Neither aspirin nor clonidine treatment used perioperatively lowers risk of kidney injury

by Bruce Sylvester: In the non-cardiac surgical setting, neither aspirin nor clonidine taken perioperatively appears to reduce the risk of acute kidney injury, researchers reported on Nov. 15, 2014 in JAMA/Journal of the American Medical Association. 

The findings were published to coincide with the presentation of the data at the American Society of Nephrology/ Kidney Week 2014 meeting.

Amit X. Garg, M.D., Ph.D., of the London Health Sciences Centre and Western University, London, Ontario, Canada, and colleagues from 22 countries enrolled and randomized 6,905 subjects undergoing non-cardiac surgery.

One group received aspirin (200 mg) or placebo 2 to 4 hours before surgery, followed by aspirin (100 mg) or placebo received daily for up to 30 days after surgery.

A second group received oral clonidine (0.2 mg) or placebo 2 to 4 hours before surgery, and then a transdermal clonidine patch or placebo patch remaining in place until 72 hours after surgery.

The investigators defined acute kidney injury as a clinically important increase in serum creatinine.

They reported that neither aspirin nor clonidine lowered the risk of acute kidney injury. Subjects in each cohort who showed acute kidney injury were 13.4 percent for aspirin vs 12.3 percent for placebo, and 13.0 percent for clonidine vs 12.7 percent for placebo.

Aspirin increased the risk of major bleeding. And major bleeding associated with an increased risk of subsequent acute kidney injury, 23.3 percent when bleeding was present vs 12.3 percent when bleeding was absent.

Clonidine increased the risk of clinically important hypotension, and hypotension associated with an increased risk of subsequent acute kidney injury, 14.3 percent when hypotension occurred vs 11.8 percent when hypotension did not occur.

The concluded that future large trials of acute kidney injury prevention in the perioperative setting should focus on interventions targeting pathways other than inhibiting platelet aggregation and alpha 2-adrenergic agonism.