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.
Highlights
Many different drugs and agents are currently being taken into consideration as the causality of nephrotoxic acute kidney injury (AKI) in children
The combination of nephrotoxic drugs in the setting of hematopoietic stem cell transplantation (HSCT) intensifies nephrotoxic probability. Renal aspects of this specific therapeutic maneuver have been reviewed elsewhere [138], so here we summarize the important aspects of AKI in this very specific group of patients
To assess AKI risk factors in our pediatric population, we carried out logistic regression analyses and found allogeneic HSCT, conditioning containing cyclophosphamide, and etoposide, septicemia, hyperbilirubinemia, venoocclusive disease, and the use of spironolactone significantly correlated with AKI
Summary
Many different drugs and agents are currently being taken into consideration as the causality of nephrotoxic acute kidney injury (AKI) in children. Prerenal AKI in children with nephrotic syndrome, impaired renal function, hypertension, congestive heart failure, or postrenal transplant patients treated with ACE inhibitors alone or in combination with AT2-receptor antagonists are well known in pediatric renal (and cardiac) clinics and have been reported [116, 117, 120,121,122]. AKI case reports of prerenal failure due to water and sodium loss caused by the tubulopathy have been published [150] Cisplatin may induce both acute and chronic renal toxicity [151]. Renal impairment during the early phase of HSCT was not predictive of later renal impairment [48, 190], whereas Kist-van Holthe et al found correlations between high serum creatinine within 3 months after BMT and chronic renal failure 1 year after BMT [49] but only a weak predictive value of acute AKI for chronic renal failure [191]
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