Renal functional reserve (RFR) is the capacity of the kidney to increase its glomerular filtration rate (GFR) in response to physiological or pathological stimuli. The most commonly used stimuli to assess this reserve are an oral load of proteins of animal origin, amino acid infusions, dopamine, glucagon...
SUMMARY OBJECTIVE Diabetes is a risk factor for acute kidney injury (AKI). However, its mechanism of pathogenesis has not been elucidated. The aim of the study was to investigate the role of inflammation and the toll-like receptor 7 (TLR7) in ischemic AKI for diabetes. METHODS A high glucose hypoxia-...
Lesión Renal Aguda/metabolismo,
Lesión Renal Aguda/fisiopatología,
Células Cultivadas,
Diabetes Mellitus/metabolismo,
Diabetes Mellitus/fisiopatología,
Citometría de Flujo,
Isquemia/metabolismo,
Isquemia/fisiopatología,
ARN Interferente Pequeño,
Transducción de Señal,
Receptor Toll-Like 7/metabolismo,
Receptor Toll-Like 7/fisiología,
Transfección
Abstract Purpose To investigate the role and related mechanisms of miR-106a in sepsis-induced AKI. Methods Serum from sepsis and healthy patients was collected, sepsis mouse model was established by cecal ligation and puncture (CLP). TCMK-1 cells were treated with lipopolysaccharide (LPS) and transfe...
Lesión Renal Aguda/metabolismo,
Lesión Renal Aguda/patología,
Apoptosis,
Estudios de Casos y Controles,
Células Cultivadas,
Citocinas/metabolismo,
Modelos Animales de Enfermedad,
Ensayo de Inmunoadsorción Enzimática,
Células Epiteliales/patología,
Riñón/citología,
MicroARNs/metabolismo,
Reacción en Cadena en Tiempo Real de la Polimerasa,
Sepsis/metabolismo,
Sepsis/patología,
Trombospondinas/farmacología,
Transfección
BACKGROUND: Acute kidney injury (AKI), which is mainly caused by sepsis, has high morbidity and mortality rates. CXCL8(3-72) K11R/G31P (G31P) can exert therapeutic effect on inflammatory diseases and malignancies. We aimed to investigate the effect and mechanism of G31P on septic AKI. METHODS: An AKI mou...
Lesión Renal Aguda/etiología,
Janus Quinasa 2/metabolismo,
FN-kappa B/metabolismo,
Factor de Transcripción STAT3/metabolismo,
Sepsis/complicaciones,
Lesión Renal Aguda/metabolismo,
Lesión Renal Aguda/patología,
Sepsis/patología,
Apoptosis,
Modelos Animales de Enfermedad,
Ratones Endogámicos C57BL,
Transducción de Señal
Abstract Sepsis is the most common cause of death in critically ill patients and it may be associated with multiorgan failure, including acute kidney injury (AKI). This situation can require acute renal support and increase mortality. Therefore, it is essential to administrate antimicrobials in dosis to ...
Abstract Introduction: It is needed for nutrition prescription correct estimate of resting energy expenditure (REE), which is a challenge given the possible daily variation in critically ill patients with acute kidney injury (AKI). Objective: To evaluate the daily variability of REE measured by indirec...
Summary Patients on intensive care present systemic, metabolic, and hormonal alterations that may adversely affect their nutritional condition and lead to fast and important depletion of lean mass and malnutrition. Several factors and medical conditions can influence the energy expenditure (EE) of critic...
ABSTRACT PURPOSE: To determine whether Toll-like receptor 7 (TLR7) is the potential targets of prevention or progression in the renal ischemia/reperfusion (I/R) injury of STZ-induced diabetic rats. METHODS: Thirty six Sprague-Dawley rats were randomly arranged to the nondiabetic (ND) or diabetic group ...
Lesión Renal Aguda/metabolismo,
Diabetes Mellitus Experimental/metabolismo,
Riñón/metabolismo,
Daño por Reperfusión/metabolismo,
Receptor Toll-Like 7/metabolismo,
Lesión Renal Aguda/patología,
Apoptosis,
Diabetes Mellitus Experimental/complicaciones,
Modelos Animales de Enfermedad,
Etiquetado Corte-Fin in Situ/métodos,
Riñón/patología,
Factor 88 de Diferenciación Mieloide/metabolismo,
FN-kappa B/metabolismo,
Distribución Aleatoria,
Ratas Sprague-Dawley,
Daño por Reperfusión/complicaciones,
Receptor Toll-Like 7/sangre
RESUMO Introdução: Priming é um mecanismo de proteção induzida pela exposição anterior de uma célula ou órgão a baixas ou mesmas concentrações de uma substância tóxica. Objetivo: analisar o mecanismo de priming induzido pela exposição a gentamicina em células tubulares proximais humana...
