title: Acetaminophen, aspirin, and chronic renal failure.
abstract: BACKGROUND
  Several epidemiologic studies have demonstrated an association between heavy consumption of nonnarcotic analgesics and the occurrence of chronic renal failure, but it is unclear which is the cause and which is the effect
  
  
  METHODS
  In a nationwide, population-based, case-control study of early-stage chronic renal failure in Sweden, face-to-face interviews were conducted with 926 patients with newly diagnosed renal failure and 998 control subjects, of whom 918 and 980, respectively, had complete data. We used logistic-regression models to estimate the relative risks of disease-specific types of chronic renal failure associated with the use of various analgesics
  
  
  RESULTS
  Aspirin and acetaminophen were used regularly by 37 percent and 25 percent, respectively, of the patients with renal failure and by 19 percent and 12 percent, respectively, of the controls. Regular use of either drug in the absence of the other was associated with an increase by a factor of 2.5 in the risk of chronic renal failure from any cause. The relative risks rose with increasing cumulative lifetime doses, rose more consistently with acetaminophen use than with aspirin use, and were increased for most disease-specific types of chronic renal failure. When we disregarded the recent use of analgesics, which could have occurred in response to antecedents of renal disease, the associations were only slightly attenuated
  
  
  CONCLUSIONS
  Our results are consistent with the existence of exacerbating effects of acetaminophen and aspirin on chronic renal failure. However, we cannot rule out the possibility of bias due to the triggering of analgesic consumption by predisposing conditions.
authors.affiliation: Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden. michael.fored@mep.ki.se
authors.forename: C M
authors.initials: CM
authors.lastname: Fored
authors.forename: E
authors.initials: E
authors.lastname: Ejerblad
authors.forename: P
authors.initials: P
authors.lastname: Lindblad
authors.forename: J P
authors.initials: JP
authors.lastname: Fryzek
authors.forename: P W
authors.initials: PW
authors.lastname: Dickman
authors.forename: L B
authors.initials: LB
authors.lastname: Signorello
authors.forename: L
authors.initials: L
authors.lastname: Lipworth
authors.forename: C G
authors.initials: CG
authors.lastname: Elinder
authors.forename: W J
authors.initials: WJ
authors.lastname: Blot
authors.forename: J K
authors.initials: JK
authors.lastname: McLaughlin
authors.forename: M M
authors.initials: MM
authors.lastname: Zack
authors.forename: O
authors.initials: O
authors.lastname: Nyrén
mesh_terms: D000082:Acetaminophen / Q000009:adverse effects*; D018712:Analgesics, Non-Narcotic / Q000009:adverse effects*; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D001241:Aspirin / Q000009:adverse effects*; D015982:Bias; D016022:Case-Control Studies; D048909:Diabetes Complications; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D006801:Humans; D007676:Kidney Failure, Chronic / Q000139:chemically induced*; D016015:Logistic Models; D016017:Odds Ratio; D012307:Risk Factors; D011795:Surveys and Questionnaires; D013548:Sweden
chemical_list: D018712:Analgesics, Non-Narcotic; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000082:Acetaminophen; D001241:Aspirin