A Multicenter Evaluation of Vancomycin-Associated Acute Kidney Injury in Hospitalized Patients with Acute Bacterial Skin and Skin Structure Infections

Jorgensen, Sarah C J; Murray, Kathryn; Lagnf, Abdalhamid M; Melvin, Sarah; Bhatia, Sahil; Shamim, Muhammad-Daniayl; Smith, Jordan R.; Brade, Karrine D.; Simon, Samuel; Nagel, Jerod; Williams, Karen; Ortwine, Jessica; Veve, Michael P; Truong, James; Huang, David B.; Davis, Susan L.; Rybak, Michael J.

doi:10.1007/s40121-019-00278-1

Cited by 27 publications

(18 citation statements)

References 69 publications

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“…Vancomycin is a glycopeptide antibiotic used for treatment of methicillin-resistant Staphylococcus aureus infections in critically ill patients. Nephrotoxicity is a serious adverse event impacting 10–20% of treated patients and is associated with increased hospital length of stay, 30-day hospital readmission rates and all-cause 30-day mortality [ 1 ]. Vancomycin associated acute kidney injury (V-AKI) is dose-related and with an onset of 4–17 days therapy initiation.…”

Section: Introductionmentioning

confidence: 99%

Urinary Exosomes Identify Inflammatory Pathways in Vancomycin Associated Acute Kidney Injury

Awdishu

Amato

et al. 2021

IJMS

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Background: Vancomycin is commonly used as a first line therapy for gram positive organisms such as methicillin resistant Staphylococcusaureus. Vancomycin-induced acute kidney injury (V-AKI) has been reported in up to 43% of patients, especially in those with higher targeted trough concentrations. The precise mechanism of injury in humans remains elusive, with recent evidence directed towards proximal tubule cell apoptosis. In this study, we investigated the protein contents of urinary exosomes in patients with V-AKI to further elucidate biomarkers of mechanisms of injury and potential responses. Methods: Urine samples from patients with V-AKI who were enrolled in the DIRECT study and matched healthy controls from the UAB-UCSD O’Brien Center Biorepository were included in the analysis. Exosomes were extracted using solvent exclusion principle and polyethylene glycol induced precipitation. Protein identity and quantification was determined by label-free liquid chromatography mass spectrometry (LC/MS). The mean peak serum creatinine was 3.7 ± 1.4 mg/dL and time to kidney injury was 4.0 ± 3.0 days. At discharge, 90% of patients demonstrated partial recovery; 33% experienced full recovery by day 28. Proteomic analyses on five V-AKI and 7 control samples revealed 2009 proteins in all samples and 251 proteins significantly associated with V-AKI (Pi-score > 1). The top discriminatory proteins were complement C3, complement C4, galectin-3-binding protein, fibrinogen, alpha-2 macroglobulin, immunoglobulin heavy constant mu and serotransferrin. Conclusion: Urinary exosomes reveal up-regulation of inflammatory proteins after nephrotoxic injury in V-AKI. Further studies are necessary in a large patient sample to confirm these findings for elucidation of pathophysiologic mechanisms and validation of potential injury biomarkers.

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Section: Introductionmentioning

confidence: 99%

Urinary Exosomes Identify Inflammatory Pathways in Vancomycin Associated Acute Kidney Injury

Awdishu

Amato

et al. 2021

IJMS

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“…Nephrotoxicity has been reported to contribute to approximately 8%–40% of all cases of acute renal injury. Since its introduction, vancomycin, a glycopeptide antibiotic often used as the last line of defense against drug resistant gram-positive bacteria, has been associated with acute renal injury [ 1 , 2 ]. Vancomycin is commonly used to treat hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) infections [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

“…infections [1]. Due to treatment failures, clinicians have been reported to be using higher doses of vancomycin [3].…”

mentioning

confidence: 99%

Protective effects of lutein against vancomycin-induced acute renal injury in mice via upregulation of peroxisome proliferator-activated receptor gamma/nuclear factor erythroid 2-related factor 2 and inhibition nuclear factor-kappaB/caspase 3

Emeka

Rasool

Morsy

et al. 2021

Korean J Physiol Pharmacol

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Kidneys are the main excretory organ for many drugs, and could easily be exposed to toxins. Nephrotoxicity has been reported to contribute to approximately 8%-40% of all cases of acute renal injury. Since its introduction, vancomycin, a glycopeptide antibiotic often used as the last line of defense against drug resistant gram-positive bacteria, has been associated with acute renal injury [1,2]. Vancomycin is commonly used to treat hospitalacquired methicillin-resistant Staphylococcus aureus (MRSA)

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“…Vancomycin is often used as a irst line empiric therapy for many moderate-to-severe gram-positive infections and has been associated with AKI [4]. Given the widespread use of vancomycin, there are reports of VA-AKI ranging between 5% to 40% [2][3][4][5][6].…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports showed that vancomycin could be both nephrotoxic and ototoxic [1]. Despite improvements in the puri ication process, literature suggests that vancomycin is still associated with 5% -40% increased incidence of acute kidney injury (AKI) [2][3][4][5][6]. A recent systematic review and meta-analysis suggested that use of vancomycin has a relative risk of 2.45 for development of AKI [7].…”

Section: Introductionmentioning

confidence: 99%

Incidence and risk factors of vancomycin-associated acute kidney injury in a single center: Retrospective study

Yalamarti¹,

Zonoozi²,

Ntoso³

et al. 2021

J Clini Nephrol

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Background: There is enough evidence to suggest that vancomycin increases the risk of acute kidney injury (AKI) but the exact mechanism is not well understood. This study aims to understand the incidence of vancomycin-associated acute kidney injury (VA-AKI) among hospitalized patients and to identify the risk factors for VA-AKI. Methods: Patients aged 18 and above who received a minimum of 24 hours of intravenous vancomycin and who had serial creatinine measurements over a 13-month period were identified through electronic records. Patients with pre-existing AKI, or eGFR of less than 30ml/min, and patients with end stage kidney disease were excluded. Results were analyzed using t-test and Fisher’s test. A logistic regression model was used to identify the predictors for VA-AKI. Results: From the 598 patients who met the inclusion criteria, 70 developed AKI. Compared to those without AKI, patients with VA-AKI had higher mean serum vancomycin trough levels (22.6 mg/L vs. 14.6 mg/L), and a statistically significant longer duration of vancomycin use (6.7 vs. 5.2 days). Multivariate analysis revealed that serum vancomycin level of > 20 mg/L was associated with a six-fold increase in odds of VA-AKI when compared to those with vancomycin levels < 15 mg/L. The presence of hypotension, iodinated contrast use, and concomitant use of piperacillin-tazobactam were all associated with increased odds of VA-AKI. Conclusion: The incidence of VA-AKI in hospitalized patients with eGFR > 30 ml/min was 11.7%. Serum vancomycin levels of > 20 mg/L, hypotension and administration of iodinated contrast significantly increased the risk of VA-AKI. Piperacillin-tazobactam, when used with vancomycin, was noted to be an independent predictor of AKI, regardless of serum vancomycin trough levels, prompting a reevaluation of the safety of this widespread practice as empiric therapy. Close monitoring of kidney function, avoiding high serum vancomycin levels, maintaining hemodynamic stability, and avoiding unnecessary use of iodinated contrast seem to be essential for the prevention of VA-AKI.

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A Multicenter Evaluation of Vancomycin-Associated Acute Kidney Injury in Hospitalized Patients with Acute Bacterial Skin and Skin Structure Infections

Cited by 27 publications

References 69 publications

Urinary Exosomes Identify Inflammatory Pathways in Vancomycin Associated Acute Kidney Injury

Urinary Exosomes Identify Inflammatory Pathways in Vancomycin Associated Acute Kidney Injury

Protective effects of lutein against vancomycin-induced acute renal injury in mice via upregulation of peroxisome proliferator-activated receptor gamma/nuclear factor erythroid 2-related factor 2 and inhibition nuclear factor-kappaB/caspase 3

Incidence and risk factors of vancomycin-associated acute kidney injury in a single center: Retrospective study

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