Abstract
Aims: Arterial stiffness increases with both advancing age and chronic kidney disease (CKD) and may contribute to kidney function decline, but evidence is inconsistent. We hypothesized that greater baseline arterial stiffness (assessed as pulse pressure (PP) and carotid-femoral pulse-wave velocity CFPWV)) was independently associated with kidney disease progression over the follow-up period (3.8 years) in the Systolic Blood Pressure Intervention Trial (SPRINT). Materials and methods: 8,815 SPRINT participants were included in the analysis of PP. 592 adults who participated in a SPRINT ancillary study that measured CFPWV were included in subgroup analyses. Cox proportional hazards analysis was used to examine the association between PP and time to kidney disease progression endpoints: (A) incident estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73m2 in non-CKD participants at baseline; (B) 50% decline in eGFR, initiation of dialysis, or transplant in those with baseline CKD. Mixed model analyses examined the association of baseline PP/CFPWV with follow-up eGFR. Results and conclusion: Mean ± SD age was 68 ± 10 years, baseline PP was 62 ± 14 mmHg, and CFPWV was 10.8 ± 2.7 m/s. In the fully adjusted model, PP ≥ median was associated with an increased hazard of kidney disease progression endpoints (HR: 1.93 (1.43 – 2.61)). The association remained significant in individuals without (2.05 (1.47 – 2.87)) but not with baseline CKD (1.28 (0.55 – 2.65)). In fully adjusted models, higher baseline PP associated with eGFR decline (p < 0.0001 (all, CKD, non-CKD)), but baseline CFPWV did not. Among older adults at high risk for cardiovascular events, baseline PP was associated with kidney disease progression.
Highlights
Arterial stiffness increases both with advancing age [1, 2] and as kidney function declines (chronic kidney disease (CKD)) [3, 4, 5] and is an important independent predictor of incident cardiovascular events and mortality [6, 7, 8, 9]
Higher baseline arterial stiffness was independently associated with incident CKD [12, 13] and eGFR decline [14, 15] in several cohorts of community-dwelling adults; evidence is not consistent across studies [13, 16] and analyses have included individuals with diabetes mellitus, who likely have greater baseline arterial stiffness [17]
We hypothesized that greater baseline arterial stiffness, as measured in the entire cohort by pulse pressure (PP) [23] and by carotid-femoral pulse-wave velocity (CFPWV) in a subgroup who participated in an ancillary study [24], would be associated with kidney disease progression over the follow-up period
Summary
Arterial stiffness increases both with advancing age [1, 2] and as kidney function declines (chronic kidney disease (CKD)) [3, 4, 5] and is an important independent predictor of incident cardiovascular events and mortality [6, 7, 8, 9]. Higher baseline arterial stiffness was independently associated with incident CKD (eGFR < 60 mL/min/1.73m2) [12, 13] and eGFR decline [14, 15] in several cohorts of community-dwelling adults; evidence is not consistent across studies [13, 16] and analyses have included individuals with diabetes mellitus, who likely have greater baseline arterial stiffness [17]. The purpose of the present study was to test the hypothesis that greater baseline arterial stiffness was independently associated with decline in kidney function over the follow-up period in older adults without baseline diabetes mellitus who participated in the recently completed Systolic Blood Pressure Intervention Trial (SPRINT). We explored any differences in these associations in individuals with and without baseline CKD
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