Drug-associated acute kidney injury: who’s at risk?

Abstract

The contribution of nephrotoxic medications to the development of acute kidney injury (AKI) is becoming better understood with the rise in incidence of AKI in children. Treatment of AKI is not yet available, so prevention continues to be the most effective approach. There is an opportunity to mitigate severity and prevent the occurrence of AKI if children at increased risk are identified early and nephrotoxins are used judiciously. Early detection of AKI is limited by the dependence on serum creatinine as an indicator. Promising new biomarkers may offer early detection of AKI prior to the rise in serum creatinine. Early detection of AKI is evolving and offers opportunities for better management of nephrotoxins. However, identification of patients at increased risk will remain an important first step both to focus the use of biomarker testing and to aid in its interpretation.

Antioxidant Potential of Ademetionine in Gentamicine Nephropathy Progression

“…Значну нішу в загальній структурі гострого пошкодження нирок (ГПН) займають нефропатії, викликані різноманітними нефротоксинами, в тому числі лікарські токсичні нефропатії [4], де провідне місце посідають аміноглікозиди -антибактеріальні засоби з широким спектром протимікробної дії та бактерицидним ефектом, однак, які одночасно, є потенційними нефротоксинами та зумовлюють пошкодження і загибель клітин канальцевого епітелію з розвитком нефропатії. Частота аміноглікозидної нефротоксичності становить 5-10% у дорослих [5] та 20-33% -у дітей після застосування антибіотика [6].…”

A child with acute kidney injury

“…Several studies indicate that among hospitalized children, nephrotoxic drug exposure is one of the most common contributors to AKI. 3 Drug-induced tubular disorders have been described with several medications that are handled through tubular transport mechanisms. 4 Several patterns have been described, ranging from isolated abnormalities (e.g.…”

“…Aminoglycosides cause damage primarily to tubular epithelial cells 3 (particularly proximal tubular cells 5 ), but can also have an adverse effect on renal function via activation of the renin-angiotensin-aldosterone system and changes of glomerular endothelial cells. 3 Other mechanisms involved are the direct and indirect effects on the mitochondria that lead to the disruption of electron transport and ATP production and the production of reactive oxygen species. 1 Patients may present with oliguric AKI, along with proximal tubule dysfunction, resulting in loss of enzymes, proteins, glucose, calcium, potassium and magnesium.…”

“…5 However, there is evidence that vancomycin has detrimental oxidative effects on proximal tubule cells. 3 The exact mechanism of nephrotoxicity remains unclear, but may be related to oxidative effects on the proximal tubule. 6 Moreover, simultaneous use of vancomycin and piperacillin/tazobactam has been linked to the development of AKI in non-critically ill children.…”

“…In hospitalized children, predisposing factors such as age 3,6 , low weight-for-age 3 , severity of illness, pharmacogenetics, dosage, duration, and concomitant nephrotoxic medication determine and influence the severity of nephrotoxic insult. 6 In this case, several risk factors can be identified for AKI, such as low weight, young age (<5 years), sepsis, dehydration, low serum albumin, association of several nephrotoxic drugs (aminoglycosides, vancomycin, piperacillin/tazobactam and amphotericin B) and a prolonged treatment with gentamicin.…”