Abstract
The impact of brachial-ankle pulse wave velocity (baPWV) and heart-femoral pulse wave velocity (hfPWV) on rapid decline of estimated glomerular filtration rate (eGFR) has been inconclusive. The database of a multicenter prospective study of 2238 patients in Korea enrolled from 2011 to 2016 was reviewed. After excluding patients with missing baPWV (n = 257) and eGFR change (n = 180), the study included 1801 non-dialysis chronic kidney disease (CKD) patients. The eGFR change <−5ml/min/1.73 m2/year was defined as rapid decline. During a mean of 2.2 years, the mean eGFR change was −3.6 ml/min/1.73 m2/year, and 31.6% of patients were classified as having rapid decline. Older age, causes of CKD, increased heart rate, systolic blood pressures, and proteinuria were associated with the highest baPWV quintile. In multivariate logistic regression analyses, the odds of a rapid decline in eGFR was 1.9 times higher in the fifth quintile than in the first quintile (P = 0.013). In a subset with baPWV and hfPWV (n = 1182), high baPWV was associated with rapid eGFR decline only when accompanied by a high hfPWV. These findings suggest that central and peripheral PWVs may simultaneously affect rapid eGFR decline.
Highlights
Chronic kidney disease (CKD) is a common form of chronic disease[1], and it contributes to an increased risk of the development of cardiovascular (CV) events and mortality[2]
The mean ΔeGFR was −3.6 ml/min/1.73 m2/year, and 31.6% of the participants were classified as having a rapid decline in the estimated glomerular filtration rate (eGFR)
We explored the association between the brachial-ankle pulse wave velocity (PWV) (baPWV) and the change of eGFR (ΔeGFR)
Summary
Chronic kidney disease (CKD) is a common form of chronic disease[1], and it contributes to an increased risk of the development of cardiovascular (CV) events and mortality[2]. Whether there is a bidirectional association between increased arterial stiffness and decreased kidney function is unclear, but a recent study suggested that increased arterial stiffness affected the decline of kidney function uni-directionally[5]. This can be explained by the fact that increased arterial stiffness limits the dampening of ventricular ejection which transmits more pressure to the end organs[6], and the increased pressure that is transmitted to the low-resistance renal afferent arterioles can damage the glomerular capillaries, resulting in reduced kidney function[7]. We performed the current multicenter study to identify the clinical importance of the baPWV on the decline in kidney function using data on a large number of adults who were enrolled in the KoreaN cohort study for Outcome in patients With Chronic Kidney Disease (KNOW-CKD)
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