Abstract: SA-PO494
Systolic Blood Pressure Modifies the Relationship Between Coronary Artery Calcification and Adverse Kidney Outcome: Results from KNOW-CKD
Session Information
- Hypertension and CVD: Clinical - II
November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1602 Hypertension and CVD: Clinical
Authors
- Joo, Young Su, Yonsei University Institute of Kidney Disease, Seodaemun-gu, Seoul, Korea (the Republic of)
- Park, Jung Tak, Yonsei University Institute of Kidney Disease, Seodaemun-gu, Seoul, Korea (the Republic of)
- Yoo, Tae-Hyun, Yonsei University Institute of Kidney Disease, Seodaemun-gu, Seoul, Korea (the Republic of)
- Oh, Kook-Hwan, Seoul National University College of Medicine, Seoul, Korea (the Republic of)
- Kang, Shin-Wook, Yonsei University Institute of Kidney Disease, Seodaemun-gu, Seoul, Korea (the Republic of)
- Han, Seung Hyeok, Yonsei University Institute of Kidney Disease, Seodaemun-gu, Seoul, Korea (the Republic of)
Background
Previous studies have shown that elevated BP and coronary artery calcification (CAC) are risk factors for adverse kidney outcomes. However, the interaction between CAC and BP in relation to CKD progression has not well been studied. In this observational study, we aimed to evaluate whether systolic blood pressure (SBP) could modify the association between CAC and CKD progression in patients with CKD.
Methods
We analyzed 1698 participants with CKD stages G1 to G5 from the KoreaN cohort study for Outcome in patients With Chronic Kidney Disease (KNOW-CKD). Participants with kidney failure with replacement therapy (KFRT) and those with missing data for CAC and SBP were excluded. We categorized the participants according to their 1-year-mean systolic BP as controlled (SBP <120 mmHg) or uncontrolled (SBP≥120 mmHg) and the CAC status (Agatston score=0 or >0 AU). CKD progression was defined as a composite of halving eGFR from baseline value or onset of KFRT.
Results
During 10,023 person-years of follow-up (median 6.2 years), the composite outcome occurred in 689 (40.7%) participants. We found a significant interaction between the Agatston score and SBP for CKD progression (P=0.02). There were 90 (27.5%), 67 (37.0%), 219 (39.5%), and 313 (49.7%) composite outcome events in participants with controlled BP without CAC (group 1), controlled BP with CAC (group 2), uncontrolled BP without CAC (group 3), and uncontrolled BP with CAC (group 4), respectively. In multivariable cause-specific Cox model, the corresponding hazard ratios (95% confidence intervals) for groups 2, 3, and 4 were 1.25 (0.88-1.77), 1.44 (1.12-1.87), and 1.78 (1.35-2.34), respectively, compared with group 1. Sensitivity analysis using a different SBP cutoff of 130 mmHg yielded similar results.
Conclusion
The clinical implication of CAC for CKD progression may be influenced by the status of controlled SBP, and CAC is more strongly associated with adverse kidney outcome when SBP is not adequately controlled.
Funding
- Government Support – Non-U.S.