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Ibuprofen-associated acute kidney injury in dehydrated children with acute gastroenteritis
Alejandro Balestracci1, Mauricio Ezquer, María Eugenia Elmo
1Nephrology Unit, Hospital General de Niños Pedro de Elizalde, Montes de Oca 40, 1270, Ciudad Autónoma de Buenos Aires, Argentina, abalestracci@yahoo.com.ar.
Insights
Ibuprofen significantly increases the risk of acute kidney injury (AKI) in dehydrated children with acute gastroenteritis (AGE). Over half of ibuprofen recipients developed AKI, highlighting this drug
Area of Science:
- Pediatric Nephrology
- Clinical Pharmacology
- Gastroenterology
Background:
- Non-steroidal anti-inflammatory drugs (NSAIDs) can cause acute kidney injury (AKI) in dehydrated individuals.
- The prevalence of NSAID-associated AKI may be underestimated, particularly in pediatric populations.
Purpose of the Study:
- To assess the impact of ibuprofen exposure on renal function in dehydrated children experiencing acute gastroenteritis (AGE).
- To characterize the prevalence and risk factors of NSAID-associated AKI in this vulnerable group.
Main Methods:
- A prospective study enrolled 105 dehydrated children with AGE over one year.
- Children were categorized into cases (AKI present, n=46) and controls (AKI absent, n=59) based on pediatric RIFLE (pRIFLE) criteria.
- Renal function and ibuprofen exposure were analyzed in relation to AKI development.
Main Results:
- The overall prevalence of AKI was 44% among the studied children.
- Ibuprofen use was significantly higher in children with AKI (74%) compared to controls (49%).
- Ibuprofen exposure was an independent risk factor for AKI (OR 2.47), even after adjusting for dehydration severity.
Conclusions:
- Ibuprofen-associated AKI occurred in 54% of exposed children within this cohort.
- Ibuprofen more than doubled the risk of developing AKI in dehydrated children with AGE.
- All affected children recovered renal function, but the findings underscore the risks of NSAIDs in this context.
Background:
Non-steroidal anti-inflammatory drugs (NSAIDs) induce acute kidney injury (AKI) in volume-depleted patients; however the prevalence of this complication is likely underestimated. We assessed the impact of ibuprofen exposure on renal function among dehydrated children with acute gastroenteritis (AGE) to further characterize NSAID-associated AKI.
Methods:
Over a 1-year period dehydrated children with AGE (n = 105) were prospectively enrolled and grouped as cases, presenting with AKI (n = 46) or controls, not presenting with AKI (n = 59). AKI was defined by pediatric RIFLE (pRIFLE) criteria.
Results:
Among the children enrolled in the study, AKI prevalence was 44 %, and 34 (54 %) of the 63 patients who received ibuprofen developed renal impairment. Relative to the controls, children presenting with AKI were younger (median age 0.66 vs. 1.74 years; p < 0.001) and received ibuprofen more frequently (74 vs. 49 %, p = 0.01). After adjusting for the degree of dehydration, ibuprofen exposure remained an independent risk factor for AKI (p < 0.001, odds ratio 2.47, 95 % confidence interval 1.78-3.42). According to the pRIFLE criteria, 17 patients were at the 'risk' stage of AKI severity, 24 were at the 'injury' stage, and five were at the 'failure' stage; none required dialysis. Distribution of patients within categories was similar regardless of ibuprofen exposure. All cases fulled recovered from AKI.
Conclusions:
Ibuprofen-associated AKI was 54 % in our cohort of dehydrated children with AGE. Drug exposure increased the risk for developing AKI by more than twofold, independent of the magnitude of the dehydration.
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