Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury

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• 作者：Robert G Fassett (1) (5) (6)
  Vincent D'Intini (1)
  Helen Healy (1)
  John Gowardman (2)
  Jay-Sen Gan (3)
  James E Sharman (4)
  Jeff S Coombes (5)
  
• 刊名：BMC Nephrology
• 出版年：2009
• 出版时间：December 2009
• 年：2009
• 卷：10
• 期：1
• 全文大小：172KB
• 参考文献：1. Blacher J, Guerin AP, Pannier B, Marchais SJ, Safar ME, London GM: Impact of aortic stiffness on survival in end-stage renal disease. / Circulation 1999,99(18): 2434-439.
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  12. The pre-publication history for this paper can be accessed here:medcentral.com/1471-2369/10/15/prepub" class="a-plus-plus">http://www.biomedcentral.com/1471-2369/10/15/prepub
  
• 作者单位：Robert G Fassett (1) (5) (6)
  Vincent D'Intini (1)
  Helen Healy (1)
  John Gowardman (2)
  Jay-Sen Gan (3)
  James E Sharman (4)
  Jeff S Coombes (5)
  
  1. Renal Medicine, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia
  5. School of Human Movement Studies The University of Queensland, Brisbane, Queensland, Australia
  6. School of Medicine The University of Queensland, Brisbane, Queensland, Australia
  2. Intensive Care Unit, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia
  3. Department of Nephrology, Royal Hobart Hospital, Hobart, Tasmania, Australia
  4. Menzies Research Institute University of Tasmania, Hobart, Tasmania, Australia
  

文摘

Background It is well know that arterial stiffness, oxidative stress and inflammation are features of chronic kidney disease. The arterial changes have a multitude of potential interconnected causes including endothelial dysfunction, oxidative stress, inflammation, atherosclerosis and vascular calcification. There is evidence that arterial stiffness becomes progressively worse as CKD progresses. The contribution of the biochemical changes of uremic toxicity to arterial stiffness is less clear. The aim of this study is to elucidate the vascular changes in acute kidney injury. We hypothesise that arterial stiffness will be increased during acute kidney injury and this will return to normal after kidney function recovers. Methods/Design One hundred and forty four patients with acute kidney injury defined as an acute increase in serum creatinine to > 133 μmol/l or urea > 14.3 mmol/l or urine output < 410 ml/day will be recruited. Baseline measures of aortic pulse wave velocity, augmentation index, and brachial and central blood pressure will be recorded along with blood measures for oxidative stress and inflammation. Repeat measures will be taken at six and 12 months after the onset of the acute kidney injury. Discussion The role and contribution of the biochemical changes to arterial stiffness in the acute phase of kidney disease is not known. This study will primarily assess the time course changes in pulse wave velocity from the onset of acute kidney injury and after recovery. In addition it will assess augmentation index, central blood pressure and oxidative stress and inflammation. This may shed light on the contribution of biochemical kidney toxins on arterial stiffness in both acute kidney injury and chronic kidney disease. Trial Registration ACTRN 12609000285257