Successful Utilization of High-Flux Hemodialysis for Treatment of Vancomycin Toxicity in a Child

Stidham, Timothy; Reiter, Pamela D.; Ford, Douglas M.; Lum, Gary; Albietz, Joseph

doi:10.1155/2011/678724

Cited by 10 publications

(12 citation statements)

References 13 publications

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“…Vancomycin causes dose‐dependent ATN, 70–75 which is attributed to oxidative stress in proximal tubule cells, autophagy, and obstructive cast formation 76, 77 (Figure 3).…”

Section: Mechanisms Of Vikimentioning

confidence: 99%

Vancomycin‐Induced Kidney Injury: Animal Models of Toxicodynamics, Mechanisms of Injury, Human Translation, and Potential Strategies for Prevention

et al. 2020

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Vancomycin is a recommended therapy in multiple national guidelines. Despite the common use, there is a poor understanding of the mechanistic drivers and potential modifiers of vancomycin-mediated kidney injury. In this review, historic and contemporary rates of vancomycin-induced kidney injury (VIKI) are described, and toxicodynamic models and mechanisms of toxicity from preclinical studies are reviewed. Aside from known clinical covariates that worsen VIKI, preclinical models have demonstrated that various factors impact VIKI, including dose, route of administration, and thresholds for pharmacokinetic parameters. The degree of acute kidney injury (AKI) is greatest with the intravenous route and higher doses that produce larger maximal concentrations and areas under the concentration curve. Troughs (i.e., minimum concentrations) have less of an impact. Mechanistically, preclinical studies have identified that VIKI is a result of drug accumulation in proximal tubule cells, which triggers cellular oxidative stress and apoptosis. Yet, there are several gaps in the knowledge that may represent viable targets to make vancomycin therapy less toxic. Potential strategies include prolonging infusions and lowering maximal concentrations, administration of antioxidants, administering agents that decrease cellular accumulation, and reformulating vancomycin to alter the renal clearance mechanism. Based on preclinical models and mechanisms of toxicity, we propose potential strategies to lessen VIKI.

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“…Vancomycin causes dose‐dependent ATN, 70–75 which is attributed to oxidative stress in proximal tubule cells, autophagy, and obstructive cast formation 76, 77 (Figure 3).…”

Section: Mechanisms Of Vikimentioning

confidence: 99%

Vancomycin‐Induced Kidney Injury: Animal Models of Toxicodynamics, Mechanisms of Injury, Human Translation, and Potential Strategies for Prevention

et al. 2020

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“…Perhaps demonstrating the strength of the dose-toxicity relationship, there are several case reports of inadvertent use of a supranormal dose of vancomycin that led to severe AKI [Stidham et al 2011;Barraclough et al 2007;Wicklow et al 2006]. In such events, the water solubility and the low protein binding of vancomycin facilitate its rapid removal by acute hemodialysis (HD) procedures.…”

Section: Vancomycin Exposure: Higher Dosesmentioning

confidence: 99%

“…2008]. Perhaps demonstrating the strength of the dose–toxicity relationship, there are several case reports of inadvertent use of a supranormal dose of vancomycin that led to severe AKI [Stidham et al . 2011; Barraclough et al .…”

Section: Predisposing Factors For Vancomycin-induced Akimentioning

confidence: 99%

Review of vancomycin-induced renal toxicity: an update

Bamgbola

2016

Therapeutic Advances in Endocrinology

176

145

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Abstract:In recent times the use of larger doses of vancomycin aimed at curbing the increasing incidence of resistant strains of Staphylococcus aureus has led to a wider report of acute kidney injury (AKI). Apart from biological plausibility, causality is implied by the predictive association of AKI with larger doses, longer duration, and graded plasma concentrations of vancomycin. AKI is more likely to occur with the concurrent use of nephrotoxic agents, and in critically ill patients who are susceptible to poor renal perfusion. Although most vancomycin-induced AKI cases are mild and therefore reversible, their occurrence may be associated with greater incidence of end-stage kidney disease and higher mortality rate. The strategy for its prevention includes adequate renal perfusion and therapeutic drug monitoring in high-risk individuals. In the near future, there is feasibility of renoprotective use of antioxidative substances in the delivery of vancomycin.

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“…Aggressive drug elimination is indicated in patients with severely elevated plasma vancomycin concentrations compounded by impaired clearance due to oliguria, as this further increases the risk of permanent renal damage. Standard membrane dialysis is ineff ective in clearing large mass molecules such as vancomycin, but high-fl ux hemodialysis allows for improved elimination of large molecules, with a reported vancomycin removal rate of up to 79% ( 10 ).…”

Section: Discussionmentioning

confidence: 99%

Acute Renal Failure Due to Vancomycin Toxicity in the Setting of Unmonitored Vancomycin Infusion

Vora¹

2016

Baylor University Medical Center Proceedings

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Successful Utilization of High-Flux Hemodialysis for Treatment of Vancomycin Toxicity in a Child

Cited by 10 publications

References 13 publications

Vancomycin‐Induced Kidney Injury: Animal Models of Toxicodynamics, Mechanisms of Injury, Human Translation, and Potential Strategies for Prevention

Vancomycin‐Induced Kidney Injury: Animal Models of Toxicodynamics, Mechanisms of Injury, Human Translation, and Potential Strategies for Prevention

Review of vancomycin-induced renal toxicity: an update

Acute Renal Failure Due to Vancomycin Toxicity in the Setting of Unmonitored Vancomycin Infusion

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