New analysis of the hypertension mechanism in bevacizumab-treated patients using 3-tesla dynamic contrast-enhanced magnetic resonance imaging.

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450 Background: Vascular endothelial growth factor (VEGF) signaling inhibitors, such as bevacizumab (BV), leads to endothelial dysfunction and microvascular rarefaction in noncancer tissue. Angiotensin II has been reported to induce VEGF production by inhibiting VEGF, but the reasons for activation of angiotensin II are unclear. We conducted a study to examine the relationship between renin-angiotensin axis and renal blood perfusion using dynamic contrast magnetic resonance imaging (DCE-MRI) in colorectal cancer patients. Methods: Sixteen patients with colorectal cancer were enrolled. They received BV+FOLFIRI regimen as second line. DCE-MRI was performed before the treatment and after 12th courses. Renin, angiotensin I, angiotensin II and aldosterone were examined before treatment and at 3, 5, 8, 12th courses. DCE-MRI parameters, Area under the time-intensity curve over the first 90 seconds after injection of contrast material (AUC90) and volume transfer constant of contrast material (Ktrans, Kep) were calculated in the normal kidney and examine the correlation with renin-angiotensin axis. Results: All DCE-MRI parameters decreased significantly after 12th courses compared with before treatment (Variables median: Ktrans -1.51, Kep -2.30, AUC90 -26.0, P < 0.001, all). A decrease in Kep correlated with higher renin, angiotensin I and angiotensin II (renin: P =0.001, angiotensin I: P =0.003, angiotensin II: P =0.002, respectively). A decrease in AUC90 correlated with higher aldosterone (P =0.005). Blood pressure did not correlate with each DCE-MRI parameters. Conclusions: VEGF inhibition decreases vessel permeability and raises interstitial pressure in normal kidney. Our data suggest that renin-angiotensin axis is also one mechanism of hypertension caused by BV. No significant financial relationships to disclose.

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