Literature DB >> 25395343

Drug-induced acute kidney injury in children.

Lauren N Faught1,2, Michael J E Greff3, Michael J Rieder1,4,5,6, Gideon Koren1,2,4,6,7,8.   

Abstract

Acute kidney injury (AKI) is a serious problem occurring in anywhere between 8 and 30% of children in the intensive care unit. Up to 25% of these cases are believed to be the result of pharmacotherapy. In this review we have focused on several relevant drugs and/or drug classes, which are known to cause AKI in children, including cancer chemotherapeutics, non-steroidal anti-inflammatory drugs and antimicrobials. AKI demonstrates a steady association with increased long term risk of poor outcomes including chronic kidney disease and death as determined by the extent of injury. For this reason it is important to understand the causality and implications of these drugs and drug classes. Children occupy a unique patient population, advocating the importance of understanding how they are affected dissimilarly compared with adults. While the kidney itself is likely more susceptible to injury than other organs, the inherent toxicity of these drugs also plays a major role in the resulting AKI. Mechanisms involved in the toxicity of these drugs include oxidative damage, hypersensitivity reactions, altered haemodynamics and tubule obstruction and may affect the glomerulus and/or the tubules. Understanding these mechanisms is critical in determining the most effective strategies for treatment and/or prevention, whether these strategies are less toxic versions of the same drugs or add-on agents to mitigate the toxic effect of the existing therapy.
© 2014 The British Pharmacological Society.

Entities:  

Keywords:  ADR; NSAID; antimicrobials; chemotherapeutics; drug-induced AKI

Mesh:

Substances:

Year:  2015        PMID: 25395343      PMCID: PMC4594733          DOI: 10.1111/bcp.12554

Source DB:  PubMed          Journal:  Br J Clin Pharmacol        ISSN: 0306-5251            Impact factor:   4.335


  105 in total

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Review 3.  Young age and the risk for ifosfamide-induced nephrotoxicity: a critical review of two opposing studies.

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4.  Evidence of renal metabolism of ifosfamide to nephrotoxic metabolites.

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Review 7.  The Predictive Role of the Biomarker Kidney Molecule-1 (KIM-1) in Acute Kidney Injury (AKI) Cisplatin-Induced Nephrotoxicity.

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