Vancomycin is a glycopeptide antibiotic that has been in clinical use for nearly 50 years as a penicillin alternative to treat penicillinase-producing strains of Staphylococcus aureus . It is one of the most widely used antibiotics in the United States for the treatment of serious gram-positive

/pdf/therapeutic-monitoring-of-vancomycin-in-adult-patients-a-40fewofi1r.pdf

Therapeutic monitoring of vancomycin in adult patients: a consensus review of the American Society of Health-System Pharmacists, the Infectious Diseases Society of America, and the Society of Infectious Diseases Pharmacists.

Purpose
Treatment failures following vancomycin therapy in patients with methicillin-resistant Staphylococcus aureus infections have led to the utilization of higher doses of this antibiotic to achieve the trough concentrations of 10–20 μg/mL recommended by the Infectious Diseases Society of America clinical practice guideline. However, many questions remain on the safety of such high doses of vancomycin, specifically their nephrotoxic effects. In this review, we have collected available evidence on the nephrotoxicity of vancomycin, particularly in terms of its mechanism, incidence, predisposing factors and special target populations.

Vancomycin-induced nephrotoxicity: mechanism, incidence, risk factors and special populations. A literature review

Although monitoring serum vancomycin concentrations in clinical practice is commonplace, the data supporting this practice are meager. The rationale for monitoring these concentrations is to improve the effectiveness and/or reduce the toxicity of the drug. However, there are no data to suggest that monitoring serum vancomycin concentrations improves the effectiveness of therapy. In addition, despite many case reports of vancomycin-associated nephrotoxicity and ototoxicity, it is unclear whether this agent truly causes such conditions. Moreover, there is no evidence that adherence to specific ranges of vancomycin concentrations will preclude these events. Finally, vancomycin pharmacokinetics are sufficiently predictable that adequate serum drug concentrations can be obtained with dosing methods that take into account the patient's age, weight, and renal function. Safe and effective vancomycin dosage regimens can be constructed with these empirical dosing methods, whereas monitoring vancomycin levels increases the cost of therapy without improving the safety or efficacy of treatment.

https://www.jstor.org/stable/pdfplus/4457746.pdf

Serum Vancomycin Concentrations: Reappraisal of Their Clinical Value

In vivo evidences suggesting the role of oxidative stress in pathogenesis of vancomycin-induced nephrotoxicity : Protection by erdosteine

Background and objectives Vancomycin has been in use for more than half a century, but whether it is truly nephrotoxic and to what extent are still highly controversial. The objective of this study was to determine the risk of AKI attributable to intravenous vancomycin. Design, setting, participants, & measurements We conducted a systematic review of randomized, controlled trials and cohort studies that compared patients treated with intravenous vancomycin with a control group of patients given a comparator nonglycopeptide antibiotic and in which kidney function or kidney injury outcomes were reported. PubMed and Cochrane Library were searched from 1990 to September of 2015. Two reviewers extracted data and assessed study risk of bias, and one reviewer adjudicated the assessments. A meta-analysis was conducted on seven randomized, controlled trials (total of 4033 patients). Results Moderate quality evidence suggested that vancomycin treatment is associated with a higher risk of AKI, with a relative risk of 2.45 (95% confidence interval, 1.69 to 3.55). The risk of kidney injury was similar in patients treated for skin and soft tissue infections compared with those treated for nosocomial pneumonia and other complicated infections. There was an uncertain risk of reporting bias, because kidney function was not a prespecified outcome in any of the trials. The preponderance of evidence was judged to be indirect, because the majority of studies compared vancomycin specifically with linezolid. Conclusions Our findings suggest that there is a measurable risk of AKI associated with vancomycin, but the strength of the evidence is moderate. A randomized, controlled trial designed to study kidney function as an outcome would be needed to draw unequivocal conclusions.

/pdf/vancomycin-and-the-risk-of-aki-a-systematic-review-and-meta-1f43j91afh.pdf

Vancomycin and the Risk of AKI: A Systematic Review and Meta-Analysis

The nephrotoxicity, as measured by urinary cell and enzyme excretion, of vancomycin was studied in rats. The lowest daily iv dose inducing significantly increased cell elimination was 25 mg/kg. Im administration caused less effects probably due to incomplete absorption from the im injection site, since im dosages of 100 mg/kg daily led to lower renal tissue concentrations than the same doses given iv. Nephrotoxicity of vancomycin increased when combined with tobramycin and was reduced when combined with D-glucaro-1.5-lactam, a beta-glucuronidase inhibitor. Vancomycin accumulated in renal tissue during repeated administration.

Renal tolerance and pharmacokinetics of vancomycin in rats

The nephrotoxicity and pharmacokinetics of LY 146032 (daptomycin) were studied in an experimental rat model. Nephrotoxicity was assessed by measuring urinary loss of tubular cells and malate dehydrogenase. LY 146032 (10-250 mg/kg daily iv) led to a dose-dependent and reversible increase of cell elimination. The tubulo-toxic threshold dose is stated to be 10 mg/kg daily. Nephrotoxicity induced by LY 146032 can be reduced by coadministration of fosfomycin or D-glucaro-1.5-lactam, and enhanced by combination with tobramycin. LY 146032 accumulated in renal tissue during repeated administration. Electron microscopy revealed histopathological changes in the kidneys. Therefore the nephrotoxic potential of LY 146032 should be taken into consideration in clinical trials.

Experimental studies on nephrotoxicity and pharmacokinetics of LY 146032 (daptomycin) in rats

The renal effects of amphotericin B alone and in combination with cyclosporin A, tobramycin, fosfomycin, D-glucaro-1,5-lactam and verapamil were studied in rats. The parameters for nephrotoxicity were urinary loss of tubular cells and malate dehydrogenase, as well as creatinine clearance. Repeated intraperitoneal injections of amphotericin B led to an increase of urinary tubular cell elimination and malate-dehydrogenase. After co-administration of amphotericin B and cyclosporin A, the urinary loss of tubular cells increased and creatinine clearance was reduced. A combination of amphotericin B and tobramycin reduced tubular cell elimination but the creatinine clearance improved. When verapamil was combined with amphotericin B, endogenous creatinine clearance increased, though the loss of tubular cells was elevated. Furthermore, fosfomycin reduced the loss of tubular cells and improved renal functional parameters in combination with amphotericin B. In addition, D-glucaro-1,5-lactam was found to reduce the urinary loss of tubular cells induced by amphotericin B.

Experimental studies on the nephrotoxicity of amphotericin B in rats.

The nephroprotective effect of fosfomycin against tubulotoxicity induced bycis-diaminedichloroplatin (DDP) and cyclosporin A (Cs) was studied in the rat. The parameter of nephrotoxicity was urinary tubular cell excretion. The experiments revealed that fosfomycin, given either concomitantly or in advance was able to reduce the nephrotoxic effect of DDP and Cs significantly. We conclude from these studies that fosfomycin is a broad-spectrum nephroprotective agent.

Fosfomycin protects against tubulotoxicity induced byCis-diaminedichloroplatin and cyclosporin A in the rat

The nephrotoxicity and pharmacokinetics of teicoplanin were studied in an experimental rat model. Nephrotoxicity was assessed by measuring urinary excretion of tubular cells and malate dehydrogenase. The experiments revealed that 1 mg/kg or more of teicoplanin daily resulted in an increase of excretion rates of tubular cells. Similarly to vancomycin, teicoplanin is accumulated in the kidneys. Nephrotoxicity induced by teicoplanin can be reduced by coadministration of fosfomycin and D-glucaro-1.5-lactam, and enhanced by administration of tobramycin. We conclude that renal function should be monitored closely during teicoplanin therapy.

Teicoplanin: renal tolerance and pharmacokinetics in rats

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