Abstract: FR-PO1162
Predicting Endothelial Cell Injury from Urine Sodium-to-Potassium Ratio in Patients with CKD
Session Information
- CKD: Screening, Diagnosis, Serum and Urine Biomarkers, and Scoring Indices
November 07, 2025 | 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
- Prakash, Pranav, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Van Buren, Peter N., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Lederer, Eleanor D., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Chen, Jing, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Background
Chronic Kidney Disease (CKD) is a salt-sensitive state associated with endothelial cell dysfunction (ECD) and higher prevalence of hypertension than the general population. Increased dietary sodium (Na) intake and/or low potassium (K) intake is associated with higher blood pressure (BP). There is emerging evidence that increased Na intake induces ECD. We analysed data from a population-based cohort and evaluated associations between urinary Na/K ratio and markers for endothelial cell injury/activation.
Methods
We conducted a cross-sectional study of CKD patients (estimated glomerular filtration rate <60 mL/min or urine albumin/creatinine [UACR]>30 mg/g) from the Dallas Heart Study (DHS). We conducted linear regression analyses with first morning spot urine Na/K as the primary predictor and intercellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM) and s-endoglin as primary outcomes in separate models controlling for age, sex, race, diabetes, BMI, renal function, albuminuria, BP, serum magnesium (Mg), glucose, albumin, and cholesterol.
Results
There were 240 participants with urine chemistry data. Mean age was 48.4 (9.3) years, with 54% women, 70% Black race, 65% with diabetes, and 27% on diuretics. Mean urine Na/K was 4.2 (3.0) and was similar between those taking vs. not taking diuretics (p=.7). Urine Na/K correlated with systolic BP (r=0.2, p=.002), Mg (r=-0.2, p=.001), ICAM (r=0.1, p=.03), VCAM (r=0.2, P=.002), and s-endoglin (r=-0.2, p=.006). In regression analyses, urine Na/K positively predicted ICAM and VCAM (β=45 and 159; p=.02 and .0007), but was negatively associated with log endoglin (β =-0.01, p=.002) when controlling for the above variables. Adding diuretics to our model did not change results.
Conclusion
Our study suggests that elevated urine Na/K ratio is independently associated with endothelial injury/activation in a diverse CKD population. Further work is needed to identify if dietary Na restriction and/or K liberalization can minimize ECD, keeping in consideration the potential hyperkalemic risks in CKD patients.
Multivariate regression analyses showing Standardized Regression coefficient and p value for each outcome
| ICAM | VCAM | Endoglin | |
| urine Sodium potassium ratio | 0.2(.02) | 0.3(.007) | -0.2(.002) |
ICAM-Intercellular adhesion molecule; VCAM- Vascular Cell adhesion molecule