Antithrombin III Protects Against Contrast-Induced Nephropathy.We previously reported that insufficiency of antithrombin III (ATIII), the major anti-coagulation molecule in vivo, exacerbated renal ischemia-reperfusion injury in animal models and possibly humans.  In the present study, we investigated the relationship between ATIII level and contrast induced nephropathy (CIN) in patients and examined therapeutic effect of ATIII on CIN in Sprague-Dawley rats.  Patients with low ATIII activity presented a higher incidence of acute kidney injury (AKI) following coronary angiography.  ATIII (500μg/kg) was intravenously injected before or after the induction of AKI in rats.  Our data demonstrated ATIII significantly attenuated the elevation of serum creatinine, blood urea nitrogen, and renal histological injury.  The beneficial effects of ATIII were accompanied by diminished renal inflammatory response, oxidative stress, cell apoptosis and improved renal blood flow in rats.  In conclusion, ATIII appears to attenuate CIN through inhibiting inflammation, oxidative stress, apoptosis and improving renal blood flow.  ATIII administration may represent a promising strategy for the prevention and treatment of contrast-induced AKI.
ATIII
Antithrombin III Protects Against Contrast-Induced Nephropathy.We previously reported that insufficiency of antithrombin III (ATIII), the major anti-coagulation molecule in vivo, exacerbated renal ischemia-reperfusion injury in animal models and possibly humans.  In the present study, we investigated the relationship between ATIII level and contrast induced nephropathy (CIN) in patients and examined therapeutic effect of ATIII on CIN in Sprague-Dawley rats.  Patients with low ATIII activity presented a higher incidence of acute kidney injury (AKI) following coronary angiography.  ATIII (500μg/kg) was intravenously injected before or after the induction of AKI in rats.  Our data demonstrated ATIII significantly attenuated the elevation of serum creatinine, blood urea nitrogen, and renal histological injury.  The beneficial effects of ATIII were accompanied by diminished renal inflammatory response, oxidative stress, cell apoptosis and improved renal blood flow in rats.  In conclusion, ATIII appears to attenuate CIN through inhibiting inflammation, oxidative stress, apoptosis and improving renal blood flow.  ATIII administration may represent a promising strategy for the prevention and treatment of contrast-induced AKI.
ATIII
Antithrombin III Protects Against Contrast-Induced Nephropathy.We previously reported that insufficiency of antithrombin III (ATIII), the major anti-coagulation molecule in vivo, exacerbated renal ischemia-reperfusion injury in animal models and possibly humans.  In the present study, we investigated the relationship between ATIII level and contrast induced nephropathy (CIN) in patients and examined therapeutic effect of ATIII on CIN in Sprague-Dawley rats.  Patients with low ATIII activity presented a higher incidence of acute kidney injury (AKI) following coronary angiography.  ATIII (500μg/kg) was intravenously injected before or after the induction of AKI in rats.  Our data demonstrated ATIII significantly attenuated the elevation of serum creatinine, blood urea nitrogen, and renal histological injury.  The beneficial effects of ATIII were accompanied by diminished renal inflammatory response, oxidative stress, cell apoptosis and improved renal blood flow in rats.  In conclusion, ATIII appears to attenuate CIN through inhibiting inflammation, oxidative stress, apoptosis and improving renal blood flow.  ATIII administration may represent a promising strategy for the prevention and treatment of contrast-induced AKI.
ATIII