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A high normal ankle-brachial index is associated with biopsy-proven severe renal small artery intimal thickening and impaired renal function in chronic kidney disease

Abstract

A significant relationship has been established between central hemodynamics and renal microvascular damage. We hypothesized that the increase in the ankle-brachial index (ABI) with age is due to increased arterial stiffness and wave reflection and is thus associated with the pathogenesis of the renal small artery in patients with chronic kidney disease (CKD). We recruited 122 patients with CKD (stages 1–5) who underwent renal biopsy and ABI measurements between 2010 and 2013. Renal small artery intimal thickening (SA-IT) severity was assessed by semiquantitative grading. The median age was 47 years, with a range of 15–86 years (47% women). The median estimated glomerular filtration rate (eGFR) was 62 mL/min/1.73 m2. Compared with patients with the lowest 1–3 SA-IT index quartile, those with the highest quartile of the SA-IT index were older in age had higher mean arterial pressure, ABI, brachial-ankle pulse wave velocity, and lower eGFR. ABI was positively associated with SA-IT severity and inversely associated with eGFR. Multivariate logistic regression analyses showed that ABI was significantly associated with the highest quartile of the SA-IT index (odds ratio per SD increase in ABI, 1.83; 95% confidence interval, 1.08–3.26) and low eGFR (<60 mL/min/1.73 m2) (odds ratio per SD increase in ABI, 1.74; 95% confidence interval, 1.03–3.03). In conclusion, a high normal ABI was associated with severe renal small artery intimal thickening and low eGFR in patients with CKD.

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Acknowledgements

We are grateful to Morihiro Ota, Masato Nohara, and Sakiko Kina-Hatoma for their skillful technical assistance in histological preparation and staining.

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Correspondence to Akio Ishida.

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Zamami, R., Ishida, A., Miyagi, T. et al. A high normal ankle-brachial index is associated with biopsy-proven severe renal small artery intimal thickening and impaired renal function in chronic kidney disease. Hypertens Res 43, 929–937 (2020). https://doi.org/10.1038/s41440-020-0443-z

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