Abstract
In subjects with chronic kidney disease (CKD), treatment of high systolic blood pressure is a key element in preventing disease progression and the occurrence of cardiovascular (CV) events. This relationship between the large arterial system and kidney function was demonstrated in different renal populations. In subjects with mild to severe renal insufficiency, increased aortic stiffness and reduced creatinine clearance are closely related and are independent of traditional CV risk factors. In renal transplant patients, aortic stiffness is significantly increased irrespective of donor type. Donor age and/or acute rejection contribute independently to the increased stiffness. In the presence of renal dysfunction, an increase in systemic pulse pressure frequently may be observed and transmitted to the glomeruli. This alteration potentially initiates renal damage and favors CV events. In subjects with end-stage renal disease and high CV risk, pharmacologic modulation of the renin-angiotensin system might prevent CKD progression and CV events.
Published Version
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