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Risk of acute kidney injury by initiation of non-steroidal anti-inflammatory drugs in hospitalised patients treated with diuretics and renin–angiotensin–aldosterone system inhibitors
  1. Mathilde Bories1,2,
  2. Astrid Bacle1,2,3,
  3. Helene Gilardi2,
  4. Pascal Le Corre1,2,3
  1. 1Laboratoire de Biopharmacie et Pharmacie Clinique, Faculté de Pharmacie, Université de Rennes 1, Rennes, France
  2. 2Pôle Pharmacie, Service Hospitalo-Universitaire de Pharmacie, CHU de Rennes, Rennes, France
  3. 3Univ Rennes, CHU Rennes, Inserm, EHESP, Irset - UMR_S 1085, Université de Rennes 1, Rennes, France
  1. Correspondence to Professor Pascal Le Corre, Laboratoire de Biopharmacie et Pharmacie Clinique, Faculté de Pharmacie, Université de Rennes 1, 35043 Rennes, France; pascal.le-corre{at}univ-rennes1.fr

Abstract

Objectives Concurrent use of non-steroidal anti-inflammatory drugs (NSAIDs) with diuretics and renin–angiotensin–aldosterone system inhibitors (RAASI) has been associated with an increased risk of developing acute kidney injury (AKI) in the ambulatory setting. There is currently no information on AKI prevalence in hospitalised patients where initiation of NSAID prescription is quite frequent. The aim of our study was to assess the prevalence of AKI in patients treated with diuretics and/or RAASI in the hospital setting when NSAIDs are initiated.

Methods This was a retrospective single centre study on inpatients receiving triple or dual association treatment. AKI was established according to evidence-based clinical practice guidelines in kidney disease (Kidney Disease Improving Global Outcome, KDIGO) using the following criteria : increase in serum creatinine (SCr) by ≥0.3 mg/dL (or ≥26.5 µmol/L) within 48 hours, or increase in SCr to ≥1.5 times baseline occurring within the last 7 days.

Results AKI was identified in 5 of 151 patients (3.3%) treated with both diuretics and RAASI in whom NSAIDs were initiated, with a 49 µM average increase in SCr within 48 hours compared with baseline. AKI was identified in 2 of 117 (1.7%) patients treated with diuretics and NSAIDs, and in 1 of 427 (0.23%) patients treated with RAASI and NSAIDs. The average increase in SCr within 2 days was 29 µM. No AKI was identified in a control group of 1886 patients treated with diuretics and RAASI but with no initiation of NSAIDs during their hospitalisation.

Conclusion Initiation of NSAID therapy in hospitalised patients already being treated with diuretics and RAASI is a risk factor for AKI. The risk of AKI with the triple association appeared higher than with the dual association treatment.

  • acute kidney injury
  • drug-related side effects and adverse reactions
  • pharmacy service
  • hospital
  • drug misuse
  • nephrology

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