Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros










Intervalo de ano de publicação
1.
Kidney Int ; 65(4): 1224-30, 2004 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15086461

RESUMO

BACKGROUND: Metabolic acidosis is a consequence of chronic renal failure and it may produce bone demineralization, muscle proteolysis, and progression of chronic renal failure. The aim of this study was to evaluate the effects of correction of metabolic acidosis with calcium citrate in an experimental model of renal mass ablation. METHODS: Wistar rats were subjected to 5/6 nephrectomy and were randomly assigned to one of 4 groups: nontreated (NFX); treated with calcium citrate (1.45 g/100 g feed) (NFX-CIT); treated with captopril (500 mg/L water) (NFX-CAP); or treated with both (NFX-CAP-CIT) during 1, 10, or 20 weeks. Body weight, systolic blood pressure, proteinuria, arterial bicarbonate concentration, urine citrate excretion, plasma calcium, and inulin clearance were measured. Histologic glomerular and tubulointerstitial damage scores were measured at 1, 10, and 20 weeks, and glomerular and tubular proliferating cell nuclear antigen (PCNA)-positive cells, alpha-smooth muscle actin, and desmin staining were studied by immunohistochemistry at 1 and 10 weeks. RESULTS: The treated groups showed significantly less glomerular and tubulointerstitial cellular proliferation in the first week (P < 0.05), less glomerular cell transdifferentiation and higher plasma bicarbonate at 10 weeks (P < 0.05), as well as diminished histologic glomerular and tubulointerstitial damage scores at 20 weeks (P < 0.05). Inulin clearances were higher (P < 0.05), and urine protein excretion rates were lower (P < 0.05) than in the NFX non-treated group, but arterial blood pressure was not significantly different in the NFX-CIT group. CONCLUSION: Calcium citrate slows the progression of chronic renal injury in the 5/6 NFX model. It improves metabolic acidosis and diminishes cell proliferation and transdifferentiation without changes in systolic blood pressure.


Assuntos
Álcalis/farmacologia , Citrato de Cálcio/farmacologia , Falência Renal Crônica/fisiopatologia , Animais , Bicarbonatos/sangue , Captopril/farmacologia , Divisão Celular , Progressão da Doença , Combinação de Medicamentos , Imuno-Histoquímica , Inulina/metabolismo , Rim/metabolismo , Rim/patologia , Falência Renal Crônica/metabolismo , Falência Renal Crônica/patologia , Falência Renal Crônica/urina , Glomérulos Renais/patologia , Túbulos Renais/patologia , Masculino , Nefrectomia , Proteinúria/etiologia , Proteinúria/urina , Distribuição Aleatória , Ratos , Ratos Wistar
2.
Arch. med. interna (Montevideo) ; 23(1): 11-21, mar. 2001. ilus, tab
Artigo em Espanhol | LILACS | ID: lil-332762

RESUMO

El compromiso túbulointersticial en las nefropatías es uno de los mecanismos responsables de la progresión a la insuficiencia renal extrema. Las pruebas funcionales renales pueden ser un instrumento útil para el diagnóstico y el seguimiento de este compromiso tubulointersticial. Los objetivos de este trabajo son evaluar un conjunto simplificado de pruebas de función tubular en el estudio de nefropatías tubulointersticiales y en glomerulopatías. Se estudiaron 75 pacientes, 38 con diagnóstico probable de nefropatía tubulointeristicial y 37 glomerulopatías. Se evaluó presencia de diskalemia, glucosurina, alteración de equilibrio ácido base y capacidad de concentración urinaria. La disfunción tubular fue frecuente en los pacientes con glomerulopatías (0,65) aún en aquellos pacientes con creatininemia menor 1.4 mg por ciento (0,45). Mediante estas pruebas es posible topografiar el sector nefronal comprometido


Assuntos
Humanos , Nefropatias , Testes de Função Renal , Túbulos Renais/fisiopatologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...