Kimio Watanabe1, Yoshihiro Tani2, Kenichi Tanaka2, Yoshimitsu Hayashi2, Koichi Asahi2, Masaaki Nakayama2, Tsuyoshi Watanabe2. 1. Department of Nephrology, Hypertension, Diabetology, Endocrinology and Metabolism, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima City, Fukushima, 960-1295, Japan. ag9t2wja@fmu.ac.jp. 2. Department of Nephrology, Hypertension, Diabetology, Endocrinology and Metabolism, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima City, Fukushima, 960-1295, Japan.
Abstract
BACKGROUND: Blood pressure (BP) transiently increases after major earthquakes. Although home BP increased in hypertensive patients after the Great East Japan Earthquake (measuring 9.0 on the Richter scale) on March 11th, 2011, such profiles in patients with chronic kidney disease (CKD) have not been investigated. METHODS: This retrospective single-center observational study included 38 patients with CKD at the predialysis stage [male, n=27 (71%); mean age 66.0 years; mean estimated glomerular filtration rate (eGFR) 46.0 mL/min/1.73 m²] who lived in Fukushima City. We compared their morning BP between two and four weeks after the quake with that of a control group of 39 non-CKD patients with hypertension. RESULTS: Systolic BP (SBP) remained elevated for one week after the quake in the CKD and non-CKD groups [before vs. after the quake 133.7±15.6 vs. 136.9±16.9 (p=0.017) and 129.9±7.8 vs. 133.3±9.3 mmHg (p=0.009), respectively]. Increases in SBP in the morning after the quake were statistically significant in the group with but not in that without CKD (7.1 and 3.4 mmHg; p=0.038 and 0.221, respectively). Multivariate analysis revealed that a low eGFR was an independent risk factor for elevated SBP after the quake. CONCLUSIONS: The quake caused acute changes in the home BP and the fact that BP elevation correlated with renal function suggests a possible mechanism of CKD, such as enhanced activity of the sympathetic nervous system in such patients.
BACKGROUND: Blood pressure (BP) transiently increases after major earthquakes. Although home BP increased in hypertensivepatients after the Great East Japan Earthquake (measuring 9.0 on the Richter scale) on March 11th, 2011, such profiles in patients with chronic kidney disease (CKD) have not been investigated. METHODS: This retrospective single-center observational study included 38 patients with CKD at the predialysis stage [male, n=27 (71%); mean age 66.0 years; mean estimated glomerular filtration rate (eGFR) 46.0 mL/min/1.73 m²] who lived in Fukushima City. We compared their morning BP between two and four weeks after the quake with that of a control group of 39 non-CKD patients with hypertension. RESULTS: Systolic BP (SBP) remained elevated for one week after the quake in the CKD and non-CKD groups [before vs. after the quake 133.7±15.6 vs. 136.9±16.9 (p=0.017) and 129.9±7.8 vs. 133.3±9.3 mmHg (p=0.009), respectively]. Increases in SBP in the morning after the quake were statistically significant in the group with but not in that without CKD (7.1 and 3.4 mmHg; p=0.038 and 0.221, respectively). Multivariate analysis revealed that a low eGFR was an independent risk factor for elevated SBP after the quake. CONCLUSIONS: The quake caused acute changes in the home BP and the fact that BP elevation correlated with renal function suggests a possible mechanism of CKD, such as enhanced activity of the sympathetic nervous system in such patients.
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