Purpose: To investigate the possibility of using combined blood oxygen level-dependent (BOLD) imaging and diffusion-weighted imaging (DWI) to detect pathological and physiological changes in renal tissue damage of the kidney induced by chronic renal hyperfiltration. Materials and Methods: The apparent diffusion coefficient (ADC) and the T2* value within the inner compartments of the kidneys of 17 rats with diabetes mellitus were compared with the results obtained from a control group (N = 16). The influence of dynamic changes of the renal function on the blood-oxygen saturation was evaluated by comparing the T2* values before and after the active reduction of tubular transport by furosemide injection. Results: All compartments of the diabetic kidney showed significantly (P < 0.05) lower T2*-values compared to the control group, In particular, the very low values in the outer stripe (OS) of the outer medulla (OM) (T2*-normal: 69.4 ± 10.9 msec; T2*-diabetic: 51.4 ± 13.9 msec) indicated either hypoxia due to hyperfiltration, or renal blood volume changes, Diffusion imaging of the same area showed significantly lower ADC values (ADC-normal: 1.45 ± 0.26: ADC-edema: 1.19 ± 0.25 [10-9m2/s]) that correlated with pathological findings on histopathology. The injection of furosemide significantly (P < 0.05) increased T2* in all compartments of both populations while the ADC remained unchanged. Conclusion: BOLD-contrast imaging appears to be able to depict tissue at risk from ischemia by revealing information about the balance between tubular workload and delivery of oxygen, and thus may reflect a measure of the reserve capacity, The diffusion measurements apparently reveal complementary information. Although ADC imaging is not sensitive to the current energy metabolism, it appears toreflect the pathological changes within the tissue. Therefore, ADC measurements may be a sensitive indicator of the severity of ischemic lesions.
|Tijdschrift||Journal of Magnetic Resonance Imaging|
|Nummer van het tijdschrift||1|
|Status||Gepubliceerd - 1 jan. 2003|