Acute kidney injury (AKI) is a common complication among acutely ill hospitalized patients. Depending on the definition used, AKI complicates 1% to 25% of intensive care unit admissions and is associated with mortality rates of 15% to 60%.1 Through a variety of mechanisms that affect the kidneys and the vasculature, patients with AKI are at increased risk for the subsequent development of not only chronic kidney disease but also hypertension, stroke, and cardiovascular disease.2 Because of the known nephroprotective and cardioprotective effects of renin angiotensin system (RAS) blockers (angiotensin converting enzyme inhibitors [ACEIs] and angiotensin receptor blockers [ARBs]),3,4 it has been postulated that these agents should be used after AKI to mitigate the risk of adverse cardiorenal outcomes in patients with AKI. Testing this hypothesis, Gayat et al5 recently reported that among 1551 intensive care unit patients enrolled in a prospective cohort, 611 of whom had AKI, those who were prescribed an RAS blocker at the time of hospital discharge had 52% lower mortality (propensity score–matched hazard ratio [HR], 0.48) than those not prescribed an RAS blocker. Of interest, in difference from those with AKI, this association was not noted in patients without AKI during the hospitalization (HR, 1.0).5
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Alpern RJ, Peixoto AJ. Use of Renin Angiotensin System Blockers After Acute Kidney Injury: Balancing Tradeoffs. JAMA Intern Med. 2018;178(12):1690–1692. doi:10.1001/jamainternmed.2018.4757
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