TY - JOUR
T1 - Predictors of abdominal aortic calcification progression in patients with chronic kidney disease without hemodialysis
AU - Yamamoto, Dai
AU - Suzuki, Susumu
AU - Ishii, Hideki
AU - Hirayama, Kenshi
AU - Harada, Kazuhiro
AU - Aoki, Toshijiro
AU - Shibata, Yohei
AU - Negishi, Yosuke
AU - Tatami, Yosuke
AU - Sumi, Takuya
AU - Ichii, Takeo
AU - Kawashima, Kazuhiro
AU - Kunimura, Ayako
AU - Kawamiya, Toshiki
AU - Morimoto, Ryota
AU - Yasuda, Yoshinari
AU - Murohara, Toyoaki
N1 - Publisher Copyright:
© 2016 Elsevier Ireland Ltd
PY - 2016/10/1
Y1 - 2016/10/1
N2 - Background and aims Abdominal aortic calcification (AAC) is an important predictor of cardiovascular mortality in patients with chronic kidney disease (CKD). However, little is known regarding AAC progression in these patients. This study aimed to identify risk factors associated with AAC progression in patients with CKD without hemodialysis. Methods We recruited 141 asymptomatic patients with CKD without hemodialysis [median estimated glomerular filtration rate (eGFR), 40.3 mL/min/1.73 m2] and evaluated the progression of the abdominal aortic calcification index (ACI) over 3 years. To identify risk factors contributing to the rate of ACI progression, the associations between baseline clinical characteristics and annual change in ACI for each CKD category were analyzed. The annual change of ACI (ΔACI/year) was calculated as follows: (second ACI − first ACI)/duration between the two evaluations. Results Median ΔACI/year values significantly increased in advanced CKD stages (0.73%, 0.87%, and 2.24%/year for CKD stages G1-2, G3, and G4-5, respectively; p for trend = 0.041). The only independent risk factor for AAC progression in mild to moderate CKD (G1-3, eGFR ≥ 30 mL/min/1.73 m2) was pulse pressure level (β = 0.258, p = 0.012). In contrast, parathyroid hormone (PTH) level was significantly correlated with ΔACI/year (β = 0.426, p = 0.007) among patients with advanced CKD (G4-5, eGFR < 30 mL/min/1.73 m2). Conclusions This study suggests that the AAC progression rate was significantly accelerated in patients with advanced CKD. In addition, measuring PTH is useful to evaluate both bone turnover and AAC progression in patients with advanced CKD.
AB - Background and aims Abdominal aortic calcification (AAC) is an important predictor of cardiovascular mortality in patients with chronic kidney disease (CKD). However, little is known regarding AAC progression in these patients. This study aimed to identify risk factors associated with AAC progression in patients with CKD without hemodialysis. Methods We recruited 141 asymptomatic patients with CKD without hemodialysis [median estimated glomerular filtration rate (eGFR), 40.3 mL/min/1.73 m2] and evaluated the progression of the abdominal aortic calcification index (ACI) over 3 years. To identify risk factors contributing to the rate of ACI progression, the associations between baseline clinical characteristics and annual change in ACI for each CKD category were analyzed. The annual change of ACI (ΔACI/year) was calculated as follows: (second ACI − first ACI)/duration between the two evaluations. Results Median ΔACI/year values significantly increased in advanced CKD stages (0.73%, 0.87%, and 2.24%/year for CKD stages G1-2, G3, and G4-5, respectively; p for trend = 0.041). The only independent risk factor for AAC progression in mild to moderate CKD (G1-3, eGFR ≥ 30 mL/min/1.73 m2) was pulse pressure level (β = 0.258, p = 0.012). In contrast, parathyroid hormone (PTH) level was significantly correlated with ΔACI/year (β = 0.426, p = 0.007) among patients with advanced CKD (G4-5, eGFR < 30 mL/min/1.73 m2). Conclusions This study suggests that the AAC progression rate was significantly accelerated in patients with advanced CKD. In addition, measuring PTH is useful to evaluate both bone turnover and AAC progression in patients with advanced CKD.
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U2 - 10.1016/j.atherosclerosis.2016.08.004
DO - 10.1016/j.atherosclerosis.2016.08.004
M3 - Article
C2 - 27573734
AN - SCOPUS:84983685810
SN - 0021-9150
VL - 253
SP - 15
EP - 21
JO - Atherosclerosis
JF - Atherosclerosis
ER -