Aortic stiffness, kidney disease, and renal transplantation

Abstract

In individuals with chronic kidney disease (CKD), treatment of elevated systolic blood pressure (SBP) is a key element in preventing disease progression and occurrence of cardiovascular events. For a given stroke volume, increased arterial stiffness is a key determinant of SBP. Therefore, the relationships between large conduit arteries and kidney function have been extensively studied in different CKD populations. In individuals with mild to severe renal insufficiency, increased aortic stiffness and reduced creatinine clearance are closely related, independently of standard cardiovascular risk factors but in the presence of significant arterial calcifications. In renal transplant patients, aortic stiffness is significantly increased irrespective of blood pressure level. In transplantation from living donors, arterial stiffness of the donor seems to contribute independently and significantly to the renal function of the recipient. In individuals with CKD, an increase in brachial pulse pressure is frequently observed, particularly in the elderly, and may be transmitted to the glomeruli, thus initiating renal damage each time a defect in renal autoregulation is present. Finally, in individuals with mild to moderate renal insufficiency, pharmacological modulation of the renin-angiotensin system may prevent both CKD progression and occurrence of cardiovascular events. © 2010 Springer-Verlag Milan.