title: The association of chronic kidney disease with the use of renin-angiotensin system inhibitors after acute myocardial infarction.
abstract: BACKGROUND
  Renin-angiotensin system (RAS) inhibitor use after acute myocardial infarction (AMI) is a quality indicator, but there may also be reasons not to use this therapy. We sought to determine how chronic kidney disease (CKD) and acute kidney injury (AKI) affected RAS inhibitor prescription after AMI in patients with and without decreased ejection fraction (EF).
  
  
  METHODS
  Participants from the TRIUMPH registry were categorized by admission estimated glomerular filtration rate (eGFR in mL/min per 1.73 m(2); severe [<30], moderate [30-59], mild [60-89], and no [≥90] CKD) and occurrence of AKI (an increase in creatinine ≥0.3 mg/dL or ≥50%). Renin-angiotensin system inhibitor prescriptions at discharge were compared across categories of CKD, AKI, and decreased EF (<40% vs ≥40%) using a hierarchical modified Poisson model.
  
  
  RESULTS
  Among 4,223 AMI patients (mean age 59.0 years, 67.0% male, 67.3% white), RAS inhibitor use decreased significantly with lower eGFR (P < .001), but there was no effect of decreased EF on this relationship (interaction P = .40). Without AKI, severe and moderate CKD were associated with significantly less RAS inhibitor use: relative risks (RRs) 0.67 (95% CIs, 0.58-0.78) and 0.94 (0.90-0.99), respectively. When AKI occurred, CKD was associated with less RAS inhibitor use: RRs 0.84 (0.76-0.93) for mild CKD, 0.78 (0.68-0.88) for moderate CKD, and 0.50 (0.42-0.61) for severe CKD. Ejection fraction <40% was associated with use (RR 1.11, 1.03-1.18), independent of renal function.
  
  
  CONCLUSIONS
  Chronic kidney disease and AKI are associated with fewer RAS inhibitor prescriptions at discharge, but in both AKI and non-AKI patients, eGFR was more strongly associated with use than EF.
authors.affiliation: Division of Nephrology, Hennepin County Medical Center, Minneapolis, MN; Chronic Disease Research Group, Hennepin County Medical Center, Minneapolis, MN. Electronic address: james.wetmore@hcmed.org.
authors.forename: James B
authors.initials: JB
authors.lastname: Wetmore
authors.affiliation: St Luke's Mid America Heart Institute, Kansas City, MO.
authors.forename: Fengming
authors.initials: F
authors.lastname: Tang
authors.affiliation: Guthrie Robert Packer Hospital, Sayre, PA.
authors.forename: Abhinav
authors.initials: A
authors.lastname: Sharma
authors.affiliation: St Luke's Mid America Heart Institute, Kansas City, MO.
authors.forename: Philip G
authors.initials: PG
authors.lastname: Jones
authors.affiliation: St Luke's Mid America Heart Institute, Kansas City, MO; University of Missouri-Kansas City, Kansas City, MO.
authors.forename: John A
authors.initials: JA
authors.lastname: Spertus
mesh_terms: D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000009:adverse effects* / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy*; D012042:Registries; D051436:Renal Insufficiency, Chronic / Q000139:chemically induced* / Q000453:epidemiology / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000187:drug effects*; D012189:Retrospective Studies
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors