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Abstract: TH-OR50

Galectin 3 and Air Pollution in Hypertensive Patients with and Without CKD

Session Information

Category: Hypertension and CVD

  • 1402 Hypertension and CVD: Clinical, Outcomes, and Trials

Authors

  • Tariq, Hafsa, Case Western Reserve University, Cleveland, Ohio, United States
  • Al-Kindi, Sadeer, Case Western Reserve University, Cleveland, Ohio, United States
  • Rahman, Mahboob, Case Western Reserve University, Cleveland, Ohio, United States
  • Wright, Jackson T., Case Western Reserve University, Cleveland, Ohio, United States
  • Rajagopalan, Sanjay, Case Western Reserve University, Cleveland, Ohio, United States
  • Dobre, Mirela A., Case Western Reserve University, Cleveland, Ohio, United States
Background

Air pollution is a major contributor to cardiovascular and kidney complications. The mechanisms linking air pollution with cardiorenal events are not well understood. We sought to assess whether Galectin 3 level, a marker of myocardial fibrosis and remodeling is associated with air pollution exposure in hypertensive patients with and without chronic kidney disease.

Methods

Satellite-derived PM2.5 measurements were linked with participants in the Systolic Blood Pressure Intervention Trial (SPRINT, Clinicaltrials.gov NCT01206062). A total of 1019 SPRINT participants with available Galectin 3 levels at study baseline and 24 months follow-up were included in these analyses. Multivariable linear regression models, adjusted for age, sex, race, eGFR, Framingham risk score, body mass index, and randomization assignment were built to assess the association between air pollution and Galectin 3 at baseline and longitudinal change at 2 years.

Results

The mean PM2.5 was 9.6 µg/m3, and the median (IQR) Galectin 3 level was 14.4 (11.5-18.0) ng/mL. In multivariable models, we found no association between PM2.5 and baseline (β=-0.02, P=0.46) or longitudinal change (β=0.05, P=0.12) in Galectin 3. In the subgroup of participants with CKD (n=201), PM2.5 was associated with change in Galectin 3 (β=0.21, P=0.002), which remained statistically significant after multivariable adjustments (β=0.23, P=0.003). In the overall cohort (n=1019), there was a significant interaction between PM2.5 and eGFR with change in Galectin 3 (p-value for interaction=0.02), (Figure).

Conclusion

Air pollution may be associated with worsening myocardial fibrosis as evidenced by increasing levels of Galectin 3 in individuals with preexisting CKD. Further studies are needed to corroborate these findings with rigorous cardiac imaging studies.

Change in Galectin 3 and PM2.5 exposure by eGFR

Funding

  • Other NIH Support