Almost one-third of in-hospital mortality after percutaneous coronary intervention (PCI) is attributable to acute kidney injury (AKI), a new study found.

Researchers calculated that 1 death could be prevented for every 9 cases of AKI that is successfully avoided, according to a report published online in Circulation. Cardiovascular Interventions (2015;8:e002212).

“These study findings stress the need for developing effective AKI preventive strategies beyond minimization of contrast dose,” the authors concluded.

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Using a regional registry of all patients undergoing PCI in Michigan, a team led by Hitinder S. Gurm, MD, of the University of Michigan Cardiovascular Center in Ann Arbor, identified 92,317 PCI patient who underwent PCI from 2010 to 2013. AKI developed in 2,141 (2.3%) of these patients. The researchers propensity score-matched 1,371 of the patients with AKI to 5,484 controls. AKI was associated with a 12.5 times increased odds of death, with 31.4% of deaths were attributable to AKI, Dr. Gurm’s group reported.

Although the study showed that a high contrast dose at time of PCI significantly increases the risk of AKI, the researchers stated that contrast dosing is only a minor contributor to the overall burden of AKI in this population. “Thus, efforts to reduce contrast dose, although worthwhile, would only moderately impact in-hospital mortality rates,” they wrote. “This suggests that efforts to reduce the incidence and impact of AKI need to move beyond contrast media choice and dosing and be targeted at other mechanistic pathways of AKI, such as inflammation and the potential role for statin preloading.”

The researchers found that the mortality risk associated with AKI was highest in those with cardiogenic shock, cardiac arrest, or presenting with ST-segment elevation myocardial infarction.

The researchers explained that AKI following PCI has a number of potential causes, including acute tubular necrosis from poor perfusion, nephrotoxicity from contrast media, use of nephrotoxic medications, cholesterol embolization, procedure-related factors, or a combination of these. “The differentiation between these etiologies is often difficult because they all result in an increase in serum creatinine within a few days post PCI, frequently in the absence of other clinical findings suggestive of a cause of injury,” they wrote.