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3.
Arq. bras. med. vet. zootec. (Online) ; 73(1): 99-107, Jan.-Feb. 2021. tab
Article in English | LILACS, VETINDEX | ID: biblio-1153067

ABSTRACT

This study evaluated the most common toxic agents affecting domestic cats, the clinical signs of toxicity, and the therapeutic approaches for recovery. A survey on poisoning in cats was conducted among small animal veterinary practitioners from 2017 to 2018. Of the 748 completed questionnaires, 543 (72.6%) were evaluated. Pesticides and household cleaning supplies were the most common causes of poisoning in cats. The toxicant groups included pesticides and household cleaning supplies (organophosphates), human drugs (acetaminophen), plants/plant derivatives (lily), and veterinary drugs (tramadol). The major clinical signs for these four groups of toxicants were (1) acetaminophen poisoning, which caused oxidative erythrocyte damage; (2) muscarinic and nicotinic cholinergic syndrome, which resulted from organophosphate poisoning; (3) acute kidney injury, which resulted from intoxication of lily; and (4) serotonin syndrome, which resulted from tramadol toxicosis. Interventions for treating poisoning in cats were based on the clinical presentation of animals. In the present study, the significant toxins identified to be dangerous for cats were characterized using the obtained data in Brazil as well as the main associated clinical signs and therapy recommended by veterinarians.(AU)


Objetiva-se com este trabalho caracterizar os principais toxicantes para gatos domésticos, bem como os prevalentes sinais clínicos e a terapêutica associada. Uma pesquisa sobre envenenamento em gatos foi realizada entre médicos veterinários no período de 2017 a 2018. Dos 748 questionários preenchidos, 543 (72,6%) foram avaliados. Pesticidas e domissanitários foram os principais causadores de intoxicação em gatos. Entre os grupos tóxicos, destacaram-se, na categoria pesticidas e domissanitários (organofosforados), medicamentos humanos (acetaminofeno), plantas e derivados de planta (lírio) e medicamentos veterinários (tramadol). Os principais sinais clínicos para os quatro grupos de substâncias tóxicas foram: (1) intoxicação por acetaminofeno, que causou dano eritrocitário oxidativo; (2) síndrome colinérgica muscarínica e nicotínica, resultante do envenenamento por organofosforado; (3) lesão renal aguda, causada pela intoxicação por lírio; e (4) síndrome serotoninérgica, resultante da exposição ao tramadol. As intervenções realizadas para o tratamento dos envenenamentos foram justificáveis mediante a apresentação clínica dos animais. Por meio dos dados obtidos, puderam-se caracterizar os principais tóxicos para gatos no Brasil, bem como os principais sinais clínicos associados e a terapêutica preconizada pelos médicos veterinários.(AU)


Subject(s)
Animals , Cats , Organophosphorus Compounds/toxicity , Poisoning/etiology , Poisoning/veterinary , Tramadol/toxicity , Lilium/toxicity , Acetaminophen/toxicity , Serotonin Agents/toxicity , Oxidative Stress , Muscarinic Antagonists/toxicity , Acute Kidney Injury/chemically induced
4.
Repert. med. cir ; 30(1): 43-47, 2021. tab.
Article in English, Spanish | LILACS, COLNAL | ID: biblio-1284478

ABSTRACT

Introducción: los cristaloides son medicamentos usados en pacientes críticamente enfermos, con resultados ambiguos cuando se utilizan soluciones balanceadas versus solución salina normal. Objetivo: conocer si existen diferencias al usar solución salina 0.9% vs. lactato de Ringer en pacientes críticamente enfermos con sepsis y choque séptico o hipovolémico, en cuanto a mortalidad, lesión renal aguda y tiempo de estancia hospitalaria. Métodos: estudio observacional de tipo cohorte retrospectiva en mayores de 18 años con diagnóstico de sepsis, choque séptico o hipovolémico. Se excluyeron aquellos con enfermedad renal crónica en diálisis, las hospitalizadas por ginecología/obstetricia y aquellos con diagnóstico de muerte encefálica o donantes de órganos. Se evaluaron los desenlaces primarios de mortalidad, lesión renal aguda y estancia hospitalaria. Resultados y discusión: se incluyeron 314 pacientes, 158 en el grupo expuesto a solución salina al 0.9% y 156 con lactato de Ringer. Se presentó lesión renal aguda en 22.7% con solución salina y 25.8% con lactato de Ringer (OR 1.18 IC 95%:0.7-2). La mortalidad con solución salina fue de 49%, y en lactato 49% (OR 1.01 IC 95%:0.63-1.63). Los factores de riesgo identificados para mortalidad fueron uso de soporte vasopresor (OR 35 IC 95% 12-83) y lesión renal aguda (1.3 IC 95% 1.01-1.69). Conclusiones: en el paciente críticamente enfermo con sepsis, choque séptico o hipovolémico el uso desolución salina 0.9% no representa diferencias al compararlo con lactato de Ringer en cuanto a mortalidad, lesión renal aguda o estancia hospitalaria. La elección de un cristaloide debe ser individualizada, teniendo en cuenta las comorbilidades, la presencia de hipercloremia o hiperpotasemia.


Objective: crystalloids are drugs used in critically ill patients, with ambiguous results when balanced solutions versus normal saline solution (NS) are used. The objective of this study is to determine if there are differences when NS (0.9%) vs. lactated Ringer ́s (LR) solution are given to critically ill patients in sepsis or septic or hypovolemic shock, in terms of mortality, acute renal injury and length of hospital stay. Methods: a retrospective observational cohort study in patients over 18 years old with sepsis or septic or hypovolemic shock. Patients with chronic renal disease on dialysis, those hospitalized by gynecology/obstetrics and those diagnosed with brain death or organ donors were excluded. The primary mortality outcomes, acute renal injury and hospital stay were evaluated. Results: 314 patients were included, 158 in the NS group and 156 in the LR group. Acute renal injury occurred in 22.7% in the NS group and 25.8% in the LR group (OR 1.18 IC 95%:0.7-2). Mortality rate was 49% in the NS group and 49% in the LR group (OR 1.01 95%: CI 0.63-1.63). Mortality risk factors included the use of vasopressor support (OR 35 95% CI 12-83) and acute renal injury (1.3 95% CI 1.01-1.69). Conclusions: no difference was found with the use of NS in critically ill patients with sepsis or septic or hypovolemic shock when compared with LR in terms of mortality, acute renal injury or hospital stay. The choice of which crystalloid to administer should be individualized, based on the comorbidities and the presence of hyperchloremia or hyperkalemia.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Aged, 80 and over , Shock/therapy , Sepsis/therapy , Ringer's Lactate/therapeutic use , Saline Solution/therapeutic use , Shock/mortality , Shock, Septic/mortality , Shock, Septic/therapy , Multivariate Analysis , Retrospective Studies , Treatment Outcome , Sepsis/mortality , Acute Kidney Injury/chemically induced , Ringer's Lactate/adverse effects , Saline Solution/adverse effects , Length of Stay
5.
Rev. bras. ter. intensiva ; 32(4): 557-563, out.-dez. 2020. tab
Article in English, Portuguese | LILACS | ID: biblio-1156243

ABSTRACT

RESUMO Objetivo: Avaliar a associação entre uso de drogas nefrotóxicas e lesão renal aguda em pacientes pediátricos graves. Métodos: Estudo de coorte retrospectivo envolvendo todas as crianças internadas na unidade de terapia intensiva de um hospital pediátrico durante o período de 1 ano. A lesão renal aguda foi definida pela classificação KDIGO. Foram incluídos pacientes com tempo de internação maior que 48 horas e idade entre 1 mês e 14 anos. Foram excluídos aqueles com nefropatia aguda ou crônica, uropatia, cardiopatia congênita ou adquirida, uso crônico de drogas nefrotóxicas, rabdomiólise e síndrome de lise tumoral. Os pacientes foram classificados quanto ao uso de drogas nefrotóxicas durante internação na unidade de terapia intensiva pediátrica. Resultados: A amostra foi composta por 226 crianças, sendo que 37,1% fizeram uso de drogas nefrotóxicas, 42,4% desenvolveram lesão renal aguda e 7,5% morreram. As medicações que, isoladamente, apresentaram associação com lesão renal aguda foram aciclovir (p < 0,001), vancomicina (p < 0,001), furosemida (p < 0,001) e ganciclovir (p = 0,008). O uso concomitante de duas ou mais drogas nefrotóxicas foi caracterizado como marcador independente de disfunção renal (p < 0,001). Após alta da unidade de terapia intensiva pediátrica, o acompanhamento da função renal na enfermaria foi inadequado em 19,8% dos casos. Conclusão: É necessário que o médico intensivista tenha conhecimento das principais drogas nefrotóxicas, de modo a prever, reduzir ou evitar danos a seus pacientes.


Abstract Objective: To evaluate the association between the use of nephrotoxic drugs and acute kidney injury in critically ill pediatric patients. Methods: This was a retrospective cohort study involving all children admitted to the intensive care unit of a pediatric hospital during a 1-year period. Acute kidney injury was defined according to the KDIGO classification. Patients with a length of hospital stay longer than 48 hours and an age between 1 month and 14 years were included. Patients with acute or chronic nephropathy, uropathy, congenital or acquired heart disease, chronic use of nephrotoxic drugs, rhabdomyolysis and tumor lysis syndrome were excluded. Patients were classified according to the use of nephrotoxic drugs during their stay at the pediatric intensive care unit. Results: The sample consisted of 226 children, of whom 37.1% used nephrotoxic drugs, 42.4% developed acute kidney injury, and 7.5% died. The following drugs, when used alone, were associated with acute kidney injury: acyclovir (p < 0.001), vancomycin (p < 0.001), furosemide (p < 0.001) and ganciclovir (p = 0.008). The concomitant use of two or more nephrotoxic drugs was characterized as an independent marker of renal dysfunction (p < 0.001). After discharge from the pediatric intensive care unit, renal function monitoring in the ward was inadequate in 19.8% of cases. Conclusion: It is necessary for intensivist physicians to have knowledge of the main nephrotoxic drugs to predict, reduce or avoid damage to their patients.


Subject(s)
Humans , Infant , Child , Pharmaceutical Preparations , Acute Kidney Injury/chemically induced , Acute Kidney Injury/epidemiology , Intensive Care Units, Pediatric , Retrospective Studies , Risk Factors , Critical Illness
6.
Int. j. morphol ; 38(4): 876-881, Aug. 2020. graf
Article in English | LILACS | ID: biblio-1124869

ABSTRACT

Acetaminophen (also called paracetamol, or APAP) causes acute kidney injury after accidental or intentional ingestion of a toxic dose of the drug. We tested whether the antioxidant and anti-inflammatory agent, quercetin (QUR) given alone can protect against acute nephrotoxicity induced by APAP overdose in a rat model of APAP-induced acute kidney injury. Rats were either given a single dose of APAP (2 g/kg) before being sacrificed after 24 hours or were pre-treated for 7 days with QUR (50 mg/kg) before being given a single dose of APAP and then sacrificed 24 hours post APAP ingestion. Kidneys were examined by light microscopy after staining with hematoxylin and eosin (H&E) and collected blood samples were assayed for biomarkers of oxidative stress, inflammation, and kidney injury. H&E stained sections of kidney from the model group of rats (APAP) showed substantial damage to the kidney architecture as demonstrated by widening of Bowman's space, tubular dilatation, vacuolization of tubular epithelium, and congested dilated blood vessels, which were partially protected by QUR. In addition, APAP significantly (p<0.05) increased blood levels of urea, creatinine, malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-a), and interleukin-6 (IL-6), which were significantly (p<0.05) reduced by QUR. These results indicate that quercetin partially protects against APAP-induced acute kidney injury in rats, which is associated with the inhibition of biomarkers of oxidative stress and inflammation and kidney injury.


El acetaminofeno (también llamado paracetamol o DCI) causa daño renal agudo después de la ingestión accidental o intencional de una dosis tóxica del medicamento. En el estudio analizamos si el agente antioxidante y antiinflamatorio, la quercetina (QUR) administrada sola, puede proteger contra la nefrotoxicidad aguda inducida por sobredosis de DCI en un modelo de rata. Las ratas recibieron una dosis única de DCI (2 g / kg) antes de ser sacrificadas después de 24 horas o fueron pretratadas durante 7 días con QUR (50 mg / kg) antes de recibir una dosis única de DCI y luego sacrificadas 24 horas post ingestión. Los riñones se examinaron mediante microscopía óptica después de la tinción con hematoxilina y eosina (H&E) y las muestras de sangre recolectadas se analizaron para detectar biomarcadores de estrés oxidativo, inflamación y daño renal. Las secciones de riñón teñidas con H&E del grupo modelo de ratas (DCI) mostraron un daño sustancial a la arquitectura del riñón, como lo demuestra la ampliación del espacio de Bowman, la dilatación tubular, la vacuolización del epitelio tubular y los vasos sanguíneos dilatados congestionados, que estaban parcialmente protegidos por QUR. Además, DCI aumentó significativamente (p <0,05) los niveles sanguíneos de la urea, creatinina, malondialdehído (MDA), factor de necrosis tumoral alfa (TNF-a) e interleucina-6 (IL-6), los que fueron reducidos significativamente (p < 0,05) por QUR. Estos resultados indican que la quercetina protege parcialmente contra la lesión renal aguda inducida por DCI en ratas, asociada con la inhibición de biomarcadores de estrés oxidativo, inflamación y lesión renal.


Subject(s)
Animals , Rats , Quercetin/administration & dosage , Acute Kidney Injury/chemically induced , Acetaminophen/toxicity , Antioxidants/administration & dosage , Quercetin/pharmacology , Biomarkers/analysis , Oxidative Stress/drug effects , Protective Agents , Creatinine , Disease Models, Animal , Inflammation , Kidney/drug effects , Antioxidants/pharmacology
7.
Int. j. morphol ; 38(2): 461-471, abr. 2020. graf
Article in English | LILACS | ID: biblio-1056463

ABSTRACT

This experiment was designed to study the administration of normal doses of one of recent antimalarial drug and coadministration of vitamin E on the kidney tissue. A total twenty-four adult male albino rats were used and divided into four groups: the first one served as a control, the second received artemether orally for three days consecutively. The rats of the third and fourth groups received the same dose of artemether concomitantly with 50 and 100 mg/kg vitamin E orally daily for 2 weeks. After the last dose, the rats were sacrificed and the kidney tissues with blood samples obtained and processed for light, electron microscopic and biochemical analysis. Histologically, artemether treated kidneys showed atrophied glomeruli with widened urinary space and kidney tubules were degenerated with disturbed contour and some vacuoles inside it. Ultrastructurally, the glomeruli of this group showed hypertrophic endothelial cells, irregularity of its basement membrane, disrupted foot processes and filtration slits. The kidney tubule cells showed loss of basal infoldings, cytoplasmic vacuolation, polymorphic damaged swollen mitochondria a loss of its microvilli towards its capillary lumen. Artemether plus vitamin E of the rat kidney groups showed improvement of morphological changes compared to the changes seen in artemether alone. These data were confirmed by biochemical findings with marked improvement of blood urea and creatinine levels and increase of anti-oxidant enzyme activities of glutathione peroxidase and superoxide dismutase in the vitamin E treated groups. The results of this study revealed that vitamins E can improve the adverse changes of artemether of rat renal tissue.


Este proyecto fue diseñado para estudiar la administración de dosis normales de uno de los medicamentos antipalúdicos y de la administración de vitamina E en el tejido renal. Se utilizaron 24 ratas albinas machos adultas divididas en cuatro grupos: el primero sirvió como control, el segundo recibió arteméter por vía oral durante tres días consecutivos. Las ratas del tercer y cuarto grupos recibieron la misma dosis de arteméter concomitantemente con 50 y 100 mg / kg de vitamina E por vía oral diariamente durante 2 semanas. Después de la última dosis, las ratas fueron sacrificadas y se obtuvo el tejido renal de cada muestra los cuales fueron procesados para análisis con microscopías de luz y electrónica, además de exámenes bioquímicos. Histológicamente, los riñones tratados con arteméter mostraron atrofia glomerular con espacio urinario ensanchado y túbulos renales degenerados con contorno alterado y algunas vacuolas en su interior. Ultraestructuralmente, los glomérulos de este grupo mostraron células endoteliales hipertróficas, irregularidad de su membrana basal, procesos alterados del pie y hendiduras de filtración. Las células del túbulo renal mostraron pérdida de inflexiones basales, vacuolación citoplasmática, mitocondrias dañadas y pérdida de sus microvellosidades hacia la luz capilar. Arteméter más vitamina E en los grupos de riñón de rata mostraron una mejora de los cambios morfológicos, en comparación con los cambios observados en arteméter solamente. Estos datos fueron confirmados por hallazgos bioquímicos con una marcada mejoría de los niveles de urea y creatinina en sangre y un aumento de las actividades enzimáticas antioxidantes de la glutatión peroxidasa y la superóxido dismutasa en los grupos tratados con vitamina E. Los resultados de este estudio revelaron que la vitamina E puede mejorar los cambios adversos del arteméter del tejido renal de la rata.


Subject(s)
Animals , Male , Rats , Vitamin E/pharmacology , Acute Kidney Injury/chemically induced , Artemether/toxicity , Vitamin E/administration & dosage , Microscopy, Electron , Biomarkers/analysis , Rats, Wistar , Kidney/drug effects , Kidney/pathology , Kidney/ultrastructure , Antimalarials/toxicity
8.
Rev. Assoc. Med. Bras. (1992) ; 66(supl.1): s82-s90, 2020. tab
Article in English | LILACS | ID: biblio-1057101

ABSTRACT

SUMMARY Acute kidney injury is a very common diagnosis, present in up to 60% of critical patients, and its third main cause is drug toxicity. Nephrotoxicity can be defined as any renal injury caused directly or indirectly by medications, with acute renal failure, tubulopathies, and glomerulopathies as common clinical presentations. Some examples of drugs commonly associated with the acute reduction of glomerular filtration rate are anti-inflammatories, antibiotics, such as vancomycin and aminoglycosides, and chemotherapeutic agents, such as cisplatin and methotrexate. Cases of tubulopathy are very common with amphotericin B, polymyxins, and tenofovir, and cases of glomerulopathies are common with VEGF inhibitors, bisphosphonates, and immunotherapy, and it is also common to have more than one clinical presentation related to a single agent. Early diagnosis is essential for the good evolution of the patient, with a reduction of renal exposure to the toxic agent, which requires knowing the risk factors and biomarkers. General measures such as correcting hydroelectrolytic disorders and hypovolemia, monitoring the serum level, avoiding combinations with the synergy of renal injury, and looking for similar options that are less toxic are the foundations for the treatment of complications that are still common and often preventable.


RESUMO A lesão renal aguda é um diagnóstico muito comum, presente em até 60% dos pacientes críticos, e sua terceira maior causa é a toxicidade de medicamentos. A nefrotoxicidade pode ser definida como qualquer lesão renal causada por medicamentos, direta ou indiretamente, tendo a insuficiência renal aguda, tubulopatias e glomerulopatias como apresentações clínicas comuns. Alguns exemplos de drogas comumente associadas à redução aguda da taxa de filtração glomerular são anti-inflamatórios, antibióticos, como a vancomicina e aminoglicosídeos, e agentes quimioterápicos, tais como cisplatina e metotrexato. Casos de tubulopatia são muito comuns com anfotericina B, polimixinas e tenofovir, já casos de glomerulopatias são comuns com inibidores de VEGF, bisfosfonatos e imunoterapia; também é comum ocorrer mais de uma apresentação clínica relacionada a um único agente. O diagnóstico precoce é essencial para a boa evolução do paciente, com a redução da exposição ao agente tóxico, o que requer conhecimento dos fatores de risco e biomarcadores. Medidas gerais, tais como a correção de distúrbios hidreletrolíticos e da hipovolemia, o monitoramento do nível sérico, evitar combinações com sinergia de lesão renal e procurar opções semelhantes e menos tóxicas são os alicerces do tratamento de complicações que são comuns e, muitas vezes, evitáveis.


Subject(s)
Humans , Drug-Related Side Effects and Adverse Reactions , Acute Kidney Injury/chemically induced , Risk Factors , Acute Kidney Injury/epidemiology , Nephrotic Syndrome/chemically induced , Nephrotic Syndrome/epidemiology
9.
Rev. Pesqui. (Univ. Fed. Estado Rio J., Online) ; 12: 460-465, jan.-dez. 2020. tab
Article in English, Portuguese | LILACS, BDENF | ID: biblio-1053063

ABSTRACT

Objetivo: Determinar a prevalência da nefropatia induzida por contraste em pacientes cardiopatas submetidos a procedimentos angiográficos de diagnóstico e/ou tratamento. Método: Estudo prospectivo, quantitativo, realizado no setor de hemodinâmica de um hospital de grande porte, situado na região norte do Rio Grande do Sul, Brasil. A amostra foi constituída por 79 participantes através do cálculo de tamanho amostral. Resultados: A amostra foi formada por 52 (65,8%) homens e 27 (34,2%) mulheres. A idade média foi de 65,9 ± 9,52 anos. A incidência de nefropatia induzida por contraste foi de 30,38%, totalizando 24 pacientes. Conclusão: Foi evidenciada uma alta prevalência de nefropatia por contraste, apesar dos pacientes apresentarem poucos fatores de risco, o que ressalta a necessidade de medidas preventivas e redução do volume de contraste


Objective: To determine the prevalence of contrast-induced nephropathy in cardiac patients undergoing diagnostic and / or treatment angiographic procedures. Method: A prospective, quantitative study in the hemodynamics sector of a large hospital, located in the northern region of Rio Grande do Sul, Brazil. The sample consisted of 79 participants through the calculation of sample size. Results: The sample consisted of 52 (65.8%) men and 27 (34.2%) women. The mean age was 65.9 ± 9.52 years. The incidence of contrast-induced nephropathy was 30,38%, totaling 24 patients. Conclusion: A high prevalence of contrast nephropathy was evidenced, despite the fact that patients presented few risk factors, which highlights the need for preventive measures and reduction of contrast volume


Objetivo: Determinar la prevalencia de la nefropatía inducida por contraste en pacientes cardiopatas sometidos a procedimientos angiográficos de diagnóstico y / o tratamiento. Método: Estudio prospectivo, cuantitativo, realizado en el sector de hemodinámica de un hospital de gran porte, situado en la región norte de Rio Grande do Sul, Brasil. La muestra fue constituida por 79 participantes a través del cálculo de tamaño muestral. Resultados: La muestra fue formada por 52 (65,8%) hombres y 27 (34,2%) mujeres. La edad media fue de 65,9 ± 9,52 años. La incidencia de nefropatía inducida por contraste fue del 30,38%, totalizando 24 pacientes. Conclusión: Se evidenció una alta prevalencia de nefropatía por contraste, a pesar de que los pacientes presentaban pocos factores de riesgo, lo que resalta la necesidad de medidas preventivas y reducción del volumen de contraste


Subject(s)
Humans , Male , Female , Middle Aged , Aged , Angiography/adverse effects , Heart Diseases/complications , Heart Diseases/diagnostic imaging , Kidney Diseases/chemically induced , Kidney Diseases/epidemiology , Prospective Studies , Contrast Media/adverse effects , Coronary Disease/complications , Acute Kidney Injury/chemically induced , Hemodynamics
10.
Int. j. morphol ; 37(4): 1335-1341, Dec. 2019. graf
Article in English | LILACS | ID: biblio-1040134

ABSTRACT

Food additives and flavour enhancers used in the food industry are potential health risks. We tested the hypothesis that the food additive and flavour enhancer, monosodium glutamate (MSG), which is the sodium salt of glutamic acid can induce ultrastructural alterations to the kidney, and the antioxidant vitamin E can protect against acute kidney injuries induced by a toxic dose of MSG in a rat model of the disease. The model group of rats received a daily dose of MSG (4 gm/kg) for 7 days, whereas the protective groups were either received a 100 mg/kg vitamin E plus MSG or 300 mg/kg vitamin E plus MSG for 7 days. Rats were then sacrificed on day 8. Transmission and light microscopy images revealed substantial kidney damage induced by MSG in the model group as demonstrated by degenerated epithelial cells with Pyknotic nuclei, swollen mitochondria, damaged brush margins, dilated tubules, and widening of Bowman's space with shrinkage and deformity of some glomeruli. Treatment of the model group with vitamin E showed a substantial protection of kidney tissue and renal ultrastructure by 300 mg/kg vitamin E compared to a partial protection by 100 mg/kg vitamin E. In addition, MSG significantly (p<0.05) increased serum levels of urea and creatinine, which were significantly (p<0.05) decreased with vitamin E. However, for serum creatinine, high doses of vitamin E (300 mg/kg) were more effective than lower doses (100 mg/kg) of vitamin E. These results indicate that vitamin E at 300 mg/kg effectively protects against MSG-induced acute kidney injury in rats.


Los aditivos alimentarios y los potenciadores del sabor utilizados en la industria alimentaria son riesgos potenciales para la salud. Probamos la hipótesis de que el aditivo alimentario y el potenciador del sabor, glutamato monosódico (MSG), la sal sódica del ácido glutámico, puede inducir alteraciones ultraestructurales del riñón, y que las propiedades antioxidantes de la vitamina E, pueden proteger contra las lesiones renales inducidas por una dosis tóxica de MSG en un modelo de rata. El grupo modelo de ratas recibió una dosis diaria de MSG (4 g / kg) durante 7 días, mientras que los grupos protectores recibieron una dosis de 100 mg / kg de vitamina E más MSG o 300 mg / kg de vitamina E más MSG durante 7 días. Las ratas se sacrificaron el día 8. Las imágenes de microscopía óptica y de transmisión revelaron un daño renal sustancial inducido por el MSG en el grupo modelo, como lo demuestran las células epiteliales degeneradas con núcleos picnóticos, mitocondrias hinchadas, bordes dañados, túbulos dilatados y ensanchamiento del espacio de Bowman, además de la deformidad de algunos glomérulos. El tratamiento del grupo modelo con vitamina E mostró una protección sustancial del tejido renal y la ultraestructura renal de 300 mg / kg de vitamina E en comparación con una protección parcial de 100 mg / kg de vitamina E. Además, el MSG aumentó significativamente (p <0,05) en el suero los niveles de urea y creatinina, disminuyeron significativamente (p <0,05) con la vitamina E. Sin embargo, para la creatinina sérica, las dosis altas de vitamina E (300 mg / kg) fueron más efectivas que las dosis más bajas (100 mg / kg) de vitamina E. Estos resultados indican que la vitamina E a 300 mg / kg protege eficazmente contra la lesión renal aguda inducida por MSG en ratas.


Subject(s)
Animals , Rats , Sodium Glutamate/toxicity , Vitamin E/therapeutic use , Acute Kidney Injury/drug therapy , Vitamin E/pharmacology , Rats, Sprague-Dawley , Microscopy, Electron, Transmission , Disease Models, Animal , Acute Kidney Injury/chemically induced , Acute Kidney Injury/pathology , Kidney/pathology , Kidney/ultrastructure
11.
Int. j. morphol ; 37(4): 1422-1428, Dec. 2019. graf
Article in English | LILACS | ID: biblio-1040148

ABSTRACT

Paracetamol (also called acetaminophen, or APAP) overdose causes acute damage to the liver and kidneys in both humans and experimental animal models via the induction of the oxidative stress pathway. We sought to determine whether the combined antioxidants and anti-inflammatory compounds, resveratrol (RES) and quercetin (QUR) can protect against kidney injury induced by a toxic dose of APAP in a rat model of APAP-induced acute kidney injury. Rats were either received a single dose of APAP (2 g/kg) before being sacrificed after 24 hours or were pre-treated for 7 days with combined doses of RES (30 mg/kg) and QUR (50 mg/kg) before being given a single dose of APAP and then sacrificed 24 hours post APAP ingestion. Harvested kidney tissues were prepared for light microscopy staining, and tissue samples were assayed for (i) biomarkers of oxidative stress and antioxidant, malondialdehyde (MDA) and superoxide dismutase (SOD); and (ii) biomarkers of inflammation, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Hematoxylin and eosin (H&E) stained images showed that APAP overdose induced acute kidney injury as demonstrated by widening of glomeruli space (Bowman space), tubular dilatation, numerous cellular debris in the renal tubules with tubular epithelial degeneration, and vacuolization, which were effectively protected by RES+QUR except a partial protection of the glomeruli space was observed. In addition, APAP significantly (p<0.05) modulated tissue levels of MDA, SOD, TNF-α, and IL-6, which were protected by RES+QUR. Furthermore, a significant (p<0.0001) positive correlation was observed between glomeruli space and TNF-α, (r=0.8899), IL-6 (r=0.8986), and MDA (r=0.8552), whereas glomeruli space scoring versus SOD showed negative correlation (r= - 0.7870). We conclude that resveratrol plus quercetin substantially protects against APAP-induced acute kidney injury in rats, possibly via the augmentation of antioxidants and inhibition of oxidative stress and inflammation.


La sobredosis de paracetamol (también llamado acetaminofen o APAP) causa un daño agudo en el hígado y los riñones, tanto en humanos como en modelos animales experimentales, a través de la inducción de la vía del estrés oxidativo. Intentamos determinar si los antioxidantes y los compuestos antiinflamatorios combinados, el resveratrol (RES) y la quercetina (QUR) pueden proteger contra la lesión renal inducida por una dosis tóxica de APAP en un modelo de rata de lesión renal aguda inducida por APAP. Las ratas recibieron una dosis única de APAP (2 g / kg) antes de ser sacrificadas después de 24 horas o se trataron previamente durante 7 días con dosis combinadas de RES (30 mg / kg) y QUR (50 mg / kg), antes de ser tratadas, se administró una dosis única de APAP y luego fueron sacrificadas 24 horas después de la ingestión. Los tejidos renales recolectados se tiñeron con H-E y fueron observados a través de microscopía óptica. Las muestras de tejido se analizaron para (i) biomarcadores de estrés oxidativo y antioxidante, malondialdehído (MDA) y superóxido dismutasa (SOD); y (ii) biomarcadores de inflamación, factor de necrosis tumoral alfa (TNF-α) e interleucina-6 (IL-6). Las imágenes teñidas con H & E mostraron que la sobredosis de APAP indujo daño renal agudo como lo demuestra la ampliación del espacio glomerular, la dilatación tubular, numerosos desechos celulares en los túbulos renales con degeneración epitelial tubular y la vacuolización, que se protegieron eficazmente con RES + QUR Se observó una protección parcial del espacio glomerular. Además, APAP modificó significativamente (p <0.05) los niveles tisulares de MDA, SOD, TNF-α e IL-6, que estaban protegidos por RES + QUR. Además, se observó una correlación positiva significativa (p <0,0001) entre el espacio glomerular y el TNF-α, (r = 0,8899), IL-6 (r = 0,8986) y MDA (r = 0,8552), mientras que la puntuación del espacio glomerular versus SOD mostró correlación negativa (r = - 0,7870). Concluimos que el resveratrol más quercetina protege sustancialmente contra la lesión renal aguda inducida por APAP en ratas, posiblemente a través del aumento de antioxidantes y la inhibición del estrés oxidativo y la inflamación.


Subject(s)
Animals , Rats , Quercetin/therapeutic use , Acute Kidney Injury/drug therapy , Resveratrol/therapeutic use , Acetaminophen/toxicity , Quercetin/pharmacology , Oxidative Stress/drug effects , Disease Models, Animal , Drug Therapy, Combination , Acute Kidney Injury/chemically induced , Resveratrol/pharmacology , Acetaminophen/antagonists & inhibitors , Anti-Inflammatory Agents/therapeutic use , Antioxidants/therapeutic use
12.
Geriatr., Gerontol. Aging (Impr.) ; 13(3): 173-176, jul-set.2019. tab
Article in English, Portuguese | LILACS | ID: biblio-1097058

ABSTRACT

As aging progresses, there is a consequent increase in chronic diseases, such as osteoporosis and osteopenia, and vitamin D (cholecalciferol) supplementation is routinely prescribed. However, indiscriminate use of this supplement can lead to intoxication and systemic changes. Seeking to raise awareness among prescribing physicians and especially older patients, the purpose of this case report was to describe the systemic symptoms and damage that can occur from intoxication due to uncontrolled use of vitamin D, such as hypercalcemia and kidney injury. This report describes the case of an older woman who reported using a cholecalciferol- containing formula for ten years to treat osteoarthritis. She arrived at the hospital with weight loss, acute kidney injury and hypercalcemia. After ruling out neoplastic diseases, she was diagnosed with vitamin D poisoning. The symptoms and laboratory results improved after treatment. Based on this report, we conclude that geriatricians play a key role in demystifying the use of vitamins and should only prescribe them when medically indicated.


Com a progressão do envelhecimento e, consequentemente, o aumento de doenças crônicas, como osteoporose e osteopenia, a suplementação da vitamina D (colecalciferol) tem sido rotineiramente prescrita, no entanto o uso indiscriminado e o não controle dessa reposição podem levar à intoxicação e, consequentemente, a alterações sistêmicas. Buscando conscientizar médicos prescritores, e principalmente pacientes idosos, o objetivo do relato do caso foi de alertar sobre o uso desregrado e divulgar os diversos sintomas sistêmicos, além dos danos dessa intoxicação, como hipercalcemia e lesão renal. Este relato trata do caso de uma idosa que afirmava usar fórmula contendo colecalciferol há dez anos para tratar osteoartrite. Chegou ao hospital com emagrecimento, lesão renal aguda e hipercalcemia. Após descartar doenças neoplásicas, foi diagnosticada com intoxicação de vitamina D. Feito tratamento, houve remissão sintomatológica e laboratorial. Com base nesse relato, concluímos que o geriatra tem um papel fundamental de desmistificar o uso de vitaminas e prescrever estritamente quando há indicação médica.


Subject(s)
Humans , Female , Aged, 80 and over , Vitamin D/adverse effects , Vitamin D/toxicity , Hypercalcemia/complications , Self Medication/adverse effects , Acute Kidney Injury/chemically induced , Hypercalcemia/rehabilitation
13.
J. bras. nefrol ; 41(1): 124-130, Jan.-Mar. 2019. tab, graf
Article in English | LILACS | ID: biblio-1040238

ABSTRACT

Abstract Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used medications associated with nephrotoxicity, especially when used chronically. Factors such as advanced age and comorbidities, which in themselves already lead to a decrease in glomerular filtration rate, increase the risk of NSAID-related nephrotoxicity. The main mechanism of NSAID action is cyclooxygenase (COX) enzyme inhibition, interfering on arachidonic acid conversion into E2 prostaglandins E2, prostacyclins and thromboxanes. Within the kidneys, prostaglandins act as vasodilators, increasing renal perfusion. This vasodilatation is a counter regulation of mechanisms, such as the renin-angiotensin-aldosterone system works and that of the sympathetic nervous system, culminating with compensation to ensure adequate flow to the organ. NSAIDs inhibit this mechanism and can lead to acute kidney injury (AKI). High doses of NSAIDs have been implicated as causes of AKI, especially in the elderly. The main form of AKI by NSAIDs is hemodynamically mediated. The second form of NSAID-induced AKI is acute interstitial nephritis, which may manifest as nephrotic proteinuria. Long-term NSAID use can lead to chronic kidney disease (CKD). In patients without renal diseases, young and without comorbidities, NSAIDs are not greatly harmful. However, because of its dose-dependent effect, caution should be exercised in chronic use, since it increases the risk of developing nephrotoxicity.


Resumo Os anti-inflamatórios não esteroidais (AINEs) são medicamentos comumente utilizados, associados à nefrotoxicidade, sobretudo quando utilizados cronicamente. Fatores como idade avançada e comorbidades, que por si só já levam à diminuição da taxa de filtração glomerular, aumentam o risco de nefrotoxicidade dos AINEs. O principal mecanismo de ação dos AINEs é a inibição da enzima ciclooxigenase (COX), interferindo na conversão do ácido araquidônico em prostaglandinas E2, prostaciclinas e tromboxanos. Nos rins, as prostaglandinas atuam como vasodilatadoras, aumentando a perfusão renal. Essa vasodilatação atua como uma contrarregulação de mecanismos, como a atuação do sistema renina-angiotensina-aldosterona e do sistema nervoso simpático, culminando com uma compensação para assegurar o fluxo adequado ao órgão. O uso de AINEs inibe esse mecanismo, podendo causar lesão renal aguda (LRA). Altas doses de AINEs têm sido implicadas como causas de LRA, especialmente em idosos. A principal forma de LRA por AINEs é a hemodinamicamente mediada. A segunda forma de apresentação da LRA induzida por AINES é a nefrite intersticial aguda, que pode se manifestar com proteinúria nefrótica. O uso de AINEs em longo prazo pode ocasionar doença renal crônica (DRC). Nos pacientes sem doenças renais, jovens e sem comorbidades, os AINEs não apresentam grandes malefícios. Entretanto, por seu efeito dose-dependente, deve-se ter grande cautela no uso crônico, por aumentar risco de desenvolver nefrotoxicidade.


Subject(s)
Humans , Infant, Newborn , Aged , Aged, 80 and over , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Cyclooxygenase Inhibitors/adverse effects , Renal Insufficiency, Chronic/chemically induced , Acute Kidney Injury/chemically induced , Nephritis, Interstitial/chemically induced , Prostaglandins E/metabolism , Proteinuria/chemically induced , Anti-Inflammatory Agents, Non-Steroidal/metabolism , Risk Factors , Cyclooxygenase Inhibitors/metabolism , Renal Insufficiency, Chronic/physiopathology , Acute Kidney Injury/physiopathology , Nephritis, Interstitial/physiopathology
14.
Clin. biomed. res ; 39(1): 1-8, 2019.
Article in Portuguese | LILACS | ID: biblio-1025955

ABSTRACT

Introdução: Exames diagnósticos contrastados oferecem riscos para o desenvolvimento de Insuficiência Renal Aguda pós-contraste (IRA-PC), principalmente em pacientes com doença renal prévia. O objetivo deste estudo foi verificar se a função renal foi avaliada antes e após a realização de exame contrastado. Métodos: Coorte retrospectiva com 2778 pacientes que realizaram tomografia computadorizada (TC) contrastada em que foi verificada a creatinina sérica (CrS) pré e pós-exame, presença de fatores de risco, incidência de IRA-PC e óbito até 10 meses pós-TC. Resultados: Somente 263 (9,5%) apresentaram avaliação da função renal pré e pós-exame dentro dos prazos estabelecidos (7 dias para pacientes internados e 180 dias para ambulatoriais pré-exame, e 48 a 72 horas pós-exame), sendo que 91,6% eram de pacientes internados. IRA-PC foi observada em 38 (14,4%) pacientes e foi associada ao uso de medicamentos nefrotóxicos (Odds Ratio 1,645; IC95%: 1,138­2,390) e maior risco de óbito pós-exame (Razão de Incidência 1,84; IC95%:1,17-2,83). Conclusão: A grande maioria dos pacientes não apresentava adequada avaliação da função renal pré e pós-TC, principalmente em nível ambulatorial. Sugere-se o estabelecimento de medidas educativas para promover a aderência do corpo clínico à avaliação da função renal para pacientes de risco para IRA-PC. (AU)


Introduction: Contrast-enhanced diagnostic tests involve risks for the development of post-contrast acute kidney injury (PC-AKI), especially in patients with previous renal disease. The aim of this study was to investigate whether renal function was evaluated before and after the contrast-enhanced test. Methods: In this retrospective cohort of 2778 patients who underwent contrast-enhanced computed tomography (CT), pre- and post-CT serum creatinine (SCr), presence of risk factors, incidence of PC-AKI, and death within 10 months post-CT were investigated. Results: Only 263 (9.5%) patients had pre- and post-CT renal function evaluation performed within the established time frames (7 days for inpatients and 180 days for outpatients pre-CT and 48 to 72 hours post-CT), with 91.6% being inpatients. PC-AKI was observed in 38 (14.4%) patients and was associated with use of nephrotoxic drugs (odds ratio: 1.645, 95% CI: 1.138-2.390) and higher risk of death post-CT (incidence ratio: 1.84; 95% CI: 1.17-2.83). Conclusion: The vast majority of patients did not undergo an adequate pre- and post-CT renal function evaluation, especially at the outpatient level. Educational measures should be developed to promote adherence of clinical staff to renal function evaluation for patients at risk for PC-AKI. (AU)


Subject(s)
Humans , Male , Female , Adolescent , Adult , Middle Aged , Aged , Aged, 80 and over , Tomography, X-Ray Computed/adverse effects , Acute Kidney Injury/chemically induced , Tomography, X-Ray Computed/mortality , Risk Factors , Acute Kidney Injury/epidemiology
15.
Braz. j. infect. dis ; 22(1): 51-54, Jan.-feb. 2018. tab, graf
Article in English | SES-SP, LILACS, SES-SP, SESSP-IDPCPROD, SES-SP | ID: biblio-1039210

ABSTRACT

ABSTRACT A retrospective cohort study, were evaluated: polymyxin B plus aminoglycosides or polymyxin B plus other antibiotics. Any degree of acute kidney injury occurred in 26 (86.6%) patients. The median time to acute kidney injury was 6.0 (95% CI 3-14) days in the polymyxin-aminoglycoside containing regimen group, against 27.0 (95% CI 6-42) days in the polymyxin with other antimicrobial combinations group (p = 0.03). Polymyxin B with aminoglycosides group progressed faster to any degree of renal dysfunction.


Subject(s)
Humans , Male , Female , Polymyxin B/therapeutic use , Enterobacteriaceae Infections/drug therapy , Kidney/drug effects , Mediastinitis/microbiology , Mediastinitis/drug therapy , Anti-Bacterial Agents/therapeutic use , Microbial Sensitivity Tests , Carbapenems/pharmacology , Retrospective Studies , Treatment Outcome , Statistics, Nonparametric , Risk Assessment , beta-Lactam Resistance/drug effects , Enterobacteriaceae Infections/mortality , Kaplan-Meier Estimate , Acute Kidney Injury/chemically induced , Aminoglycosides/therapeutic use , Mediastinitis/mortality
16.
Yonsei Medical Journal ; : 107-112, 2018.
Article in English | WPRIM | ID: wpr-742497

ABSTRACT

PURPOSE: Contrast-induced acute kidney injury (CI-AKI) is associated with poor outcomes after percutaneous coronary intervention. However, CI-AKI has rarely been evaluated within the neurovascular field. The aim of this study was to investigate the incidence and clinical implication of CI-AKI after coil embolization in patients with an aneurysmal subarachnoid hemorrhage (aSAH). MATERIALS AND METHODS: Between January 2005 and March 2016, 192 patients who underwent coil embolization were enrolled in this study. CI-AKI was defined as an increase from baseline serum creatinine concentration of >25% or >0.5 mg/dL within 72 hours after coil embolization. A poor clinical outcome was defined as a score of ≥3 on the modified Rankin Scale at one-year post-treatment. RESULTS: A total of 16 patients (8.3%) died as a result of medical problems within one year. CI-AKI was identified in 14 patients (7.3%). Prominent risk factors for one-year mortality included CI-AKI [odds ratio (OR): 16.856; 95% confidence interval (CI): 3.437–82.664] and an initial Glasgow Coma Scale (GCS) score ≤8 (OR: 5.565; 95% CI: 1.703–18.184). A poor clinical outcome was associated with old age (≥65 years) (OR: 7.921; 95% CI: 2.977–21.076), CI-AKI (OR: 11.281; 95% CI: 2.138–59.525), an initial GCS score ≤8 (OR 31.02; 95% CI, 10.669–90.187), and a ruptured aneurysm (p=0.016, OR: 4.278) in posterior circulation. CONCLUSION: CI-AKI seems to be an independent predictor of the overall outcomes of aSAH after endovascular treatment.


Subject(s)
Acute Kidney Injury/chemically induced , Acute Kidney Injury/diagnostic imaging , Acute Kidney Injury/etiology , Acute Kidney Injury/mortality , Adult , Aged , Aged, 80 and over , Aneurysm/complications , Aneurysm/diagnostic imaging , Aneurysm/therapy , Angiography , Contrast Media/adverse effects , Embolization, Therapeutic/adverse effects , Female , Humans , Incidence , Male , Middle Aged , Subarachnoid Hemorrhage/complications , Subarachnoid Hemorrhage/diagnostic imaging , Subarachnoid Hemorrhage/therapy , Treatment Outcome , Young Adult
17.
Braz. j. med. biol. res ; 51(2): e6373, 2018. tab, graf
Article in English | LILACS | ID: biblio-889016

ABSTRACT

Cyclosporin-A (CsA) is an immunosuppressant associated with acute kidney injury and chronic kidney disease. Nephrotoxicity associated with CsA involves the increase in afferent and efferent arteriole resistance, decreased renal blood flow (RBF) and glomerular filtration. The aim of this study was to evaluate the effect of Endothelin-1 (ET-1) receptor blockade with bosentan (BOS) and macitentan (MAC) antagonists on altered renal function induced by CsA in normotensive and hypertensive animals. Wistar and genetically hypertensive rats (SHR) were separated into control group, CsA group that received intraperitoneal injections of CsA (40 mg/kg) for 15 days, CsA+BOS and CsA+MAC that received CsA and BOS (5 mg/kg) or MAC (25 mg/kg) by gavage for 15 days. Plasma creatinine and urea, mean arterial pressure (MAP), RBF and renal vascular resistance (RVR), and immunohistochemistry for ET-1 in the kidney cortex were measured. CsA decreased renal function, as shown by increased creatinine and urea. There was a decrease in RBF and an increase in MAP and RVR in normotensive and hypertensive animals. These effects were partially reversed by ET-1 antagonists, especially in SHR where increased ET-1 production was observed in the kidney. Most MAC effects were similar to BOS, but BOS seemed to be better at reversing cyclosporine-induced changes in renal function in hypertensive animals. The results of this work suggested the direct participation of ET-1 in renal hemodynamics changes induced by cyclosporin in normotensive and hypertensive rats. The antagonists of ET-1 MAC and BOS reversed part of these effects.


Subject(s)
Animals , Male , Pyrimidines/pharmacology , Cyclosporine/toxicity , Acute Kidney Injury/chemically induced , Acute Kidney Injury/prevention & control , Endothelin Receptor Antagonists/pharmacology , Immunosuppressive Agents/toxicity , Urea/blood , Immunohistochemistry , Immunoblotting , Reproducibility of Results , Rats, Wistar , Creatinine/blood , Acute Kidney Injury/physiopathology , Endothelin Receptor Antagonists/therapeutic use , Bosentan , Hemodynamics , Kidney/drug effects
18.
Braz. j. med. biol. res ; 51(4): e6487, 2018. tab, graf
Article in English | LILACS | ID: biblio-889057

ABSTRACT

Contrast-induced acute kidney injury (CI-AKI) is a serious complication of diagnostic coronary angiograph and percutaneous coronary intervention (PCI). However, the exact pathophysiological mechanisms underlying CI-AKI development are largely unknown. The present study examined whether urinary semaphorin 3A levels predict the development of CI-AKI in patients undergoing PCI. This study enrolled 168 patients with stable angina undergoing elective PCI. Serial urine samples, obtained at baseline and 2, 6, 12, 24, 36, and 48 h post-PCI were analyzed by semaphorin 3A and neutrophil gelatinase-associated lipocalin (NGAL) ELISA kit. AKI was defined as an increase in serum creatinine beyond 50% according to the RIFLE classification system. Receiver operator characteristic (ROC) curve analyses identified optimal semaphorin 3A and NGAL values for diagnosing CI-AKI. CI-AKI occurred in 20 of 168 patients. There were no significant differences in the baseline clinical characteristics and angiographic findings between non-AKI patients group and AKI patients group. Both urinary semaphorin 3A and NGAL levels significantly increased at 2 and 6 h post-PCI. ROC analysis showed that the cut-off value of 389.5 pg/mg semaphorin 3A at 2 h post-PCI corresponds to 94% sensitivity and 75% specificity and the cut-off value of 94.4 ng/mg NGAL at 2 h post-PCI corresponds to 74% sensitivity and 82% specificity. Logistic regression showed that semaphorin 3A levels at 2 and 6 h post-PCI were the significant predictors of AKI in our cohort. Urinary semaphorin 3A may be a promising early biomarker for predicting CI-AKI in patients undergoing PCI.


Subject(s)
Humans , Male , Female , Middle Aged , Contrast Media/adverse effects , Semaphorin-3A/urine , Acute Kidney Injury/chemically induced , Acute Kidney Injury/urine , Percutaneous Coronary Intervention/adverse effects , Biomarkers/urine , Predictive Value of Tests , ROC Curve , Acute Kidney Injury/diagnosis
19.
Biol. Res ; 51: 31, 2018. graf
Article in English | LILACS | ID: biblio-983936

ABSTRACT

BACKGROUND: miR-214 was demonstrated to be upregulated in models of renal disease and promoted fibrosis in renal injury independent of TGF-ß signaling in vivo. However, the detailed role of miR-214 in acute kidney injury (AKI) and its underlying mechanism are still largely unknown. METHODS: In this study, an I/R-induced rat AKI model and a hypoxia-induced NRK-52E cell model were used to study AKI. The concentrations of kidney injury markers serum creatinine, blood urea nitrogen, and kidney injury molecule-1 were measured. The expressions of miR-214, tumor necrosis factor-α, interleukin (IL)-1ß, IL-6, were detected by RT-qPCR. The protein levels of Bcl-2, Bax, Dickkopf-related protein 3, ß-catenin, c-myc, and cyclinD1 were determined by western blot. Cell apoptosis and caspase 3 activity were evaluated by flow cytometry analysis and caspase 3 activity assay, respectively. Luciferase reporter assay was used to confirm the interaction between miR-214 and Dkk3. RESULTS: miR-214 expression was induced in ischemia-reperfusion (I/R)-induced AKI rat and hypoxic incubation of NRK-52E cells. Overexpression of miR-214 alleviated hypoxia-induced NRK-52E cell apoptosis while inhibition of miR-214 expression exerted the opposite effect. Dkk3 was identified as a target of miR-214. Anti-miR-214 abolished the inhibitory effects of DKK3 knockdown on hypoxia-induced NRK-52E cell apoptosis by inactivation of Wnt/ß-catenin signaling. Moreover, miR-214 ameliorated AKI in vivo by inhibiting apoptosis and fibrosis through targeting Dkk3 and activating Wnt/ß -catenin pathway. CONCLUSION: miR-214 ameliorates AKI by inhibiting apoptosis through targeting Dkk3 and activating Wnt/ß -catenin signaling pathway, offering the possibility of miR-214 in the therapy of ischemic AKI.


Subject(s)
Animals , Male , Rats , Intercellular Signaling Peptides and Proteins/metabolism , MicroRNAs/metabolism , Catenins/metabolism , Acute Kidney Injury/metabolism , Wnt Signaling Pathway/genetics , Rats, Sprague-Dawley , Chemokines , Intercellular Signaling Peptides and Proteins/genetics , MicroRNAs/genetics , Adaptor Proteins, Signal Transducing , Cell Proliferation , Disease Models, Animal , Catenins/genetics , Acute Kidney Injury/chemically induced
20.
J. bras. nefrol ; 39(4): 467-469, Oct.-Dec. 2017.
Article in English | LILACS | ID: biblio-893796

ABSTRACT

Abstract A previously healthy 24 yo male presented with a two-month history of epigastric pain, nausea, vomiting, fatigue and malaise. He reported abuse of different substances, including an injectable veterinary vitamin compound, which contains high doses of vitamin A, D and E, and an oily vehicle that induces local edema and enhances muscle volume. Serum creatinine was 3.1 mg/dL, alanine transaminase 160 mg/dL, aspartate transaminase 11 mg/dL, total testosterone 23 ng/dL, 25-OH-vitamin D >150 ng/mL (toxicity >100), 1,25-OH-vitamin D 80 pg/mL, vitamin A 0.7 mg/dL, parathormone <3 pg/mL, total calcium 13.6 mg/dL, 24-hour urinary calcium 635 mg/24h (RV 42-353). A urinary tract ultrasound demonstrated signs of parenchymal nephropathy. The diagnosis was hypercalcemia and acute renal failure secondary to vitamin D intoxication. He was initially treated with intravenous hydration, furosemide and prednisone. On the fifth day of hospitalization a dose of pamidronate disodium was added. The patient evolved with serum calcium and renal function normalization. Thirty days later he presented normal clinical and laboratory tests, except 25-OH-vitamin D that was persistently increased (107 ng/mL), as it may take several months to normalize. This case report is a warning of the risks related to the use of veterinary substances for aesthetics purposes.


Resumo Um paciente de 24 anos do sexo masculino, previamente hígido, apresentou-se com uma história de dois meses de dor epigástrica, náuseas, vômitos, fadiga e mal-estar. Ele relatava abuso de diferentes substâncias, incluindo um composto vitamínico veterinário injetável contendo altas doses de vitamina A, D e E, e um veículo oleoso que induz edema local com aumento de volume muscular. A creatinina sérica estava 3,1 mg/dL, alanina transaminase 160 mg/dL, aspartato transaminase 11 mg/dL, testosterona total 23 ng/dL, 25-OH-vitamina D > 150 ng/mL (toxicidade > 100), 1,25-OH-vitamina D 80 pg/mL, vitamina A 0,7 mg/dL, paratormônio < 3 pg/mL, cálcio total 13,6 mg/dL, cálcio urinário de 24h 635 mg/24h (VR 42-353). Uma ultrassonografia do trato urinário demonstrou sinais de nefropatia parenquimatosa. O diagnóstico foi hipercalcemia e insuficiência renal aguda secundária a intoxicação por vitamina D. Ele foi tratado inicialmente com hidratação intravenosa, furosemida e prednisona. No quinto dia de hospitalização uma dose de pamidronato dissódico foi adicionada. O paciente evoluiu com normalização do cálcio sérico e da função renal. Trinta dias depois ele apresentou testes clínicos e laboratoriais normais, exceto a 25-OH-vitamina D que estava persistentemente elevada (107 ng/mL), já que ela pode demorar vários meses para normalizar. Este relato de caso é um alerta aos riscos relacionados ao uso de substâncias veterinárias para fins estéticos.


Subject(s)
Humans , Male , Young Adult , Vitamin A/adverse effects , Vitamin D/adverse effects , Vitamin E/adverse effects , Veterinary Drugs/adverse effects , Acute Kidney Injury/chemically induced , Hypercalcemia/chemically induced , Vitamins/adverse effects , Acute Kidney Injury/complications , Hypercalcemia/complications
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