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Functional MRI

Rationale and Objectives

To evaluate the functional alterations of chronic kidney disease (CKD) with magnetic resonance dynamic perfusion imaging.

Materials and methods

Twenty-one healthy subjects (42 kidneys) and 20 CKD patients (40 kidneys) underwent routine scans with fat-saturated T1-weighted fast low angle shot (FLASH) and true-fast imaging with steady-state precession (FISP) sequences followed by dynamic perfusion scans using a turbo-FLASH T1-weighted sequence. Signal intensity (SI) of the cortex and medulla on images was measured and plotted as a function of time. Peak height (P) and time to peak (T) of the cortex and medulla SI were estimated, and P/T ratio and the area under the time-intensity curves were calculated. We also tested the correlation between these data and serum creatinine (sCr) levels in patients.

Results

P, P/T ratio, and the area under the curve of patients’ cortex and medulla were significantly decreased compared to control subjects, and T was delayed. In patients, P and P/T ratio of the cortex and P of the medulla were negatively correlated with sCr levels ( r = −0.469, r = −0.419, and r = −0.423, respectively; P < 0.01).

Conclusion

Renal dysfunction in CKD can be evaluated by magnetic resonance dynamic perfusion imaging.

Magnetic resonance imaging (MRI) has several distinct advantages in the kidney compared to other imaging methods. Ultrasound scanning (US) is suitable for morphologic evaluation but does not supply information about renal function. Intravenous urography (IVU) allows visualization of general morphology and simple functional evaluation of the kidney. Contrast-enhanced computed tomography (CT) has excellent spatial and temporal resolution, but the contrast used during IVU and CT is nephrotoxic and unfit for patients with renal dysfunction. Although nuclear medicine has provided reliable functional data, inability to visualize the kidney and lack of spatial resolution limit morphologic evaluation.

Dynamic contrast-enhanced MRI has great potential in providing both morphologic and functional information in the kidney ( ). Dynamic T1 contrast-enhancement is a commonly used MRI technique. T1 (longitudinal relaxation time) is shortened because of the dipole–dipole interaction of the contrast agent, which corresponds to increased signal intensity (SI) in T1-weighted imaging. A common contrast agent, gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA) is not contraindicated in patients with impaired renal function ( ), and it is therefore possible to study renal perfusion and excretion in patients with chronic renal dysfunction using dynamic MRI.

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Materials and Methods

Subjects

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MRI

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Pathology

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Data Analysis

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Results

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Figure 1, Dynamic perfusion images from a healthy subject. Enhancement of the cortex was normally followed by enhancement of medulla. Corticomedullary differentiation was preserved. Both kidneys were equally enhanced. The images in Figures 1–3 were chosen at the same time point during dynamic perfusion imaging, with uniform width and level.

Figure 2, Dynamic perfusion images from a CKD patient (sCr 191 μmol/L). Enhancement of cortex and medulla were subdued, compared with Figure 1 . Corticomedullary differentiation was preserved.

Figure 3, Dynamic perfusion images from a CKD patient (sCr 295 μmol/L). Enhancement of cortex and medulla were distinctly delayed and subdued, especially in the left kidney. Corticomedullary differentiation was decreased. There was a small cyst at the inferior pole of the right kidney.

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Table 1

Statistical Results in CKD Patients and Controls

Healthy Controls CKD Patients_t__P_ Value Cortex Time to peak (Tc) 25.8 ± 3.0 31.4 ± 8.1 4.230 <.01 Peak height (Pc) 57.0 ± 12.2 49.6 ± 13.1 2.642 <.05 Pc/Tc 2.2 ± 0.5 1.7 ± 0.7 3.919 <.01 Medulla Time to peak (Tm) 85.5 ± 15.8 96.1 ± 28.0 2.111 <.05 Peak height (Pm) 55.9 ± 10.7 45.9 ± 13.0 3.818 <.01 Pm/Tm 0.67 ± 0.15 0.50 ± 0.19 4.486 <.01

Figure 4, (a, b) Perfusion curve of a healthy subject and of a patient (sCr 295 μmol/L). In the patient, peak height and the area under the curve of the cortex and medulla were decreased and time to peak of the cortex and medulla were delayed compared with the control subject. Focal proliferative sclerosing glomerulonephritis with ischemic injury was confirmed pathologically.

Figure 5, (a, b) The same patient as Figure 3 . Peak height of cortex and medulla of the left kidney were distinctly lower than the right kidney.

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Table 2

Correlation Between sCr and P, T, and P/T of Cortex and Medulla in CKD Patients

r__P Value Cortex Time to peak (Tc) 0.127 <.05 Peak height (Pc) −0.469 <.01 Pc/Tc −0.419 <.01 Medulla Time to peak (Tm) −0.059 <.05 Peak height (Pm) −0.423 <.01 Pm/Tm −0.298 <.05

Figure 6, With increased serum creatinine (sCr) level, ( a ) peak height of cortex (Pc), ( b ) Pc/time to peak of cortex (Tc), and ( c ) peak height of medulla (Pm) of kidneys reduced gradually in patients.

Table 3

The Area Under the Time-intensity Curves in CKD Patients and Controls

Healthy Controls CKD Patients_t__P_ Value Cortex 132.6 ± 27.6 105.6 ± 30.3 3.951 <.01 Medulla 116.6 ± 22.5 90.6 ± 22.1 4.892 <.01

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Figure 7, Immunoglobulin A (IgA) glomerulonephritis with ischemic injury at 20× magnification. ( a ) PASM stain. ( b ) Masson stain. Note the sclerosing glomerulus, crescents, and extensive proliferation of the mesangial cells and extracellular matrix. Atrophy of renal tubules, monocyte and fibrosis in interstitium, and light thickening of arteriolar walls were observed.

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Discussion

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Summary

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Acknowledgment

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