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Published on: July 17, 2016
Nephrotoxicity as a cause of acute kidney injury in children
1Children's Hospital St. Elisabeth and St. Barbara, Mauerstrasse 5, 06110, Halle/S., Germany. patzer@krankenhaus-halle-saale.de
Insights
Nephrotoxic drugs are a significant cause of acute kidney injury (AKI) in children, with factors like age and other medications influencing severity. Early identification and avoidance of nephrotoxic agents are crucial for prevention.
Area of Science:
- Pediatric Nephrology
- Clinical Pharmacology
- Toxicology
Background:
- Acute kidney injury (AKI) in children lacks defined incidence and etiology.
- Pediatric intensive care unit (PICU) studies report AKI incidence between 8-30%, with neonates at higher risk.
- Nephrotoxic drugs contribute to approximately 16% of pediatric AKI cases.
Purpose of the Study:
- To review the causes, risk factors, and mechanisms of drug-induced nephrotoxicity in children.
- To highlight the importance of identifying and managing nephrotoxic agents in pediatric AKI.
Main Methods:
- Review of pediatric retrospective and prospective studies on AKI incidence.
- Analysis of common nephrotoxic agents and their association with pediatric AKI.
- Discussion of pathophysiological mechanisms of drug-induced kidney damage.
Main Results:
- Nephrotoxic drugs are a common cause of AKI in children, particularly older children and adolescents.
- Key nephrotoxic agents include NSAIDs, antibiotics, amphotericin B, ACE inhibitors, and radiocontrast media.
- Mechanisms include intrarenal vasoconstriction, acute tubular necrosis, and interstitial nephritis.
Conclusions:
- Drug-induced nephrotoxicity is a significant risk factor for AKI in children.
- Predisposing factors like age, genetics, and concurrent medications influence AKI severity.
- Management involves avoiding dehydration and co-administered nephrotoxic drugs, especially in children with pre-existing kidney issues.
Abstract:
Many different drugs and agents may cause nephrotoxic acute kidney injury (AKI) in children. Predisposing factors such as age, pharmacogenetics, underlying disease, the dosage of the toxin, and concomitant medication determine and influence the severity of nephrotoxic insult. In childhood AKI, incidence, prevalence, and etiology are not well defined. Pediatric retrospective studies have reported incidences of AKI in pediatric intensive care units (PICU) of between 8% and 30%. It is widely recognized that neonates have higher rates of AKI, especially following cardiac surgery, severe asphyxia, or premature birth. The only two prospective studies in children found incidence rates of 4.5% and 2.5% of AKI in children admitted to PICU, respectively. Nephrotoxic drugs account for about 16% of all AKIs most commonly associated with AKI in older children and adolescents. Nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics, amphotericin B, antiviral agents, angiotensin-converting enzyme (ACE) inhibitors, calcineurin inhibitors, radiocontrast media, and cytostatics are the most important drugs to indicate AKI as significant risk factor in children. Direct pathophysiological mechanisms of nephrotoxicity include constriction of intrarenal vessels, acute tubular necrosis, acute interstitial nephritis, and-more infrequently-tubular obstruction. Furthermore, AKI may also be caused indirectly by rhabdomyolysis. Frequent therapeutic measures consist of avoiding dehydration and concomitant nephrotoxic medication, especially in children with preexisting impaired renal function.
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