The Role of Urinary Biomarkers as Diagnostic and Prognostic Predictors of Acute Kidney Injury Associated With Vancomycin

Garms, Durval Sampaio de Souza; Eid, Karina Zanchetta Cardoso; Burdmann, Emmanuel A.; Marçal, Lia Junqueira; Antonângelo, Leila; Santos, Adriano dos; Ponce, Daniela

doi:10.3389/fphar.2021.705636

Cited by 11 publications

(5 citation statements)

References 32 publications

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“…[38] However, despite its potential role as a predictor of vancomycin-induced AKI, studies comparing urinary biomarkers, including KIM-1, as early detection markers for drug-induced AKI have yielded inconsistent results. [37,39,40] Therefore, further studies with a larger population are warranted to elucidate the role of KIM-1.…”

Section: Discussionmentioning

confidence: 99%

Serum and urinary biomarkers of vancomycin-induced acute kidney injury: A prospective, observational analysis

Park,

Yu,

et al. 2024

Medicine

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Vancomycin, a first-line drug for treating methicillin-resistant Staphylococcus aureus infections, is associated with acute kidney injury (AKI). This study involved an evaluation of biomarkers for AKI detection and their comparison with traditional serum creatinine (SCr). We prospectively enrolled patients scheduled to receive intravenous vancomycin for methicillin-resistant S aureus infection. Blood samples for pharmacokinetic assessment and SCr and cystatin C (CysC) measurements were collected at baseline and on days 3, 7, and 10 from the initiation of vancomycin administration (day 1). Urinary biomarkers, including kidney injury molecule 1 (KIM-1), neutrophil gelatinase-associated lipocalin, and clusterin, were collected from days 1 to 7 and adjusted for urinary creatinine levels. The estimated glomerular filtration rate (eGFR) was calculated using the Chronic Kidney Disease Epidemiology Collaboration equation. Of the 42 patients, 6 experienced vancomycin-induced AKI. On day 7, the change from baseline eGFR using CysC (ΔeGFRCysC) showed a stronger correlation with vancomycin area under the curve (r = −0.634, P < .001) than that using SCr (ΔeGFRSCr; r = −0.437, P = .020). ΔeGFRSCr showed no significant correlation with vancomycin pharmacokinetic in patients with body mass index ≥23. The median (interquartile range) level of KIM-1 (μg/mg) was significantly higher in the AKI group (0.006 [0.005–0.008]) than in the non-AKI group (0.004 [0.001–0.005]) (P = .039, Mann–Whitney U test), with area under the receiver operating characteristic curve (95% confidence interval) of 0.788 (0.587–0.990). Serum CysC, particularly in overweight individuals or those with obesity, along with urinary KIM-1 are important predictors of vancomycin-induced AKI. These results may aid in selecting better biomarkers than traditional SCr for detecting vancomycin-induced AKI.

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Section: Discussionmentioning

confidence: 99%

Serum and urinary biomarkers of vancomycin-induced acute kidney injury: A prospective, observational analysis

Park,

Yu,

et al. 2024

Medicine

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“…The [TIMP-2] × [IGFBP-7] value obtained on day 1 of vancomycin administration was independently associated with VA-AKI (p < 0.001) [65]. A prospective cohort study of 94 patients receiving vancomycin found that the urinary NGAL level between 96 and 144 hrs (OR 1.123, 95%CI 1.096-1.290, p = 0.03) was a predictor of AKI development, whereas a higher urinary x[IGFBP-7]/Cr between 144 and 192 hrs (OR 1.26, 95%CI 1.092-1.543, p = 0.03) was a predictor of non-recovery of VA-AKI [64]. In addition, a recent study by Awdishu et al [12] found that urinary concentrations of some inflammatory proteins (namely, complement C3, C4, galectin-3-binding protein, fibrinogen, alpha-2 macroglobulin, immunoglobulin heavy constant mu, and serotransferrin) increased after nephrotoxic injury in patients with VA-AKI.…”

Section: Biomarkers For Detecting Va-akimentioning

confidence: 99%

Vancomycin-Associated Acute Kidney Injury: A Narrative Review from Pathophysiology to Clinical Application

Chen

Shiao

2022

IJMS

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Vancomycin is the most frequently used antibiotic, accounting for up to 35% of hospitalized patients with infection, because of its optimal bactericidal effectiveness and relatively low price. Vancomycin-associated AKI (VA-AKI) is a clinically relevant but not yet clearly understood entity in critically ill patients. The current review comprehensively summarizes the pathophysiological mechanisms of, biomarkers for, preventive strategies for, and some crucial issues with VA-AKI. The pathological manifestations of VA-AKI include acute tubular necrosis, acute tubulointerstitial nephritis (ATIN), and intratubular crystal obstruction. The proposed pathological mechanisms of VA-AKI include oxidative stress and allergic reactions induced by vancomycin and vancomycin-associated tubular casts. Concomitant administration with other nephrotoxic antibiotics, such as piperacillin–tazobactam, high vancomycin doses, and intermittent infusion strategies compared to the continuous infusion are associated with a higher risk of VA-AKI. Several biomarkers could be applied to predict and diagnose VA-AKI. To date, no promising therapy is available. Oral steroids could be considered for patients with ATIN, whereas hemodialysis might be applied to remove vancomycin from the patient. In the future, disclosing more promising biomarkers that could precisely identify populations susceptible to VA-AKI and detect VA-AKI occurrence early on, and developing pharmacological agents that could prevent or treat VA-AKI, are the keys to improve the prognoses of patients with severe infection who probably need vancomycin therapy.

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“…Interestingly, cyclosporine dose reduction in these patients led to decreased urine β2-microglobulin [60]. In addition, based on results of a cohort investigation, urinary NGAL levels between 96 and 144 h and urinary [TIMP-2]•[IGFBP7] normalized by urinary creatinine between 144 and 192 h of vancomycin use were predictors of developing AKI during hospital stay and recovery of AKI at the time of hospital discharge, respectively [61]. There is the possibility of tracking patients' improvement with DIKD using novel biomarkers.…”

Section: Movement Between Categoriesmentioning

confidence: 99%

Moving toward a contemporary classification of drug-induced kidney disease

Karimzadeh,

Barreto,

Kellum

et al. 2023

Crit Care

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Drug-induced kidney disease (DIKD) accounts for about one-fourth of all cases of acute kidney injury (AKI) in hospitalized patients, especially in critically ill setting. There is no standard definition or classification system of DIKD. To address this, a phenotype definition of DIKD using expert consensus was introduced in 2015. Recently, a novel framework for DIKD classification was proposed that incorporated functional change and tissue damage biomarkers. Medications were stratified into four categories, including “dysfunction without damage,” “damage without dysfunction,” “both dysfunction and damage,” and “neither dysfunction nor damage” using this novel framework along with predominant mechanism(s) of nephrotoxicity for drugs and drug classes. Here, we briefly describe mechanisms and provide examples of drugs/drug classes related to the categories in the proposed framework. In addition, the possible movement of a patient’s kidney disease between certain categories in specific conditions is considered. Finally, opportunities and barriers to adoption of this framework for DIKD classification in real clinical practice are discussed. This new classification system allows congruencies for DIKD with the proposed categorization of AKI, offering clarity as well as consistency for clinicians and researchers.

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The Role of Urinary Biomarkers as Diagnostic and Prognostic Predictors of Acute Kidney Injury Associated With Vancomycin

Cited by 11 publications

References 32 publications

Serum and urinary biomarkers of vancomycin-induced acute kidney injury: A prospective, observational analysis

Serum and urinary biomarkers of vancomycin-induced acute kidney injury: A prospective, observational analysis

Vancomycin-Associated Acute Kidney Injury: A Narrative Review from Pathophysiology to Clinical Application

Moving toward a contemporary classification of drug-induced kidney disease

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