Abstract: SA-PO1087
Hyperuricemia Treatment Reduces ESKD Risk and Mortality in Patients with CKD: A Causal Inference Analysis Using the G-formula Approach
Session Information
- CKD: Epidemiology, Risk Factors, and Prevention - 3
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: CKD (Non-Dialysis)
- 2301 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention
Authors
- Ko, Ara, Seoul National University Hospital Department of Internal Medicine, Jongno-gu, Seoul, Korea (the Republic of)
- Lee, Jeonghwan, Seoul National University Hospital Boramae Medical Center, Seoul, Korea (the Republic of)
- Lim, Chun Soo, Seoul National University Hospital Boramae Medical Center, Seoul, Korea (the Republic of)
- Lee, Jung Pyo, Seoul National University Hospital Boramae Medical Center, Seoul, Korea (the Republic of)
Background
Hyperuricemia is recognized as an independent predictor of chronic kidney disease(CKD), but the role of treating it in CKD, especially when asymptomatic, remains under debate. The g-formula, valuable for epidemiological causal inference, allows estimation of effects in complex relationships among time-varying covariates. We used the g-formula to assess the impact of treating hyperuricemia in CKD patients using urate-lowering agents(ULAs).
Methods
Employing the g-formula, we analyzed data from 27,260 CKD patients to build regression models, evaluating relationships among time-varying covariates: serum urate(sUA), creatinine, and ULA prescription status, measured every 6 months. We also adjusted for time-invariant factors like diabetes and hypertension. Our focus was the impact of various strategies for managing hyperuricemia (treating if sUA ≥7, 8, 9, or 10mg/dL, or never treating) on end-stage kidney disease(ESKD) and all-cause mortality, supported by 1,000 bootstrap replicates for 95% confidence intervals(CIs).
Results
Of the cohort, 5,361 patients had been prescribed allopurinol, febuxostat, or benzbromarone. We found that hyperuricemia treatment generally decreased ESKD and all-cause mortality risks compared to never treating. Lower sUA thresholds were linked to dose-responsive decrease in risk, particularly at 7mg/dL [RR of 0.960 for ESKD (95% CI: 0.956 to 0.964), and 0.988 for mortality (0.984 to 0.992) compared to never treating]. Compared to no intervention, initiating treatment ≥9 or 10mg/dL, or never treating, significantly increased ESKD and mortality with a protective effect observed only at the threshold of 8mg/dL or below.
Conclusion
Our study demonstrates that treating hyperuricemia in CKD patients significantly reduces the risk of ESKD and mortality. This suggests potential harm in not treating hyperuricemia at urate levels of 9mg/dL or higher.