Abstract: SA-PO1095
Association of Changes in Albuminuria with Change in Estimated Glomerular Filtration Rate (eGFR) in Macroalbuminuric CKD (CKD): Post Hoc Analysis of a 5-Year Randomized Trial
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
- Goraya, Nimrit, Baylor Scott & White Medical Center Temple, Temple, Texas, United States
- Simoni, Jan, Texas Tech University System, Lubbock, Texas, United States
- Kahlon, Maninder, The University of Texas at Austin Dell Medical School, Austin, Texas, United States
- Aksan, Nazan, The University of Texas at Austin Dell Medical School, Austin, Texas, United States
- Wesson, Donald E., The University of Texas at Austin Dell Medical School, Austin, Texas, United States
Background
Previous studies show changes in albuminuria associate inversely with the rate of eGFR change in patients with CKD and normoalbuminuria (urine albumin [mg]-to-creatinine [g] ratio [UACR] < 30) or microalbuminuria (UACR 30 to <300). In this post hoc analysis, we hypothesized that this inverse association also holds for patients with macroalbuminuric (UACR ≥ 300) kidney injury and non-diabetic CKD with initially normal eGFR (> 90 ml/min/m2 or stage G1).
Methods
One hundred fifty-three macroalbuminuric, non-diabetic G1 participants on ACEI were randomized to receive F&V (n=51), oral NaHCO3 (HCO3, n=51), or Usual Care, n=51. They were followed annually for 5 years, measuring eGFR (CKD-EPI) and UACR. Mixed linear regressions with random person intercepts tested differential group trajectories, p-values from relevant interaction terms are included below. We conducted preliminary causal mediation analyses examining participant level improvements in eGFR from the first year after randomization until the last study year (time-5) as the outcome. We examined the cumulative impact of change from first year after randomization to year 4 in UACR. In both the mediator and the outcome equations, baseline levels of eGFR and UACR were partialled out.
Results
Baseline eGFR and UACR were not different among groups. The observed mean rate of eGFR decline [mean (SE)] from baseline to year 5 for F&V [-1.08 (0.06) ml/min/1.73m2/ yr] and HCO3 [-1.17 (0.07) ml/min/1.73m2/ yr] were both lower (p<0.001) than UC [-1.94 (0.11) ml/min/1.73m2/yr. Interaction terms indicated that the UACR trajectories for F&V and HCO3 were each lower (consistent with less kidney injury) than UC (p<0.001). Although the direction of the UACR change vs. eGFR change varied among groups, the interaction for the entire sample was inverse (r= -0.41) and significant (p<0.001).
Conclusion
Like in patients with CKD and normoalbuminuria or microalbuminuria, this post hoc analysis showed that directional changes in albuminuria associate inversely with the rate of eGFR changes in patients with CKD and baseline macroalbuminuria. The data support future studies to test if interventions that reduce albuminuria might also be kidney protective in patients with macroalbuminuric level of kidney injury.