In vitro evaluation of biomarkers of nephrotoxicity through gene expression using gentamicin

Campos, Maria Augusta Amaral; Almeida, Leonardo Augusto de; Grossi, Marina Felipe; Tagliati, Carlos Alberto

doi:10.1002/jbt.22189

Cited by 13 publications

(8 citation statements)

References 21 publications

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“…In addition, the regulation of these genes produced proteins capable of cleaving specific substrates leading to cell death. Moreover, a decrease in antiapoptotic genes e.g., BCL2L1 has been found [ 53 ]. In an experimental study carried out on drug-induced, predominantly tubular (gentamicin and cisplatine) and glomerular (puromycin and doxorubicin) kidney injury, among several commonly downregulated miRNAs, miR-143-3p and miR-122-5p were proposed as potential tubular and miR-3473 as glomerular biomarker candidates [ 54 ].…”

Section: Gentamicin-induced Nephrotoxicity Pathophysiology and Biomentioning

confidence: 99%

Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A Review

Petejová

Martínek

Zadrazil

et al. 2020

IJMS

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Acute kidney injury is a common complication in critically ill patients with sepsis and/or septic shock. Further, some essential antimicrobial treatment drugs are themselves nephrotoxic. For this reason, timely diagnosis and adequate therapeutic management are paramount. Of potential acute kidney injury (AKI) biomarkers, non-protein-coding RNAs are a subject of ongoing research. This review covers the pathophysiology of vancomycin and gentamicin nephrotoxicity in particular, septic AKI and the microRNAs involved in the pathophysiology of both syndromes. PubMED, UptoDate, MEDLINE and Cochrane databases were searched, using the terms: biomarkers, acute kidney injury, antibiotic nephrotoxicity, sepsis, miRNA and nephrotoxicity. A comprehensive review describing pathophysiology and potential biomarkers of septic and toxic acute kidney injury in septic patients was conducted. In addition, five miRNAs: miR-15a-5p, miR-192-5p, miR-155-5p, miR-486-5p and miR-423-5p specific to septic and toxic acute kidney injury in septic patients, treated by nephrotoxic antibiotic agents (vancomycin and gentamicin) were identified. However, while these are at the stage of clinical testing, preclinical and clinical trials are needed before they can be considered useful biomarkers or therapeutic targets of AKI in the context of antibiotic nephrotoxicity or septic injury.

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Section: Gentamicin-induced Nephrotoxicity Pathophysiology and Biomentioning

confidence: 99%

Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A Review

Petejová

Martínek

Zadrazil

et al. 2020

IJMS

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“…Glucosa alta (25 mM, 48 h) (Habib, Yadav, Kidane, Weiss, & Liang, 2016) Células mesangiales glomerulares de rata (HBZY-1) Diabetes Productos finales de glicación avanzada (200 μg/mL), Glucosa alta (25 mM, 24-72 h) (Lu et al, 2015;Zhang et al, 2014) Células murinas del conducto colector medular interno (mIMCD3) Deshidratación 100-150 mM NaCl (osmolaridad 500-600 mOsm/kg H2O, 48-72 h) (Leroy et al, 2000;Neuhofer et al, 2004) Células humanas del epitelio del túbulo proximal (HK2) Aminoglucósidos Gentamicina (2-8 mM, 24 h) (Bae et al, 2013;Campos et al, 2018) Diabetes Glucosa alta (25 mM , 48 h-168 h) (Hills et al, 2018) Deshidratación 120 mM NaCl (Berry et al, 2017) Células porcinas del epitelio de riñones (LLC-PK1) Aminoglucósidos Gentamicina (2-3 mM, 96 h) (El Mouedden et al, 2000;Peyrou & Cribb, 2007) Tabla 1 Modelos in vitro de distintos factores etiológicos de daño renal Arjinajarn et al, 2016;Bae et al, 2013;El-Kashef et al, 2015;Guo et al, 2013;P. Liu et al, 2014;Mahmoud, 2017;Morales et al, 2010;Pedraza-Chaverri et al, 2004…”

Section: Diabetesunclassified

“…La función renal reducida se ve cuando el proceso de regeneración no puede compensar el daño tisular causado por el agente tóxico. Algunos modelos in vitro se han desarrollado a partir de líneas celulares expuestas a GM para evaluar biomarcadores y potenciales candidatos en células de esta región de la nefrona, como células caninas del epitelio tubular renal Madin-Darby (MDCK), epiteliales renales de rata (NRK-52) y humanas del epitelio del túbulo proximal (HK2) (Bae et al, 2013;Campos et al, 2018;Chen et al, 2015;El Mouedden et al, 2000;Peyrou & Cribb, 2007).…”

Section: Diabetesunclassified

“…Diversos estímulos inducen la agregación de Bax y la translocación a las mitocondria, provocando la activación de caspasa-9, que luego escinde y activa la caspasa efectora, caspasa-3, lo que conduce a una pérdida del potencial transmembrana mitocondrial y a la muerte celular apoptótica (Bae et al, 2013;Campos et al, 2018;Hao et al, 2000;Milagres et al, 2018;Tong et al, 2019).…”

Section: Apoptosisunclassified

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Biomarcadores traslacionales de modelos in vitro e in vivo de daño renal: Una perspectiva para abordar nefrotoxicidad desde múltiples factores etiológicos

Castañeda¹,

Ortiz²,

Aldana³

et al. 2020

CTS

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La prevalencia de enfermedad renal ha aumentado considerablemente en la última década y está previsto que crezca en los próximos años. Recientemente, diversos modelos se han utilizado para entender los procesos fisiopatológicos de daño renal y para la búsqueda de futuros candidatos farmacológicos. El objetivo de esta revisión es proporcionar una descripción de la evidencia actual de modelos in vitro e in vivo de nefrotoxicidad, nefropatía diabética y deshidratación, y los fundamentos de las principales vías de señalización fisiopatológicas, con el fin de proponer biomarcadores candidatos para futura investigación farmacológica. Actualmente, los roedores constituyen un pilar importante en estudios de daño renal, existiendo diferencias específicas según el estímulo nocivo, lo que sugiere considerar para un modelo relevante aspectos como especie, cepa, género y estructuras renales objetivo. Diversas estructuras renales se han complementado in vitro, principalmente a partir de líneas celulares, como del epitelio tubular, podocitos, células mesangiales glomerulares y conducto colector medular interno. Este enfoque se ha utilizado como complementario en modelos de nefrotoxicidad por exposición a aminoglucósidos (principalmente), deshidratación por cloruro de sodio hiperosmolar, y nefropatía diabética por medio de glucosa alta y productos derivados de glucólisis y glicación. Recientemente, estos modelos han mostrado similitud en diversas rutas de señalización celular, con algunos biomarcadores en común, entre múltiples causas de daño renal como el daño oxidativo, disfunción mitocondrial, procesos inflamatorios, desregulación de sistemas de defensa y sobrevivencia celular, y apoptosis. El enfoque en seleccionar biomarcadores relevantes contribuirá al diseño de estrategias terapéuticas de nefroprotectores sobre múltiples factores etiológicos.

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“…Thus, the discovery of the initial renal injury required new biomarkers which are more sensitive and highly specific that gives an insight into the site of underlying renal damage. [15]…”

Section: Biomarkers Of Nephrotoxicitymentioning

confidence: 99%

Nephrotoxicity: Role and significance of renal biomarkers in the early detection of acute renal injury

Al-Naimi

Rasheed

Hussien

et al. 2019

J Adv Pharm Technol Res

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Nephrotoxicity is defining as rapid deterioration in the kidney function due to toxic effect of medications and chemicals. There are various forms, and some drugs may affect renal function in more than one way. Nephrotoxins are substances displaying nephrotoxicity. Different mechanisms lead to nephrotoxicity, including renal tubular toxicity, inflammation, glomerular damage, crystal nephropathy, and thrombotic microangiopathy. The traditional markers of nephrotoxicity and renal dysfunction are blood urea and serum creatinine which are regarded as low sensitive in the detection of early renal damage. Thus, the detection of the initial renal injures required new biomarkers which are more sensitive and highly specific that gives an insight into the site of underlying renal damage. Kidney injury molecule-1, Cystatin C, and neutrophil gelatinase-associated lipocalin sera levels are more sensitive than blood urea and serum creatinine in the detection of acute kidney injury during nephrotoxicity.

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In vitro evaluation of biomarkers of nephrotoxicity through gene expression using gentamicin

Cited by 13 publications

References 21 publications

Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A Review

Acute Kidney Injury in Septic Patients Treated by Selected Nephrotoxic Antibiotic Agents—Pathophysiology and Biomarkers—A Review

Biomarcadores traslacionales de modelos in vitro e in vivo de daño renal: Una perspectiva para abordar nefrotoxicidad desde múltiples factores etiológicos

Nephrotoxicity: Role and significance of renal biomarkers in the early detection of acute renal injury

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