magnetic resonance imaging based markers to identify early changes in CKD.

Methods: Fifty-nine subjects (22 healthy, 7 anemics with no renal disease, 30 subjects with CKD) participated. Data using 3D volume imaging, blood oxygenation level dependent (BOLD) and Diffusion MRI was acquired. BOLD MRI acquisition was repeated after 20 mg of iv furosemide.

Results: Compared to healthy subjects, those with CKD have lower renal parenchymal volumes (329.6±66.4 vs. 257.1±87.0 ml, p<0.005), higher cortical R2* values (19.7±3.2 vs. 23.2±6.3 s(-1), p = 0.013) (suggesting higher levels of hypoxia) and lower response to furosemide on medullary R2* (6.9±3.3 vs. 3.1±7.5 s(-1), p = 0.02). All three parameters showed significant correlation with estimated glomerular filtration rate (eGFR). When the groups were matched for age and sex, cortical R2* and kidney volume still showed significant differences between CKD and healthy controls. The most interesting observation is that a small number of subjects (8 of 29) contributed to the increase in mean value observed in CKD. The difference in cortical R2* between these subjects compared to the rest were highly significant and had a large effect size (Cohen's d = 3.5). While highly suggestive, future studies may be necessary to verify if such higher levels of hypoxia are indicative of progressive disease. Diffusion MRI showed no differences between CKD and healthy controls.

Conclusions: These data demonstrate that BOLD MRI can be used to identify enhanced hypoxia associated with CKD and the preliminary observations are consistent with the chronic hypoxia model for disease progression in CKD. Longitudinal studies are warranted to further verify these findings and assess their predictive value.

No MeSH data available.


Related in: MedlinePlus