Renin-angiotensin system inhibitors and arterial stiffness in chronic kidney disease: results from the chronic renal insufficiency cohort

Abstract Chronic kidney disease (CKD) is associated with accelerated arterial stiffness, which contributes to its high burden cardiovascular disease. There is conflicting evidence on whether renin-angiotensin system inhibitors (RASIs) prevent arterial stiffness. We investigated the association between RASIs versus non-RASI antihypertensive medications and yearly changes in carotid-femoral pulse wave velocity (cfPWV) – a measure of arterial stiffness –using a linear mixed-effects model among participants in the Chronic Renal Insufficiency Cohort (CRIC) Study. As a secondary analysis, we restricted the cohort to participants on one antihypertensive medication at baseline. Lastly, we used a linear mixed-effects model to evaluate the relationship between RASI use and systolic blood pressure over time. Of the 1 201 participants who met inclusion criteria, 982 were on RASI and 219 were on a non-RASI medication. Individuals on RASI had a non-significant increase in cfPWV (adjusted cfPWV 0.19 m/s per year, 95% CI 0.14 to 0.25) compared to non-RASI users (adjusted cfPWV 0.15 m/s per year, 95% CI 0.00 to 0.30; p = 0.61). In the monotherapy cohort (N = 283), there was no difference in adjusted yearly change in cfPWV between RASI (0.11 m/s per year, 95% CI 0.02 to 0.21) and non-RASI users (0.03 m/s per year, 95% CI −0.14 to 0.20; p = 0.41). In both cohorts, there was no significant difference in systolic blood pressure over time between RASI and non-RASI users. Future research to mitigate the accelerated large artery stiffness in patients with CKD should focus on targetable mechanisms beyond the renin-angiotensin system.