Serum 5-Hydroxyindoleacetic Acid and Ratio of 5-Hydroxyindoleacetic Acid to Serotonin as Metabolomics Indicators for Acute Oxidative Stress and Inflammation in Vancomycin-Associated Acute Kidney Injury

Lee, Hyunseung; Kim, Sang-Mi; Jang, Ja‐Hyun; Park, Hyung-Doo; Lee, Soo-Youn

doi:10.3390/antiox10060895

Cited by 14 publications

(11 citation statements)

References 53 publications

(72 reference statements)

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“…Previous studies have shown that oxidative stress is an important mechanism related to glycopeptide antibiotics, such as vancomycin, bleomycin, etc.,induced cytotoxicity [39][40][41].It has been documented that TIGAR prevents apoptosis via directing glucose to PPP and increasing the levels of NADPH and 5-ribose phosphate, thus signi cantly reducing intracellular ROS [13,38]. Here, we observed that teicoplanin caused ROS accumulation in HEI-OC1 cells, and the overexpression of TIGAR decreased the cellular level of ROS and the loss of ΔΨm in HEI-OC1 cells exposed to teicoplanin, but TIGAR knockdown has the opposite effect (Fig.…”

Section: Discussionmentioning

confidence: 52%

TIGAR protects cochlear hair cells against teicoplanin-induced damage

zhang

Yao

Chen

et al. 2022

Preprint

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Teicoplanin, a glycopeptide antibiotic, is used for the treatment of severe staphylococcal infections. Teicoplanin is reported to have an ototoxic potential but its toxic effects on cochlea hair cells (HCs) remains unclear. TP53-induced glycolysis and apoptosis regulator (TIGAR) plays a key role to promote cell survival, our previous study shown that TIGAR protected inner ear spiral ganglion neuron against cisplatin injury. However, the role of TIGAR in mammalian HCs damage has not been explored yet. In this study, firstly, we found that teicoplanin induced significant cell loss of both HEI-OC1 cells and cochlea HCs in a dose-dependent manner in vitro. Next, we discovered that the expression of TIGAR was significantly decreased after teicoplanin treatment in HCs and HEI-OC1 cells. To explore the role of TIGAR in inner ear after teicoplanin damage, the expression of TIGAR was upregulated via recombinant adenovirus or knocked down by shRNA in HEI-OC1 cells, respectively. We found that the overexpression of TIGAR increased cell viability, decreased apoptosis and reduced intracellular reactive oxygen species (ROS) level after teicoplanin injury, whereas downregulation of TIGAR by shRNA decreased cell viability, exacerbated apoptosis and elevated ROS level. Finally, antioxidant treatment with N-acetyl-L-cysteine lowered ROS level, rescued cell loss as well as restored p38/phosphorylation-p38 expression levels induced by TIGAR deficiency in HEI-OC1 cells after teicoplanin injury. This study provides evidences that TIGAR might be a new potential target for prevention from the teicoplanin-induced ototoxicity.

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Section: Discussionmentioning

confidence: 52%

TIGAR protects cochlear hair cells against teicoplanin-induced damage

zhang

Yao

Chen

et al. 2022

Preprint

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“…Study design and subject selection are summarized in Figure 4 . The current study included subjects from our previous study cohort [ 66 ]. In brief, 23,182 cases referred for vancomycin concentration measurement from January 2018 to December 2019 were screened.…”

Section: Methodsmentioning

confidence: 99%

Diagnostic Value of Multiple Serum Biomarkers for Vancomycin-Induced Kidney Injury

Kim

Lee

Kim

et al. 2021

JCM

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Acute kidney injury (AKI) is a major contributor to in-hospital morbidity and mortality. Vancomycin, one of the most commonly used antibiotics in a clinical setting, is associated with AKI, with its incidence ranging up to 43%. Despite the high demand, few studies have investigated serum biomarkers to detect vancomycin-induced kidney injury (VIKI). Here, we evaluated the diagnostic value of nine candidate serum biomarkers for VIKI. A total of 23,182 cases referred for vancomycin concentration measurement from January 2018 to December 2019 were screened and 28 subjects with confirmed VIKI were enrolled (VIKI group). Age- and sex- matched control group consisted of 21 subjects who underwent vancomycin therapy without developing VIKI (non-VIKI group), and 23 healthy controls (HC group). The serum concentrations of clusterin, retinol binding protein 4 (RBP4), interleukin-18 (IL-18), tumor necrosis factor receptor 1 (TNF-R1), C-X-C motif chemokine ligand 10 (CXCL10), neutrophil gelatinase-associated lipocalin (NGAL), osteopontin, trefoil factor-3 (TFF3), and cystatin C were compared among the three groups, and their correlations with estimated glomerular filtration rate (eGFR) and diagnostic values for VIKI were assessed. All of the biomarkers except clusterin and RBP4 exhibited significant elevation in the VIKI group. Serum TFF3, cystatin C, TNF-R1, and osteopontin demonstrated an excellent diagnostic value for VIKI (TFF3, area under the curve (AUC) 0.932; cystatin C, AUC 0.917; TNF-R1, AUC 0.866; osteopontin, AUC 0.787); and except osteopontin, a strong negative correlation with eGFR (TFF3, r = −0.71; cystatin C, r = −0.70; TNF-R1, r = −0.60). IL-18, CXCL10, and NGAL showed weak correlation with eGFR and moderate diagnostic value for VIKI. This study tested multiple serum biomarkers for VIKI and showed that serum TFF3, cystatin C, TNF-R1, and osteopontin could efficiently discriminate VIKI patients. Further studies are warranted to clarify the diagnostic value of these biomarkers in VIKI.

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“…A recent human study demonstrated that lower serum serotonin (5-HT), higher serum 5-hydroxy indole acetic acid (5-HIAA), and a higher ratio of 5-HIAA to 5-HT was associated with the occurrence of VA-AKI. The finding suggests that the high 5-HIAA/5-HT ratio could be a potential surrogate biomarker for VA-AKI, and indicates that acute oxidative stress and inflammation are involved in in the mechanism of VA-AKI [32].…”

Section: Oxidative Stressmentioning

confidence: 86%

“…As mentioned earlier, a high 5-HIAA/5-HT ratio in serum (AUC 0.88 (0.88-0.96)) was proposed as a potential surrogate biomarker for VA-AKI in humans [32]. Furthermore, Kim et al retrospectively compared serum biomarkers among patients with and without 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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Serum 5-Hydroxyindoleacetic Acid and Ratio of 5-Hydroxyindoleacetic Acid to Serotonin as Metabolomics Indicators for Acute Oxidative Stress and Inflammation in Vancomycin-Associated Acute Kidney Injury

Cited by 14 publications

References 53 publications

TIGAR protects cochlear hair cells against teicoplanin-induced damage

TIGAR protects cochlear hair cells against teicoplanin-induced damage

Diagnostic Value of Multiple Serum Biomarkers for Vancomycin-Induced Kidney Injury

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

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