2008
DOI: 10.1016/j.lpm.2007.10.013
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Hépatites virales chroniques chez les patients insuffisants rénaux

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Cited by 4 publications
(2 citation statements)
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“…In the present study, the risk estimates of death due to intracerebral haemorrhage did not change materially after adjusting for the presence of chronic hepatitis or cirrhosis at baseline, suggesting that advanced liver damage might not be the causal intermediate between HBV infection and intracerebral haemorrhage. HBV-induced proinflammatory effect25 and steatosis,26 further leading to endothelial dysfunction and acceleration of atherosclerosis, may play an essential role in the development of cardiovascular diseases. The individual pathophysiological mechanisms that link the HBV infection and different cardiovascular endpoints still warrant further elucidation.…”
Section: Discussionmentioning
confidence: 99%
“…In the present study, the risk estimates of death due to intracerebral haemorrhage did not change materially after adjusting for the presence of chronic hepatitis or cirrhosis at baseline, suggesting that advanced liver damage might not be the causal intermediate between HBV infection and intracerebral haemorrhage. HBV-induced proinflammatory effect25 and steatosis,26 further leading to endothelial dysfunction and acceleration of atherosclerosis, may play an essential role in the development of cardiovascular diseases. The individual pathophysiological mechanisms that link the HBV infection and different cardiovascular endpoints still warrant further elucidation.…”
Section: Discussionmentioning
confidence: 99%
“…The pathogenesis of HBV-associated nephropathy remains unclear, and several mechanisms have been implicated. Steatosis, a typical feature of chronic HBV infection, could induce lipid peroxidation and increase plasma inflammatory biomarkers, leading to endothelial dysfunction and renal injury [ 18 ]. It is also suggested that HBV carriers are more likely to have increased insulin resistance and a higher circulating level of transforming growth factor ß, contributing to the potentiation of apoptosis and renal fibrosis [ 19 , 20 ].…”
Section: Discussionmentioning
confidence: 99%