12 resultados para Cystatin C

em Repositório Institucional UNESP - Universidade Estadual Paulista "Julio de Mesquita Filho"


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OBJECTIVE: Pneumoperitoneum during laparoscopy results in transient oliguria and decreased glomerular filtration and renal blood flow. The presence of oliguria and elevated serum creatinine is suggestive of acute renal injury. Serum cystatin C has been described as a new marker for the detection of this type of injury. In this study, our aim was to compare the glomerular filtration rate estimated using cystatin C levels with the rate estimated using serum creatinine in patients with normal renal function who were undergoing laparoscopic surgery. METHODS: In total, 41 patients undergoing laparoscopic cholecystectomy or hiatoplasty were recruited for the study. Blood samples were collected at three time intervals: first, before intubation (T1); second, 30 minutes after the establishment of pneumoperitoneum (T2); and third, 30 minutes after deflation of the pneumoperitoneum (T3). These blood samples were then analyzed for serum cystatin C, creatinine, and vasopressin. The Larsson formula was used to calculate the glomerular filtration rate based on the serum cystatin C levels, and the Cockcroft-Gault formula was used to calculate the glomerular filtration rate according to the serum creatinine levels. RESULTS: Serum cystatin C levels increased during the study (T1 = T2creatinine levels decreased (T1 = T2>T3; p<0.05). The calculated eGlomerular filtration rate-Larsson decreased, whereas the eGlomerular filtration rate-Cockcroft-Gault increased. There was no correlation between cystatin C and serum creatinine. Additionally, Pearson's analysis showed a better correlation between serum cystatin C and the eGlomerular filtration rate than between serum creatinine and the eGlomerular filtration rate. CONCLUSION: This study demonstrates that serum cystatin C is a more sensitive indicator of changes in the glomerular filtration rate than serum creatinine is in patients with normal renal function who are undergoing laparoscopic procedures.

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OBJETIVO: Avaliar a cistatina C como marcador de função renal em pacientes submetidos à cirurgia de cardíaca com circulação extracorpórea, comparando com a dosagem sérica de creatinina. MÉTODOS: Foram analisados 50 pacientes consecutivos submetidos à cirurgia de revascularização do miocárdio. A função renal foi avaliada com a dosagem sérica de cistatina C e de creatinina no pré-operatório, no primeiro e no quinto dia de pós-operatório. Foram utilizadas as fórmulas de Cockcroft-Gault (CG) e Modification of Diet in Renal Disease (MDRD) para calcular a taxa de filtração glomerular estimada (TFG) através da creatinina, e a fórmula de Larsson para a TFG estimada através da cistatina C (TFG-Cis). RESULTADOS: A creatinina e o TFG através das fórmulas de CG e MDRD não mostraram diferença significativa nos momentos estudados. Após a agressão renal pela cirurgia, houve um aumento da cistatina C no 1º e 5º pós-operatório, sendo que no 5º pós-operatório com diferença estatisticamente significativa (P < 0,01). Houve uma queda da TFG estimada pela cistatina C de 105,2 ± 41,0 ml/min, no pré-operatório, para 89,5 ± 31,5 ml/min no 5º dia pós-operatório (P < 0,012). CONCLUSÃO: A cistatina C e a TFG-Cis apresentaram mudanças significativas no pós-operatório de cirurgia de revascularização do miocárdio quando comparadas a creatinina e a respectiva TFG estimada pelas fórmulas de Cockcroft-Gault e MDRD

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Pós-graduação em Bases Gerais da Cirurgia - FMB

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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The cysteine proteinase inhibitor cystatin C inhibited RANKL-stimulated osteoclast formation in mouse bone marrow macrophage cultures, an effect associated with decreased mRNA expression of Acp5, Calcr, Ctsk, Mmp9, Itgb3, and Atp6i, without effect on proliferation or apoptosis. The effects were concentration dependent with half-maximal inhibition at 0.3 μM. Cystatin C also inhibited osteoclast formation when RANKL-stimulated osteoclasts were cultured on bone, leading to decreased formation of resorption pits. RANKL-stimulated cells retained characteristics of phagocytotic macrophages when cotreated with cystatin C. Three other cysteine proteinase inhibitors, cystatin D, Z-RLVG-CHN2 (IC50 0.1 μM), and E-64 (IC 50 3 μM), also inhibited osteoclast formation in RANKL-stimulated macrophages. In addition, cystatin C, Z-RLVG-CHN2, and E-64 inhibited osteoclastic differentiation of RANKL-stimulated CD14+ human monocytes. The effect by cystatin C on differentiation of bone marrow macrophages was exerted at an early stage after RANKL stimulation and was associated with early (4 h) inhibition of c-Fos expression and decreased protein and nuclear translocation of c-Fos. Subsequently, p52, p65, IκBα, and Nfatc1 mRNA were decreased. Cystatin C was internalized in osteoclast progenitors, a process requiring RANKL stimulation. These data show that cystatin C inhibits osteoclast differentiation and formation by interfering intracellularly with signaling pathways downstream RANK. © FASEB.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)