Abstract: FR-PO536

Plasma Biomarkers and Response to Intensive Blood Pressure Control: The ACCORD Trial

Session Information

Category: Hypertension

  • 1104 Hypertension: Clinical and Translational - Salt and Hypertension

Authors

  • Nadkarni, Girish N., Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Pollack-Zollman, Martine, Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Chauhan, Kinsuk, Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Rao, Veena, Yale University, New Haven, Connecticut, United States
  • Poojary, Priti, Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Saha, Aparna, Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Parikh, Chirag R., Yale University and VAMC, New Haven, Connecticut, United States
  • Coca, Steven G., Icahn School of Medicine at Mount Sinai, New York, New York, United States
Background

Plasma biomarkers of inflammation [ tumour necrosis factor 1 (TNFR1); monocyte chemoattractant protein (MCP1) and interleukin 18 (IL18)] , renal injury [Kidney Injury Molecule 1 (KIM1)] and fibrosis [YKL40] are associated with estimated glomerular filtration rate (eGFR) decline. There are limited data on association between these markers and response to intensive sytolic blood pressure (SBP) control. We examined the relationship between baseline plasma biomarker levels and longitudinal SBP change in the ACCORD trial.

Methods

We used a multiplex platform to measure plasma biomarkers in baseline plasma specimens from randomly selected ACCORD trial participants with type 2 diabetes in intensive SBP arm (goal <120; n=260) vs. standard SBP arm (goal <140; n=269). We estimated the association between longitudinal SBP change and baseline biomarker tertiles after stratifying by intensive vs. standard SBP arm using linear mixed models.

Results

Mean age was 61.7 years, 46.6% were female and baseline eGFR was 88 ml/min. There were no significant differences between the intensive and standard SBP arm. Participants in the third tertile of KIM-1 had a higher SBP at baseline after adjusting for eGFR, UACR and demographics [+3.7 mmHg, SE 1.6]. After randomization, participants in the third tertile of KIM-1 in intensive SBP group had a smaller change in sBP compared to the first tertile [-5.1 mmHg; SE 1.5; p<0.001]. There were no associations with other biomarkers and SBP change in either arm. (Figure 1)

Conclusion

Higher levels of plasma KIM-1 at baseline are associated with attenuated SBP changes with intensive control. These findings indicate that subclinical renal tubular injury is associated with poorer response to intensive SBP control, even in persons with normal eGFR.

Figure 1. Relationship between Biomarker Tertiles and Response to Blood Pressure Control Stratified by Intensive vs. Standard Arms

Funding

  • NIDDK Support