RECTAL NSAIDS FOR POST-ERCP PANCREATITIS PROPHYLAXIS AND RISK OF ACUTE KIDNEY INJURY

Introduction:
Rectal non-steroidal anti-inflammatory drugs (NSAIDs) reduce post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP). There is limited data regarding the risk of acute kidney injury (AKI) with one-time rectally administered NSAIDs (NSAID-PR). This study aims to evaluate the risk of AKI following NSAIDs-PR for PEP.
Methods:
We conducted a retrospective case-control study at a tertiary care center to evaluate the risk of AKI in patients >18 years old undergoing ERCP from 2018 - 2023. Cases were individuals with a native papilla who received a one-time dose NSAID-PR while controls were randomly chosen individuals who did not receive an NSAID. Patients on hemodialysis (HD) at the time of ERCP were excluded. NSAID-PR were either diclofenac or indomethacin. Relevant information was obtained from EMR. AKI was defined as an increase in serum creatinine measured within 7 days of ERCP of at least 1.5x the baseline measure. Baseline creatinine was the average creatinine over 90 days prior to ERCP. Continuous variables were summarized using mean and standard deviation (SD), and categorical variables were summarized using frequency and percentage. Variable comparisons between groups were performed using Wilcoxon rank sum test for continuous variables and Fisher’s exact test or χ2 tests for categorical variables. Univariate and multivariable logistic regression was used to assess factors associated with incidence of AKI. All tests were 2-sided, and a P value <0.05 was considered statistically significant.
Results:
Of 540 patients originally selected using a 2:1 random sample, 113 were excluded due to presenting with or having a resolving AKI, actively receiving HD, or having missing data. There were 144 controls and 283 cases analyzed. In univariate analysis (Table 1), diuretics and eGFR baseline were found to be significantly associated with AKI. Patients on diuretics have a higher risk of AKI than those not on diuretics (OR=2.54, 95% CI, 0.99, 6.10, p=0.041). Patients with eGFR<60 are at higher risk of AKI vs. those with GFR >60 (OR=3.11, 95% CI, 1.25, 7.39, p=0.011). There was no significant difference in the frequency of NSAIDs given to those with eGFR <60 vs. >60 (p=0.22).
After controlling for baseline eGFR in a multivariable logistic regression model (Table 2), receiving NSAID-PR is not significant for incidence of AKI (OR = 1.09, 95% CI 0.43, 2.63, p > 0.9). Finally, we looked at risk of PEP among those that received NSAIDs and found no significant difference by type of NSAID (p=0.3).
Conclusion:
Our study shows that a one-time dose of rectally-administered NSAID for PEP prophylaxis does not increase AKI risk. Endoscopists should take into consideration baseline eGFR as we found this to be associated with development AKI. Additional studies are needed to further evaluate these findings.