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

Fassett, Robert G., D'Intini, Vincent, Healy, Helen, Gowardman, John, Gan, Jay-Sen, Sharman, James E . and Coombes, Jeff S. (2009) Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury. BMC Nephrology, 10 15: Article number 15.


Author Fassett, Robert G.
D'Intini, Vincent
Healy, Helen
Gowardman, John
Gan, Jay-Sen
Sharman, James E .
Coombes, Jeff S.
Title Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury
Journal name BMC Nephrology  (ERA 2012 Listed)    (ERA 2010 Rank C)   Check publisher's open access policy
Publication date 2009-06-18
Sub-type Article
Year available 2009
DOI 10.1186/1471-2369-10-15
Volume number 10
Issue number 15
ISSN 1471-2369
Start page Article number 15
Total pages 5
Place of publication London, United Kingdom
Publisher BioMed Central
Collection year 2010
Language eng
Subject 110312 Nephrology and Urology
920103 Cardiovascular System and Diseases
1102 Cardiovascular Medicine and Haematology
Formatted abstract 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 mol/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.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

 
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