Questions: 

Contrast induced acute kidney injury (CI-AKI) is an important type of AKI. Key feature of the pathophysiology of CI-AKI is the reduction in glomerular filtration rate. The present study tests the hypothesis that contrast media impair the renal microvasculature function in a manner that contributes to decrease the effective glomerular filtration pressure.

Methods: 

Isolated afferent arteriole (AA) and efferent arteriole (EA) of C57BL/6 mice were perfused with either contrast media (23mg iodine/ml) or vehicle solution for 20 min, followed by angiotensin II dose response curves. Groups of AA were also treated with L-NAME. Changes in diameter served for analysis of tone and reactivity. DAF-FM and dihydroethidium fluorescence were used for quantification of nitric oxide bioavailability and superoxide concentration, respectively in AA.

Results: 

Contrast media reduced AA diameters (to 86.3%) and further increased AA response to angiotensin II, while EA was unaffected by contrast media. L-NAME (70.7%) and contrast media+L-NAME (52.9%) both constricted AA, but only contrast media+L-NAME enhanced the angiotensin II response. The DAF-FM fluorescence intensity was reduced similarly during contrast media (4.0%) and L-NAME (3.6%) treatment compared to control group (10.6%). The dihydroethidium ratio was increased during contrast media (13.4%) application for 3 min. TEMPOL diminished this contrast media effect.

Conclusions: 

The results suggest that a reduction in the effective glomerular filtration pressure might contribute to the reduced glomerular filtration rate in CI-AKI.