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

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Vascular disease, characterised by premature atherosclerosis and large artery stiffness, is a feature of advanced chronic kidney disease (CKD) [1, 2]. Central pulse pressure, augmentation index (AIx) and aortic pulse wave velocity (PWV) are all predictors of morbidity and mortality in patients with CKD [1, 3, 4]. Large artery stiffness may also be related to the progression of CKD. The mechanisms and time frames for the development of arterial stiffness are unclear but may include traditional cardiovascular risk factors such as dyslipidemia and hypertension as well as non-traditional risk factors such as oxidative stress and inflammation. Moreover, to our knowledge no studies have assessed the relationship between arterial stiffness in the uraemic environment of acute kidney injury. Measuring arterial stiffness in this setting would enable us to determine whether changes in arterial stiffness occur due to the biochemical changes associated with acute kidney injury without the interference of factors that exist in chronic kidney disease. This may in turn help to understand the potential for reversibility of uremic biochemical effects on arterial stiffness.

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