Radiological iodinated contrasts (IC) agents cause acute kidney injury (AKI). To evaluate the renoprotective effect of sodium bicarbonate (Bic) on renal function (creatinine clearance {Clcr}, Jaffé, and Clcr mL·min-1⋅100 g-1) and the oxidative profile (peroxide excretion, urinary peroxides, urinary malondialdehyde, FOX-2 expression, and thiobarbituric acid reactive substance {TBARS; nmol/mg Cr}) in rats treated with an IC agent. Adult male Wistar rats weighing 250 - 300 g were treated once daily for 5 days with one of the following treatments: saline (0.9%, 3 mL·kg-1⋅day-1intraperitoneally {i.p.}), IC agent (sodium and meglumine ioxitalamate, 3 mL/kg, i.p.), Bic + Saline (3-mL/kg Bic, i.p., 1 h before and after saline treatment), and Bic + IC (3-mL/kg Bic, i.p., 1 h before and after the IC treatment). The IC agent induced AKI, and the antioxidant renoprotective effect of Bic was confirmed (Clcr/TBARS/urinary peroxide: saline group, 0.59 ± 0.03/0.11 ± 0.02/1.29 ± 0.24; Bic + Saline group, 0.58 ± 0.03/0.13 ± 0.02/1.32 ± 0.64; IC group, 0.22 ± 0.02/0.19 ± 0.02/4.77 ± 0.24; Bic + CI group, 0.51 ± 0.04/0.13 ± 0.3/1.80 ± 0.04; p<0.05). The protective effect of Bic in the IC-induced AKI was confirmed; hence, Bic administration may be considered as a therapeutic option for patients undergoing IC-enhanced radiography.
Acute kidney injury; Contrast media; Iodine; Sodium bicarbonate; Therapeutics