Biopsy-Proven Acute Tubular Necrosis due to Vancomycin Toxicity

Shah-Khan, Farheen; Scheetz, Marc H.; Ghossein, Cybele

doi:10.4061/2011/436856

Cited by 23 publications

(13 citation statements)

References 31 publications

(31 reference statements)

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“…Increases in KIM-1 urinary expression greater than 1.87-fold compared with that for the controls has over 95% specificity for AKI (8). Ample preclinical (8,9,38) and clinical (39,40) data demonstrate that vancomycin can induce proximal tubular damage. Although the exact mechanism by which vancomycin causes proximal tubule damage remains unclear, data suggest that this damage may be due to oxidative stress and mitochondrial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Vancomycin Exposures Associated with Elevations in Novel Urinary Biomarkers of Acute Kidney Injury in Vancomycin-Treated Rats

Rhodes

Prozialeck

Lodise

et al. 2016

Antimicrob Agents Chemother

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Vancomycin has been associated with acute kidney injury (AKI).A cute kidney injury (AKI) is a major contributor to patient morbidity and mortality in the hospital setting (1, 2). While the etiology of AKI is multifactorial, many cases among hospital patients are related to medication exposure (2). Not surprisingly, the risk of drug-induced AKI is highest among critically ill, hospitalized patients (3), who carry multiple risk factors for the development and progression of AKI. Vancomycin, the antibiotic most frequently administered in the hospital setting (4), has been implicated as a cause of AKI in a number of clinical (5-7) and animal (8-10) studies. Among the clinical studies, the incidence of vancomycin-induced AKI has been associated with higher doses of vancomycin (11, 12), increasing numbers of vancomycin doses (12), and elevated trough concentrations (7, 13).While a number of clinical studies have shown that more intensive vancomycin dosing regimens are associated with an increased risk of AKI, these studies could only suggest an association with kidney injury. As these studies were largely observational in nature, it is difficult to discern if the association was reflective of a true effect or was biased due to confounders. For example, patient confounder factors, such as severity of illness, residence in an intensive care unit, and concurrent receipt of nephrotoxins, may influence the vancomycin exposure-response profile that best predicts clinical AKI.Animal systems are ideally suited to define exposure-response relationships, as they provide flexibility to titrate dosing groups and minimize the influence of external covariates on the observed results. To date, animal models of AKI have confirmed that vancomycin is a nephrotoxin. Dose-ranging studies have revealed that an increase in the vancomycin dose and an increase in the duration of treatment in rats are associated with increases in histopathological damage and elevations in novel urinary biomarkers of AKI (8-10). However, a prospectively derived ex-

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Section: Discussionmentioning

confidence: 99%

Evaluation of Vancomycin Exposures Associated with Elevations in Novel Urinary Biomarkers of Acute Kidney Injury in Vancomycin-Treated Rats

Rhodes

Prozialeck

Lodise

et al. 2016

Antimicrob Agents Chemother

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“…Human data also suggest that vancomycin toxicity involves both the proximal tubules and the medullary region of the kidney [41]. However, cases of AKI in humans where a kidney biopsy was performed have mostly shown acute interstitial nephritis [42][43][44] with acute tubular injury being reported rarely [45,46].…”

Section: Discussionmentioning

confidence: 99%

Vancomycin-Associated Acute Kidney Injury in a Large Veteran Population

et al. 2019

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Background: To determine the association of vancomycin with acute kidney injury (AKI) in relation to its serum concentration value and to examine the risk of AKI in patients treated with vancomycin when compared with a matched cohort of patients receiving non-glycopeptide antibiotics (linezolid/daptomycin). Methods: From a cohort of > 3 million US veterans with baseline estimated glomerular filtration rate ≥60 mL/min/1.73 m², we identified 33,527 patients who received either intravenous vancomycin (n = 22,057) or non-glycopeptide antibiotics (linezolid/daptomycin, n = 11,470). We examined the association of the serum trough vancomycin level recorded within the first 48 h of administration with subsequent AKI in all patients treated with vancomycin and association of vancomycin vs. non-glycopeptide antibiotics use with the risk of incident AKI. Results: The overall multivariable adjusted ORs of AKI stages 1, 2, and 3 in patients on vancomycin vs. non-glycopeptides were 1.1 (1.1–1.2), 1.2 (1–1.4), and 1.4 (1.1–1.7), respectively. When examined in strata divided by vancomycin trough level, the odds of AKI were similar or lower in patients receiving vancomycin compared to non-glycopeptide antibiotics as long as serum vancomycin levels were ≤20 mg/L. However, in patients with serum vancomycin levels > 20 mg/L, the ORs of AKI stages 1, 2, and 3 in patients on vancomycin vs. non-glycopeptide antibiotics were 1.5 (1.4–1.7), 1.9 (1.5–2.3), and 2.7 (2–3.5), respectively. Conclusions: Vancomycin use is associated with a higher risk of AKI when serum levels exceed > 20 mg/L.

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“…It is only the second report documenting VAN as the sole etiologic cause of ATN. 1 Moreover, this case also demonstrates the rapidity in the development of VAN nephrotoxicity (within 72 hours of admission). The primary risk factors associated with VAN-induced nephrotoxicity are directly related to the total amount of VAN being administered, either the total daily dosage or the length of use of more than 7 days.…”

Section: Discussionmentioning

confidence: 93%

“…Despite its extensive use, only one prior case of VAN-induced and biopsyproven acute tubular necrosis (ATN) has been described in the literature. 1 Vancomycin is a parenteral glycopeptide antibiotic obtained from Nocardia orientalis and has proven efficacy against many gram-positive bacteria. 2 Since its initial use in the 1950s, VAN has been associated with acute kidney injury (AKI).…”

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confidence: 99%