Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury
<p>Abstract</p> <p>Background</p> <p>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...
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Format: | Article |
Language: | English |
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BMC
2009-06-01
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Series: | BMC Nephrology |
Online Access: | http://www.biomedcentral.com/1471-2369/10/15 |
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author | Fassett Robert G D'Intini Vincent Healy Helen Gowardman John Gan Jay-Sen Sharman James E Coombes Jeff S |
author_facet | Fassett Robert G D'Intini Vincent Healy Helen Gowardman John Gan Jay-Sen Sharman James E Coombes Jeff S |
author_sort | Fassett Robert G |
collection | DOAJ |
description | <p>Abstract</p> <p>Background</p> <p>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.</p> <p>Methods/Design</p> <p>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.</p> <p>Discussion</p> <p>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.</p> <p>Trial Registration</p> <p><b>ACTRN </b>12609000285257</p> |
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format | Article |
id | doaj.art-fd8efe77db0c4d0f8d57ee51d3c4e257 |
institution | Directory Open Access Journal |
issn | 1471-2369 |
language | English |
last_indexed | 2024-04-13T12:28:31Z |
publishDate | 2009-06-01 |
publisher | BMC |
record_format | Article |
series | BMC Nephrology |
spelling | doaj.art-fd8efe77db0c4d0f8d57ee51d3c4e2572022-12-22T02:46:57ZengBMCBMC Nephrology1471-23692009-06-011011510.1186/1471-2369-10-15Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injuryFassett Robert GD'Intini VincentHealy HelenGowardman JohnGan Jay-SenSharman James ECoombes Jeff S<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Methods/Design</p> <p>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.</p> <p>Discussion</p> <p>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.</p> <p>Trial Registration</p> <p><b>ACTRN </b>12609000285257</p>http://www.biomedcentral.com/1471-2369/10/15 |
spellingShingle | Fassett Robert G D'Intini Vincent Healy Helen Gowardman John Gan Jay-Sen Sharman James E Coombes Jeff S Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury BMC Nephrology |
title | Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury |
title_full | Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury |
title_fullStr | Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury |
title_full_unstemmed | Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury |
title_short | Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury |
title_sort | assessment of arterial stiffness oxidative stress and inflammation in acute kidney injury |
url | http://www.biomedcentral.com/1471-2369/10/15 |
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