Young Su Joo1,2, Changhyun Lee1,3, Hyung Woo Kim1, Jonghyun Jhee1,4, Hae-Ryong Yun1, Jung Tak Park1, Tae Ik Chang5, Tae-Hyun Yoo1, Shin-Wook Kang1,6, Seung Hyeok Han7. 1. Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea. 2. Division of Nephrology, Department of Internal Medicine, Myongji Hospital, Goyang, Gyeonggi-do, Republic of Korea. 3. Division of Integrated Medicine, Department of Internal Medicine, National Health Insurance Service Medical Center, Ilsan Hospital, Goyang, Gyeonggi-do, Republic of Korea. 4. Division of Nephrology, Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea. 5. Department of Internal Medicine, National Health Insurance Service Medical Center, Ilsan Hospital, Goyang, Gyeonggi-do, Republic of Korea. 6. Department of Internal Medicine, College of Medicine, Severance Biomedical Science Institute, Brain Korea 21 PLUS, Yonsei University, Seoul, Republic of Korea. 7. Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of Korea hansh@yuhs.ac.
Abstract
BACKGROUND: Although hypertension is a well known risk factor for CKD, few studies have evaluated the association between temporal trends of systolic BP and kidney function decline in persons without hypertension. METHODS: We studied whether changes in systolic BP over time could influence incident CKD development in 4643 individuals without CKD and hypertension participating in the Korean Genome and Epidemiology Study, a prospective community-based cohort study. Using group-based trajectory modeling, we categorized three distinct systolic BP trajectories: decreasing, stable, and increasing. The primary outcome was incident CKD development, defined as two consecutive eGFR measurements <60 ml/min per 1.73 m2. RESULTS: Among participants with an increasing systolic BP trajectory, systolic BP increased from 105 to 124 mm Hg. During 31,936 person-years of follow-up (median 7.7 years), 339 participants developed incident CKD. CKD incidence rates were 8.9, 9.6, and 17.8 cases per 1000 person-years in participants with decreasing, stable, and increasing systolic BP trajectories, respectively. In multivariable cause-specific Cox analysis, after adjustment of baseline eGFR, systolic BP, and other confounders, increasing systolic BP trajectory associated with a 1.57-fold higher risk of incident CKD (95% confidence interval, 1.20 to 2.06) compared with a stable trajectory. There was a significant effect modification of baseline systolic BP on the association between systolic BP trajectories and CKD risk (P value for interaction =0.02), and this association was particularly evident in participants with baseline systolic BP <120 mm Hg. In addition, increasing systolic BP trajectory versus a stable trajectory was associated with higher risk of new development of albuminuria. CONCLUSIONS: Increasing systolic BP over time without reaching the hypertension threshold is associated with a significantly increased risk of incident CKD in healthy adults.
BACKGROUND: Although hypertension is a well known risk factor for CKD, few studies have evaluated the association between temporal trends of systolic BP and kidney function decline in persons without hypertension. METHODS: We studied whether changes in systolic BP over time could influence incident CKD development in 4643 individuals without CKD and hypertension participating in the Korean Genome and Epidemiology Study, a prospective community-based cohort study. Using group-based trajectory modeling, we categorized three distinct systolic BP trajectories: decreasing, stable, and increasing. The primary outcome was incident CKD development, defined as two consecutive eGFR measurements <60 ml/min per 1.73 m2. RESULTS: Among participants with an increasing systolic BP trajectory, systolic BP increased from 105 to 124 mm Hg. During 31,936 person-years of follow-up (median 7.7 years), 339 participants developed incident CKD. CKD incidence rates were 8.9, 9.6, and 17.8 cases per 1000 person-years in participants with decreasing, stable, and increasing systolic BP trajectories, respectively. In multivariable cause-specific Cox analysis, after adjustment of baseline eGFR, systolic BP, and other confounders, increasing systolic BP trajectory associated with a 1.57-fold higher risk of incident CKD (95% confidence interval, 1.20 to 2.06) compared with a stable trajectory. There was a significant effect modification of baseline systolic BP on the association between systolic BP trajectories and CKD risk (P value for interaction =0.02), and this association was particularly evident in participants with baseline systolic BP <120 mm Hg. In addition, increasing systolic BP trajectory versus a stable trajectory was associated with higher risk of new development of albuminuria. CONCLUSIONS: Increasing systolic BP over time without reaching the hypertension threshold is associated with a significantly increased risk of incident CKD in healthy adults.
Authors: Kristi Reynolds; Dongfeng Gu; Paul Muntner; John W Kusek; Jing Chen; Xigui Wu; Xiufang Duan; Chung-Shiuan Chen; Michael J Klag; Paul K Whelton; Jiang He Journal: J Am Soc Nephrol Date: 2007-05-02 Impact factor: 10.121
Authors: Caroline S Fox; Martin G Larson; Eric P Leip; Bruce Culleton; Peter W F Wilson; Daniel Levy Journal: JAMA Date: 2004-02-18 Impact factor: 56.272