乌鸦传媒視頻

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PHILADELPHIA -- Neither aspirin nor clonidine reduced the risk of acute kidney injury (AKI) in patients having noncardiac surgery, researchers reported here.

In the POISE-2 acute kidney injury substudy, aspirin did not lower the risk of AKI compared with placebo (13.4% versus 12.3%, respectively, adjusted relative risk 1.10, 95% CI 0.96-1.25), reported , of London Health Sciences Center in Ontario in Canada, and colleagues online in the and at the American Society of Nephrology Kidney Week meeting.

The risk of AKI was not any lower with clonidine versus placebo (13% versus 12.7%, aRR 1.03, 95% CI 0.90-1.18), they stated.

However, they did find that aspirin increased the risk for major bleeding.

Some studies have suggested that perioperative aspirin or clonidine may reduce the risk of AKI in surgical patients, but those effects are uncertain and each intervention has the potential for harm: aspirin carries the risk of perioperative bleeding, while clonidine could cause perioperative hypotension.

To determine whether aspirin or clonidine compared with placebo could alter the risk of perioperative AKI, Garg and colleagues completed the Perioperative Ischemia Evaluation-2 (POISE-2) AKI substudy.

The trial enrolled 6,905 patients having noncardiac surgery from 88 centers in 22 countries between January 2011 and December 2013. Patients were enrolled in a 2-by-2 factorial analysis to one of the following interventions:

• Aspirin 200 mg or placebo 2 to 4 hours before surgery, and then aspirin 100 mg or placebo daily for up to 30 days after surgery
• Oral clonidine 0.2 mg or placebo 2 to 4 hours before surgery and transdermal clonidine patch 0.2 mg/day
• Placebo patch worn for 72 hours after surgery

The authors defined AKI as "an increase in serum creatinine concentration from the preoperative concentration by either an increase of 0.3 mg/dL or greater (≥26.5 micromoles/L) within 48 hours of surgery or an increase of 50% or greater within 7 days of surgery."

In a post-hoc analysis, major bleeding was associated with a greater risk of subsequent AKI (23.3% when bleeding was present versus 12.3% when bleeding was absent, adjusted hazard ratio 2.20, 95% CI 1.72-2.83).

They also saw that clonidine increased the risk of clinically important hypotension, and in the post-hoc analysis, clinically important hypotension was associated with a greater risk of subsequent AKI (14.3% versus 11.8%, aHR 1.34, 95% CI 1.14-1.58).

The researchers cautioned that a key limitation of their protocol was the reliance on the serum creatinine concentration collected during routine care as the sole measure of kidney function. It would have been preferable to have multiple baseline measures of serum creatinine and other assessments of kidney function, along with additional follow-up measures during the perioperative period, they explained.

Still, they said the findings can now guide similar analyses in other ongoing trials to determine if these signals are replicated.

Future large trials to prevent AKI in the surgical setting, they added, should focus on interventions that target pathways other than inhibiting platelet aggregation or alpha2-adrenergic agonism. Interventions that prevent perioperative bleeding and perioperative hypotension may prove useful, they wrote.

In an accompanying editorial, , of Baylor College of Medicine, and , of the University of Texas, both in Houston, wrote that the results "are sobering and constitute a setback to finding effective interventions to prevent AKI and the burden of its consequences."

They also noted that the next iteration of AKI guidelines will be able to increase the evidence level of the recommendations against using these therapies, adding that the "next therapeutic batter is already warming up and hoping to have more luck against the formidable opponent AKI."