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High temporal resolution parametric MRI monitoring of the initial ischemia/reperfusion phase in experimental acute kidney injury.

Pohlmann A, Hentschel J, Fechner M, Hoff U, Bubalo G, Arakelyan K, Cantow K, Seeliger E, Flemming B, Waiczies H, Waiczies S, Schunck WH, Dragun D, Niendorf T - PLoS ONE (2013)

Bottom Line: There is an unmet need to better understand the mechanisms operative during the initial phase of ischemic AKI.Our study demonstrated for the first time that continuous and high temporal resolution parametric MRI is feasible for in-vivo monitoring and characterization of I/R induced AKI in rats.This technique may help in the identification of the timeline of key events responsible for development of renal damage in hypoperfusion-induced AKI.

View Article: PubMed Central - PubMed

Affiliation: Berlin Ultrahigh Field Facility, Max Delbrück Center for Molecular Medicine, Berlin, Germany. andreas.pohlmann@mdc-berlin.de

ABSTRACT
Ischemia/reperfusion (I/R) injury, a consequence of kidney hypoperfusion or temporary interruption of blood flow is a common cause of acute kidney injury (AKI). There is an unmet need to better understand the mechanisms operative during the initial phase of ischemic AKI. Non-invasive in vivo parametric magnetic resonance imaging (MRI) may elucidate spatio-temporal pathophysiological changes in the kidney by monitoring the MR relaxation parameters T2* and T2, which are known to be sensitive to blood oxygenation. The aim of our study was to establish the technical feasibility of fast continuous T2*/T2 mapping throughout renal I/R. MRI was combined with a remotely controlled I/R model and a segmentation model based semi-automated quantitative analysis. This technique enabled the detailed assessment of in vivo changes in all kidney regions during ischemia and early reperfusion. Significant changes in T2* and T2 were observed shortly after induction of renal ischemia and during the initial reperfusion phase. Our study demonstrated for the first time that continuous and high temporal resolution parametric MRI is feasible for in-vivo monitoring and characterization of I/R induced AKI in rats. This technique may help in the identification of the timeline of key events responsible for development of renal damage in hypoperfusion-induced AKI.

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Ischemia reperfusion results derived from the standardized segmentation model of the kidney: Plots of T2* (mean ±SEM averaged over six animals) versus time for the ROIs in the cortex (C1, C2, C3; top row), in the outer medulla (O1, O2, O3; middle row), and in the inner medulla (I1, I2, I3; bottom row).Ischemia (shaded in gray) led to an immediate and significant T2* decrease in all kidney ROIs (p≤0.01 in C1, p≤0.001 in all other ROIs). Clear differences between cortex, outer medulla and inner medulla were observed. At the end of the reperfusion period T2* was close to baseline (dashed line) in the cortex (p>0.2), below baseline in the outer medulla (p≤0.05 (C1), p≤0.001 (C2), p≤0.01 (C3)), and above baseline in the inner medulla (non-significant). The three ROIs within each kidney regions showed very similar but not identical trends.
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pone-0057411-g005: Ischemia reperfusion results derived from the standardized segmentation model of the kidney: Plots of T2* (mean ±SEM averaged over six animals) versus time for the ROIs in the cortex (C1, C2, C3; top row), in the outer medulla (O1, O2, O3; middle row), and in the inner medulla (I1, I2, I3; bottom row).Ischemia (shaded in gray) led to an immediate and significant T2* decrease in all kidney ROIs (p≤0.01 in C1, p≤0.001 in all other ROIs). Clear differences between cortex, outer medulla and inner medulla were observed. At the end of the reperfusion period T2* was close to baseline (dashed line) in the cortex (p>0.2), below baseline in the outer medulla (p≤0.05 (C1), p≤0.001 (C2), p≤0.01 (C3)), and above baseline in the inner medulla (non-significant). The three ROIs within each kidney regions showed very similar but not identical trends.

Mentions: Quantitative examination of T2* and T2 changes used the standardized renal segmentation model. Plots of T2* (mean ±SEM averaged over six animals) versus time for these ROIs are shown in Figure 5. The T2* time courses revealed an immediate drop in T2* after onset of ischemia followed by a slow and steady decrease in T2*. During ischemia T2* was significantly reduced in all ROIs (p≤0.01 in C1, p≤0.001 in all other ROIs), which clearly distinguished this condition from baseline. The time courses of T2 were very similar to those of T2*. During reperfusion, T2* and T2 did return to baseline in the cortex, but not in the medulla. While no major differences among the cortical, outer medullary, and inner medullary T2* changes were found during ischemia, there was a clear regional dynamics during reperfusion. After onset of reperfusion T2* returned close to baseline for cortical segments (p = 0.97 (C1), p = 0.22 (C2), p = 0.65 (C3)). For the outer medulla T2* remained below baseline throughout reperfusion and was at 40–47% below baseline after 100 minutes (p≤0.05 (C1), p≤0.001 (C2), p≤0.01 (C3)). T2 was 19–21% below baseline at 100 minutes reperfusion. In the inner medulla T2* and T2 exceeded baseline by 17–28% and 14–18% respectively (non-significant) at the end of reperfusion. These differences among the layers were pronounced during early reperfusion and remained stable throughout reperfusion. The assessment of the heterogeneity among segments within one kidney layer revealed an almost equal time course in T2* for the cortical, outer medullary and inner medullary segments, respectively.


High temporal resolution parametric MRI monitoring of the initial ischemia/reperfusion phase in experimental acute kidney injury.

Pohlmann A, Hentschel J, Fechner M, Hoff U, Bubalo G, Arakelyan K, Cantow K, Seeliger E, Flemming B, Waiczies H, Waiczies S, Schunck WH, Dragun D, Niendorf T - PLoS ONE (2013)

Ischemia reperfusion results derived from the standardized segmentation model of the kidney: Plots of T2* (mean ±SEM averaged over six animals) versus time for the ROIs in the cortex (C1, C2, C3; top row), in the outer medulla (O1, O2, O3; middle row), and in the inner medulla (I1, I2, I3; bottom row).Ischemia (shaded in gray) led to an immediate and significant T2* decrease in all kidney ROIs (p≤0.01 in C1, p≤0.001 in all other ROIs). Clear differences between cortex, outer medulla and inner medulla were observed. At the end of the reperfusion period T2* was close to baseline (dashed line) in the cortex (p>0.2), below baseline in the outer medulla (p≤0.05 (C1), p≤0.001 (C2), p≤0.01 (C3)), and above baseline in the inner medulla (non-significant). The three ROIs within each kidney regions showed very similar but not identical trends.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3585384&req=5

pone-0057411-g005: Ischemia reperfusion results derived from the standardized segmentation model of the kidney: Plots of T2* (mean ±SEM averaged over six animals) versus time for the ROIs in the cortex (C1, C2, C3; top row), in the outer medulla (O1, O2, O3; middle row), and in the inner medulla (I1, I2, I3; bottom row).Ischemia (shaded in gray) led to an immediate and significant T2* decrease in all kidney ROIs (p≤0.01 in C1, p≤0.001 in all other ROIs). Clear differences between cortex, outer medulla and inner medulla were observed. At the end of the reperfusion period T2* was close to baseline (dashed line) in the cortex (p>0.2), below baseline in the outer medulla (p≤0.05 (C1), p≤0.001 (C2), p≤0.01 (C3)), and above baseline in the inner medulla (non-significant). The three ROIs within each kidney regions showed very similar but not identical trends.
Mentions: Quantitative examination of T2* and T2 changes used the standardized renal segmentation model. Plots of T2* (mean ±SEM averaged over six animals) versus time for these ROIs are shown in Figure 5. The T2* time courses revealed an immediate drop in T2* after onset of ischemia followed by a slow and steady decrease in T2*. During ischemia T2* was significantly reduced in all ROIs (p≤0.01 in C1, p≤0.001 in all other ROIs), which clearly distinguished this condition from baseline. The time courses of T2 were very similar to those of T2*. During reperfusion, T2* and T2 did return to baseline in the cortex, but not in the medulla. While no major differences among the cortical, outer medullary, and inner medullary T2* changes were found during ischemia, there was a clear regional dynamics during reperfusion. After onset of reperfusion T2* returned close to baseline for cortical segments (p = 0.97 (C1), p = 0.22 (C2), p = 0.65 (C3)). For the outer medulla T2* remained below baseline throughout reperfusion and was at 40–47% below baseline after 100 minutes (p≤0.05 (C1), p≤0.001 (C2), p≤0.01 (C3)). T2 was 19–21% below baseline at 100 minutes reperfusion. In the inner medulla T2* and T2 exceeded baseline by 17–28% and 14–18% respectively (non-significant) at the end of reperfusion. These differences among the layers were pronounced during early reperfusion and remained stable throughout reperfusion. The assessment of the heterogeneity among segments within one kidney layer revealed an almost equal time course in T2* for the cortical, outer medullary and inner medullary segments, respectively.

Bottom Line: There is an unmet need to better understand the mechanisms operative during the initial phase of ischemic AKI.Our study demonstrated for the first time that continuous and high temporal resolution parametric MRI is feasible for in-vivo monitoring and characterization of I/R induced AKI in rats.This technique may help in the identification of the timeline of key events responsible for development of renal damage in hypoperfusion-induced AKI.

View Article: PubMed Central - PubMed

Affiliation: Berlin Ultrahigh Field Facility, Max Delbrück Center for Molecular Medicine, Berlin, Germany. andreas.pohlmann@mdc-berlin.de

ABSTRACT
Ischemia/reperfusion (I/R) injury, a consequence of kidney hypoperfusion or temporary interruption of blood flow is a common cause of acute kidney injury (AKI). There is an unmet need to better understand the mechanisms operative during the initial phase of ischemic AKI. Non-invasive in vivo parametric magnetic resonance imaging (MRI) may elucidate spatio-temporal pathophysiological changes in the kidney by monitoring the MR relaxation parameters T2* and T2, which are known to be sensitive to blood oxygenation. The aim of our study was to establish the technical feasibility of fast continuous T2*/T2 mapping throughout renal I/R. MRI was combined with a remotely controlled I/R model and a segmentation model based semi-automated quantitative analysis. This technique enabled the detailed assessment of in vivo changes in all kidney regions during ischemia and early reperfusion. Significant changes in T2* and T2 were observed shortly after induction of renal ischemia and during the initial reperfusion phase. Our study demonstrated for the first time that continuous and high temporal resolution parametric MRI is feasible for in-vivo monitoring and characterization of I/R induced AKI in rats. This technique may help in the identification of the timeline of key events responsible for development of renal damage in hypoperfusion-induced AKI.

Show MeSH
Related in: MedlinePlus