SP551
RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM INHIBITORS (RAASI) AND CLINICAL OUTCOMES IN HEMODIALYSIS PATIENTS: RESULTS FROM THE DOPPS

INTRODUCTION AND AIMS: Prescription of RAASi is often indicated for hemodialysis (HD) patients due to the high rates of congestive heart failure (CHF) and cardiovascular (CV) disease. Hyperkalemia, a potential side effect of RAASi, is a risk factor for arrhythmias and sudden death. However, this potential risk may be outweighed by the wide-ranging benefits of RAAS inhibition. We investigated the association between RAASi and clinical outcomes in an international cohort of HD patients.

METHODS: Data were from phases 2-5 (2002-2015) of the Dialysis Outcomes and Practice Patterns Study (DOPPS), a prospective cohort study. The exposure was RAASi prescription at study entry; RAASi included angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARB), renin inhibitors, and aldosterone antagonists. We used Cox regression to estimate the effect of RAASi on our primary outcome of all-cause mortality. Secondary outcomes included (1) an arrhythmia composite, defined as sudden death or inpatient hospitalization caused by arrhythmia event, and (2) a CV composite, defined as death by CV cause (excluding sudden death) or inpatient hospitalization caused by CV event (excluding arrhythmias). Models were stratified by DOPPS phase and country and adjusted for age, gender, black race, vintage, 13 comorbidities, catheter use, treatment time, BMI, hemoglobin, serum albumin, calcium, and phosphorus. Because medication prescription at HD start largely reflects care patients received prior to HD, we performed all analyses separately for incident (≤ 120 days on HD) and prevalent (>120 days on HD) patients.

RESULTS: Among incident patients, the adjusted all-cause mortality hazard ratio (HR, 95% CI) for patients prescribed (vs. not prescribed) RAASi was 0.87 (0.79-0.96); results for both cause-specific composite outcomes were directionally consistent (Table 1). Among prevalent patients, the adjusted all-cause mortality HR (95% CI) for RAASi was 0.93 (0.89-0.98); in contrast, HR’s greater than 1 were observed for both cause-specific composite outcomes (Table 1). Further adjustment for serum K, a potential mediator of clinical outcomes, did not impact any HR.

CONCLUSIONS: RAASi prescription was associated with lower all-cause mortality rates in both incident and prevalent cohorts of HD patients. Mixed results were observed in analyses of cause-specific hospitalizations and cause of death, possibly reflecting outcome misclassification or selection bias. Future research should explore potential effects of RAASi type (e.g., ACEi vs. ARB) and other anti-hypertensive medication classes (e.g., beta blockers) on adverse events in HD patients.