Biopsy-Proven Acute Tubular Necrosis Associated with Vancomycin in an Adult Patient

Belen, Cary; Budhiraja, Pooja; Bracamonte, Erika; Popovtzer, Mordecai M.

doi:10.3109/0886022x.2012.655683

Cited by 15 publications

(8 citation statements)

References 11 publications

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“…On the other hand, biopsy specimens in cases 8 and 9 revealed acute tubular injury. Further, 2 published cases from this series (cases 13 and 14) as well as others [39, 40] also reported histopathological evidence of acute tubular injury. Therefore, while we cannot conclude that any particular histological pattern of injury specifically associates with this syndrome, these data suggest that acute tubular injury can be present.…”

Section: Discussionmentioning

confidence: 99%

Vancomycin-Associated Acute Kidney Injury with a Steep Rise in Serum Creatinine

Obadan

Kaushal

Alzubaidi

et al. 2018

Nephron

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Background: Vancomycin-associated (VA) acute kidney injury (AKI) is being increasingly recognized. A distinct pattern of rapid rise in serum creatinine (sCr) during VA-AKI has occasionally been observed. However, such scenarios remain underreported. Methods: We conducted an online survey at the American Society of Nephrology Communities forum and reviewed publications of VA-AKI via PubMed or Google searching for cases of precipitous AKI (those with rise in sCr ≥1.5 mg/dL/day) attributable to vancomycin. Results: We identified 12 original cases compiled from 6 different hospitals and 4 published cases (n = 16; 38% women, age 43.5 ± 16 years, weight 108 ± 23 kg, body mass index 35 ± 7 kg/m²) of precipitous AKI observed shortly after large cumulative doses of VA (8.8 ± 5 g). The median steepest 24-h rise in sCr was 2.6 mg/dL (range 1.5–3.5 mg/dL) and the slope of the initial 48-h sCr rise was greater than that of a control AKI (non-VA, n = 48) group (2.03 ± 0.1 vs. 0.62 ± 0.0 mg/dL/day; p < 0.0001). The steep rise in sCr in the VA-AKI was not accompanied by anuria. Overt rhabdomyolysis was absent in all cases. Further, in 3 precipitous VA-AKI cases, simultaneous serum cystatin C values did not rise precipitously, suggesting that the reductions in glomerular filtration rate were overestimated by the sCr increase. Conclusions: VA-AKI can manifest with a precipitous rise in sCr shortly after a high cumulative dose of vancomycin. True toxic tubular injury overrepresented by the sCr rise is postulated.

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Section: Discussionmentioning

confidence: 99%

Vancomycin-Associated Acute Kidney Injury with a Steep Rise in Serum Creatinine

Obadan

Kaushal

Alzubaidi

et al. 2018

Nephron

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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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“…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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Biopsy-Proven Acute Tubular Necrosis Associated with Vancomycin in an Adult Patient

Cited by 15 publications

References 11 publications

Vancomycin-Associated Acute Kidney Injury with a Steep Rise in Serum Creatinine

Vancomycin-Associated Acute Kidney Injury with a Steep Rise in Serum Creatinine

Vancomycin-Associated Acute Kidney Injury in a Large Veteran Population

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

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