Stepwise increase in arterial stiffness corresponding with the stages of chronic kidney disease

Wang, Mingcheng; Tsai, Wei-Chuan; Chen, Ju‐Yi; Huang, Jeng-Jong

doi:10.1053/j.ajkd.2004.11.011

Cited by 300 publications

(255 citation statements)

References 51 publications

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“…Numerous studies have shown that increased arterial stiffness may be associated with reduced GFR and increased albuminuria. [10][11][12][13][14] Although CFPWV was not related to urine ACR in our study participants, greater CFPWV was associated with a lower GFR. Mediation analysis provided useful insights into potential specific mechanisms by which aortic stiffness may have affected the kidney microvasculature and reduced function in our sample.…”

Section: Discussionmentioning

confidence: 64%

Mediation Analysis of Aortic Stiffness and Renal Microvascular Function

Woodard

Sigurðsson

Gotal

et al. 2015

Journal of the American Society of Nephrology

104

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Aortic stiffening, assessed by carotid-femoral pulse wave velocity, is associated with CKD. Transmission of excessive flow pulsatility into the low-impedance renal microvasculature may mediate this association. However, direct analyses of macrovascular-microvascular relations in the kidney are limited. Using arterial tonometry, iohexol clearance, and magnetic resonance imaging, we related arterial stiffness, GFR, urinary albumin excretion, and potential mediators, including renal artery pulsatility index, renal vascular resistance, and arterial volume in the cortex, in 367 older adults (ages 72-92 years) participating in the Age, Gene/ Environment Susceptibility-Reykjavik Study. In a model adjusted for age, sex, heart rate, and body size, aortic stiffness was related to GFR (Slope of regression B=22.2860.85 ml/min per SD, P=0.008) but not urine albumin (P=0.09). After accounting for pulsatility index, the relation between aortic stiffness and GFR was no longer significant (P=0.10). Mediation analysis showed that 34% of the relation between aortic stiffness and GFR was mediated by pulsatility index (95% confidence interval of indirect effect, 21.35 to 20.29). An additional 20% or 36% of the relation was mediated by lower arterial volume in the cortex or higher renal vascular resistance, respectively, when offered as mediators downstream from higher pulsatility index (95% confidence interval of indirect effect including arterial volume in the cortex, 22.22 to 20.40; 95% confidence interval of indirect effect including renal vascular resistance, 22.51 to 20.76). These analyses provide the first evidence that aortic stiffness may contribute to lower GFR by transferring excessive flow pulsatility into the susceptible renal microvasculature, leading to dynamic constriction or vessel loss.

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Section: Discussionmentioning

confidence: 64%

Mediation Analysis of Aortic Stiffness and Renal Microvascular Function

Woodard

Sigurðsson

Gotal

et al. 2015

Journal of the American Society of Nephrology

104

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“…16 -19,21 These studies have been limited by small samples of patients with CKD, 16 -19,21 lack of CFPVW, 18 or the use of eGFRcrea as a continuous exposure in samples without CKD. 17,18,21 In longitudinal analyses, we found that baseline arterial stiffness measures were not associated with incident CKD over a 7-to 10-yr period. Our observations using widely accepted kidney function assessment tools and the standard array of tonometry measures suggest that central arterial stiffness is unlikely to be an important characteristic in community-dwelling individuals with primarily stage 3 CKD.…”

Section: Discussionmentioning

confidence: 84%

Arterial Stiffness in Mild-to-Moderate CKD

Upadhyay¹,

Hwang

Mitchell

et al. 2009

Journal of the American Society of Nephrology

127

116

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Whether arterial stiffness correlates with mild-to-moderate CKD and albuminuria in the community is unclear. We studied the association between arterial stiffness and mild-to-moderate CKD and albuminuria in the Framingham Heart Study. CKD was present in 6.7% (181 of 2682) of participants and microalbuminuria was present in 8.2% (479 of 5818). The measures of arterial stiffness were the carotid femoral pulse wave velocity, forward pressure wave amplitude, central pulse pressure, augmentation pressure, augmentation index, and mean arterial pressure. In cross-sectional analyses, arterial stiffness did not associate with CKD (defined by estimated GFR Ͻ60 ml/min/1.73 m 2 ) in either age-and gender-adjusted or multivariable-adjusted linear regression models. Carotid femoral pulse wave velocity associated with both urinary albumin-to-creatinine ratio and microalbuminuria (P Ͻ 0.0001 after multivariable adjustment). In longitudinal analyses, we used logistic regression models to examine the associations between baseline arterial stiffness measures (exposure variables) and incident CKD or microalbuminuria (n ϭ 1675 for CKD analyses and n ϭ 1252 for microalbuminuria analyses). Baseline arterial measures did not associate with incident CKD or incident microalbuminuria. In summary, arterial stiffness correlates with albuminuria but not with mild-to-moderate CKD.

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“…A simple and noninvasive method to automatically measure brachial-ankle PWV (baPWV) was recently developed to screen large populations (13,14). In several reports that included patients with different stages of CKD, PWV increased proportionally to decreased estimated GFR (eGFR) or creatinine clearance (15)(16)(17). Recently, an eGFR for Japanese patients was proposed by the Japanese Society of Nephrology (18); however, its clinical usefulness has not yet been fully established.…”

Section: Introductionmentioning

confidence: 99%