Association of Angiotensin-Converting Enzyme Inhibitor or Angiotensin Receptor Blocker Use With Outcomes After Acute Kidney Injury

Abstract

; for the Interdisciplinary Chronic Disease Collaboration IMPORTANCE Patients with acute kidney injury (AKI) are at an increased long-term risk of death. Effective strategies that improve long-term outcomes in patients with AKI are unknown. OBJECTIVE To evaluate whether the use of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) after hospital discharge is associated with better outcomes in patients with AKI. DESIGN, SETTING, AND PARTICIPANTS This retrospective cohort study used data from the Alberta Kidney Disease Network population database to evaluate 46 253 adults 18 years or older with an episode of AKI during a hospitalization between July 1, 2008, and March 31, 2015, in Alberta, Canada. All patients who survived to hospital discharge were followed up for a minimum of 2 years. EXPOSURES Use of an ACEI or ARB within 6 months after hospital discharge. MAIN OUTCOMES AND MEASURES The primary outcome was mortality; secondary outcomes included hospitalization for a renal cause, end-stage renal disease (ESRD), and a composite outcome of ESRD or sustained doubling of serum creatinine concentration. An AKI was defined as a 50% increase between prehospital and peak in-hospital serum creatinine concentrations. Propensity scores were used to construct a matched-pairs cohort of patients who did and did not have a prescription for an ACEI or ARB within 6 months after hospital discharge. RESULTS The study evaluated 46 253 adults (mean [SD] age, 68.6 [16.4] years; 24 436 [52.8%] male). Within 6 months of discharge, 22 193 (48.0%) of the participants were prescribed an ACEI or ARB. After adjustment for comorbidities, ACEI or ARB use before admission, demographics, baseline kidney function, other factors related to index hospitalization, and prior health care services, ACEI or ARB use was associated with lower mortality in patients with AKI after 2 years (adjusted hazard ratio, 0.85; 95% CI, 0.81-0.89). However, patients who received an ACEI or ARB had a higher risk of hospitalization for a renal cause (adjusted hazard ratio, 1.28; 95% CI, 1.12-1.46). No association was found between ACEI or ARB use and progression to ESRD. CONCLUSIONS AND RELEVANCE Among patients with AKI, ACEI or ARB therapy appeared to be associated with lower mortality but a higher risk of hospitalization for a renal cause. These results suggest a potential benefit of ACEI or ARB use after AKI, but cautious monitoring for renal-specific complications may be warranted.

Improving Care for Patients after Hospitalization with AKI

“…Several recent observational studies attempting to quantify the risks and benefits of continued RAAS inhibition have been published, with conflicting findings. [8][9][10] Some studies have suggested an increased risk for hospitalization for kidney events, whereas others have shown no increase in risk for recurrent AKI. However, studies have also demonstrated that the potential risks of these medications may be offset by favorable effects on survival and long-term kidney function, if applied cautiously.…”

Quality of Care for Acute Kidney Disease: Current Knowledge Gaps and Future Directions

“…However, in humans, after an episode of AKI, administration of RAAS agents may increase the risk for hyperkalemia as well as the need for nephrology-based hospitalization. 29 In a retrospective cohort study of US adults, post-AKI patients had a 22% increase in the odds of developing hypertension. 31 However, RAAS agents are associated with functional AKI, especially in the setting of acute hypovolemia.…”

Iatrogenic Decompensated Heart Failure

“…RAASi is often misunderstood as a nephrotoxic drug. Introduction of the UK electronic acute kidney injury alert (AKI e-alert) system has exacerbated this anxiety, and a reflex cessation of RAASi amongst hospital and community practitioners occurs when a small serum urea or creatinine (sCr) rise is seen [6]. RAASi induces renal efferent arterial vasodilatation, and a resultant fall in intra-glomerular pressure is expected, reflected by an initial sCr rise and a decline in glomerular filtration rate (GFR) in the first 2 weeks.…”