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1.
Nephron Clin Pract ; 108(1): c56-66, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-18097149

RESUMO

BACKGROUND: The established risk factors for atherosclerotic renal artery stenosis (ARAS) include hypertension, diabetes mellitus, dyslipidemia, obesity, smoking, old age and family history. In the last few years, several emerging risk factors have been proposed as predictors of ARAS, namely homocysteine, fibrinogen, C-reactive protein, lipoprotein(a) and creatinine. METHODS: We searched Pubmed/Medline for studies investigating the prognostic value of each of these emerging risk factors in ARAS. RESULTS: Creatinine and C-reactive protein seem to be the most promising predictors of ARAS, whereas the prognostic value of homocysteine, lipoprotein(a) and fibrinogen is not yet fully determined. CONCLUSION: The establishment of a definite role for these emerging risk factors could result in earlier recognition and/or better management of ARAS with potential regression/slowing down of progression of stenosis. Modifying these markers may also improve the therapeutic approach of the associated systemic atherosclerosis in these high-risk patients. Future trials should focus on the effect of different classes of drugs (e.g. statins and fibrates) on the levels of the emerging risk factors and the association with ARAS progression.


Assuntos
Aterosclerose/sangue , Aterosclerose/complicações , Obstrução da Artéria Renal/sangue , Obstrução da Artéria Renal/complicações , Proteína C-Reativa/metabolismo , Homocisteína/sangue , Humanos , Doenças Vasculares Periféricas/sangue , Doenças Vasculares Periféricas/complicações , Fatores de Risco
3.
Kidney Int ; 63(4): 1433-42, 2003 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-12631359

RESUMO

BACKGROUND: Chronic renal failure is associated with impaired endothelium-dependent vasodilation and accelerated atherogenesis. To examine whether endogenous reactive oxygen species (ROS) modify endothelial function in renal failure, we evaluated the effect of the antioxidant vitamin C on endothelium-dependent responses in both the conduit and resistance vasculature of subjects with severe renal impairment. METHODS: Endothelial function of the forearm resistance vasculature was assessed using plethysmography to measure the dilator response to intra-arterial acetylcholine (Ach) (25 to 100 nmol/min). Endothelial function of radial and brachial arteries was assessed using vascular ultrasound to measure the dilator response to flow during reactive hyperemia [flow-mediated dilatation (FMD)]. Studies were performed before and after administration of vitamin C by intra-arterial infusion (25 mg/min) in 33 predialysis patients or by intravenous infusion (3 g) in 17 hemodialysis patients. RESULTS: Parenteral administration of vitamin C resulted in a 100-fold increase (intra-arterial studies) and a 4.5-fold increase (intravenous studies) in serum antioxidant activity. Vitamin C administration increased the dilator response to ACh in resistance vessels (P = 0.01), but did not alter the dilator response to flow in conduit vessels of either dialysis (P = 0.3) or predialysis subjects (P = 0.8). In the presence of the nitric oxide (NO) synthase inhibitor NGmonomethyl-L-arginine (L-NMMA), there was no effect of vitamin C on resistance vessel endothelial function. In all cases the dilator response to the endothelium-independent dilators was unaffected by vitamin C. CONCLUSION: Acute administration of vitamin C reduces oxidant stress in renal failure and improves NO-mediated resistance vessel dilatation.


Assuntos
Antioxidantes/administração & dosagem , Ácido Ascórbico/administração & dosagem , Endotélio Vascular/fisiologia , Falência Renal Crônica/tratamento farmacológico , Falência Renal Crônica/fisiopatologia , Resistência Vascular/efeitos dos fármacos , Adulto , Biomarcadores , Artéria Braquial/fisiologia , Endotélio Vascular/efeitos dos fármacos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Óxido Nítrico/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Artéria Radial/fisiologia , Diálise Renal , Vasodilatação/efeitos dos fármacos
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