Large arteries and the kidney

In subjects with chronic renal disease, high systolic blood pressure (SBP) is the most modifiable cardiovascular (CV) risk factor that enables prevention of the progression of chronic kidney disease renal failure and the occurrence of CV events. Although large-artery stiffness and wave reflections are the principal hemodynamic determinants of SBP, their precise role in the progression of chronic renal disease has been poorly investigated. However, in subjects with mild to severe renal insufficiency, increased arterial stiffness and reduced creatinine clearance are closely related, independently of age; mean arterial pressure level; and presence of other traditional risk factors, including atherosclerotic plaques. Through inflammatory mechanisms, as well as through the development of arterial calcifications (including microscopic) and sodium-related alterations in extracellular matrix composition, arterial stiffness is associated with significant SBP and increased pulse pressure (PP). In the presence of renal dysfunction, frequently observed in elderly hypertensive or diabetic subjects, or even in some living donors, the resulting increase in PP may be transmitted toward and across glomeruli, even when peripheral blood pressure values are maintained. This alteration alone may initiate glomerulosclerosis and/or tubulointerstitial damage, eventually leading to CV events. In subjects with end-stage renal disease and high CV risk, pharmacological modulation of the renin–angiotensin system has been shown to prevent independently such complications.