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Updated: Jun 12, 2026
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Causal Effects of Renin-Angiotensin-Aldosterone System Inhibition on Renal Function in Patients With Chronic Kidney
Tae Ryom Oh1, Jiyong Park2, Hong Sang Choi3,4
1Department of Internal Medicine, Mokpo Hankook Hospital, Mokpo, Korea.
Abstract:
Renin-angiotensin-aldosterone system inhibitors are widely prescribed for chronic kidney disease, but their causal effect on kidney function remains uncertain. This study investigated the impact of starting renin-angiotensin blockade on renal function in adults with kidney disease. A retrospective cohort study was conducted in Korea using a quasi-experimental staggered difference-in-differences design with propensity score matching to estimate time-varying treatment effects. Overall, 1,204 adults (375 treated and 829 contemporaneous not-yet-treated controls) were followed for 3 years. Initiation of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers was recorded, and treatment exposure was categorized monthly. The primary outcome was a change in estimated glomerular filtration rate after initiation, evaluated over sequential intervals up to 12 months. The overall average treatment effect of two-way fixed effects model was not statistically significant (-1.47 mL/min/1.73 m2; p = 0.33). However, initiation was associated with an immediate and significant decline in eGFR at event time 0 (estimate: -3.87 mL/min/1.73 m2, p < 0.05) and at event time 1 and 3 (p < 0.05). Beyond these early intervals, there was no evidence of progressive deterioration in kidney function during the 1-year follow-up. Declines following initiation of renin-angiotensin blockade are early, transient, and primarily hemodynamic in nature rather than reflective of structural kidney injury. Importantly, this quasi-experimental analysis of real-world data reproduced the findings of randomized trials, reinforcing current guideline recommendations to continue therapy in chronic kidney disease provided that reduction in filtration rate remains below the accepted threshold of 30%.
Insights
Starting renin-angiotensin blockade for kidney disease causes an early, temporary drop in kidney function. This effect is hemodynamic, not structural damage, supporting continued use in chronic kidney disease.
Area of Science:
- Nephrology
- Pharmacology
- Epidemiology
Background:
- Renin-angiotensin-aldosterone system (RAAS) inhibitors are standard for chronic kidney disease (CKD).
- Their precise impact on kidney function progression is debated.
- Uncertainty exists regarding whether initial declines in kidney function reflect harm or a hemodynamic effect.
Purpose of the Study:
- To investigate the causal effect of initiating RAAS blockade on renal function in adults with CKD.
- To differentiate between hemodynamic and structural kidney injury after RAAS inhibitor initiation.
- To assess the long-term impact of RAAS blockade on estimated glomerular filtration rate (eGFR) in CKD patients.
Main Methods:
- Retrospective cohort study in Korea with a quasi-experimental staggered difference-in-differences design.
- Propensity score matching used to control for confounding variables.
- Analysis of 1,204 adult CKD patients (375 treated, 829 controls) over 3 years, focusing on eGFR changes within 12 months of treatment initiation.
Main Results:
- The overall average treatment effect on eGFR was not statistically significant (-1.47 mL/min/1.73 m²).
- Initiation of RAAS blockade was associated with a significant, immediate eGFR decline at event times 0, 1, and 3 months (p < 0.05).
- No progressive kidney function deterioration was observed beyond these early intervals within the 1-year follow-up.
Conclusions:
- Early declines in eGFR after starting RAAS inhibitors are transient and primarily hemodynamic.
- These findings suggest that RAAS blockade does not cause progressive structural kidney injury.
- The results support current guidelines recommending continuation of RAAS inhibitors in CKD patients if eGFR decline is within acceptable limits (<30%).
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