Abstract: FR-PO0527
Associations of P-Cresol Sulfate with Heart Rate Variability in the Chronic Renal Insufficiency Cohort Study
Session Information
- CKM: Clinical - Trials, Epidemiology, and Biomarkers
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Cardiovascular-Kidney-Metabolic Health
- 602 Cardiovascular-Kidney-Metabolic Health: Clinical
Authors
- Moloney, Brona, Brigham and Women's Hospital, Boston, Massachusetts, United States
- Song, Emily Haejin, Brigham and Women's Hospital, Boston, Massachusetts, United States
- Walker, Judith, Brigham and Women's Hospital, Boston, Massachusetts, United States
- Waikar, Sushrut S., Boston Medical Center, Boston, Massachusetts, United States
- Mc Causland, Finnian R., Brigham and Women's Hospital, Boston, Massachusetts, United States
Background
Gut dysbiosis & autonomic dysfunction are common in chronic kidney disease (CKD) and independently associated with cardiovascular (CV) outcomes. A gut-kidney-brain axis has been proposed, whereby dysbiosis, uremic toxins, and autonomic dysfunction synergistically drive CV disease. We hypothesized that higher plasma P-cresol sulfate (PCS) concentrations (reflecting dysbiosis and uremic toxin burden) would be associated with lower heart rate variability (HRV), a marker of autonomic dysfunction, in the Chronic Renal Insufficiency Cohort (CRIC) Study.
Methods
Baseline plasma PCS and HRV data were available in 2857 (51%) of participants. We used linear regression models to explore the association of PCS (modeled continuously per 5µg/mL and as quartiles) with log-transformed SDNN and RMSSD (HRV metrics, derived from 10-second ECGs). Multivariable models adjusted for clinically relevant covariates. Multiplicative interaction terms explored differential associations according to baseline eGFR (linear) and diabetes status.
Results
Mean age was 57 ± 11 years, 46% were female, 40% were Black, and mean plasma PCS was 10.3 ±8.2 µg/mL. Higher plasma PCS (per 5µg/mL) was associated with a 4% lower SDNN (95%CI –6, –2%) and a 4% lower RMSSD (95% CI –5, –2%). A monotonic inverse association was observed across quartiles, with the highest PCS quartile (versus lowest) associated with an 18% lower SDNN (95% CI –25, –10%) and 17% lower RMSSD (95% CI –24, –9%). There was a suggestion of differential association of plasma PCS with SDNN by baseline eGFR and diabetes status (P-interaction 0.09 and 0.03, respectively); associations appeared more pronounced among those with CKD stages 1-2 vs. stages 3-5 and among patients with diabetes (Fig. 1).
Conclusion
Among patients with CKD, higher PCS is associated with lower HRV, a proxy for autonomic dysfunction. As PCS may represent a modifiable therapeutic target, strategies targeting dysbiosis & uremic toxin burden warrant further investigation.