Arterial stiffness and incidence of chronic kidney disease

The progression of arterial stiffness, which arises from biological ageing and averse cardiometabolic processes, gives rise to increasing pulsatile pressure. This can cause damage to organs with high flow and low resistance, with the kidneys being particularly susceptible.

Studies have demonstrated a cross-sectional correlation between greater arterial stiffness, as measured by higher pulse wave velocity (PWV), and lower kidney function. Most were, however, limited to participants with chronic kidney disease (CKD) and in the arterial segments that were measured. 

The study by Yao and colleagues investigated the association of arterial stiffness, as assessed by PWVs measured at six different arterial segments, with the incidence of CKD and changes in kidney function. They used data from the Atherosclerosis Risk in Communities (ARIC) study, which enrolled participants aged 45–64 years between 1987 and 1989, and followed them over seven visits, the last being in 2019. Data at visit 5 (2011–2013) were used as the baseline in the present study.

In the primary analysis, 3161 participants without CKD (eGFR ≥60 mL/min/1.73 m²) at baseline were followed until they had incident CKD, were lost to follow-up, died or to the end of follow-up. The secondary analysis included 4341 participants with any eGFR record across visits 5 to 7, with changes in eGFR as an outcome variable.

Measures of PWV in six sites were investigated: carotid–femoral (cfPWV), heart–femoral (hfPWV), heart–ankle (haPWV), brachial–ankle (baPWV), heart–carotid (hcPWV) and femoral–ankle (faPWV). 

Over a median follow-up of 6.6 years, 460 participants developed incident CKD (incidence rate, 22.0/1000 person-years). After adjusting for confounders, the highest quartiles (Q4) of cfPWV, hfPWV and haPWV were associated with an increased risk of incident CKD compared to the lowest quartile (Q1) (HRs, 1.53 [95% CI, 1.15 to 2.04], 1.49 [1.12 to 1.99] and 1.56 [1.16 to 2.08], respectively). The results were consistent in demographic and clinical subgroups. 

In the secondary analysis, after adjusting, participants in the Q4 of cfPWV had a faster eGFR decline than those in the Q1 (eGFR slope, –0.44 mL/min/1.73 m²/year [–0.56 to –0.33] vs –0.37 mL/min/1.73 m²/year [–0.48 to –0.26], respectively). The findings for other PWVs were consistent with the primary analysis. Only faPWV was not associated with incident CKD or eGFR slope.

The findings of this large, community-based study support the pathophysiological contribution of aortic stiffness pre-dating the development or progression of CKD. Future research should assess whether aortic stiffness can be a therapeutic target to prevent CKD. The study also supports cfPWV as the preferred measure for evaluating arterial stiffness. 

The full article can be read here.