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Abstract: SA-OR052

The Effect of Intensive Blood Pressure Lowering on Kidney Tubule Injury in a Subgroup of Participants in the ACCORD Trial

Session Information

Category: Hypertension and CVD

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


  • Nadkarni, Girish N., 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
  • Ix, Joachim H., UCSD, San Diego, California, United States
  • Shlipak, Michael, San Francisco VA Medical Center, San Francisco, California, 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

Randomization to the intensive (SBP<120 mm Hg) arm in the ACCORD-BP trial resulted in more rapid decline in estimated glomerular filtration rate (eGFR) than in the standard arm (SBP <140 mm Hg). Whether this change reflects hemodynamic effects or accelerated intrinsic kidney damage is unknown.


Longitudinal sub-group analysis of 529 participants in the ACCORD-Blood Pressure clinical trial. We measured urine biomarkers of tubule injury (kidney injury molecule-1 [KIM-1], interleukin-18 [IL-18]), repair (YKL-40) and inflammation (monocyte chemoattractant protein [MCP-1]) at baseline and year 2. We compared changes between arms using ANCOVA.


Of the 529 participants, 260 were randomized to intensive and 269 to standard blood pressure arm. Mean age was 62 ± 6.5 and eGFR 90 ml/min/1.73m2. Baseline clinical characteristics, eGFR, urinary albumin-to-creatinine ratio (ACR), and all 4 biomarkers were similar between arms. Compared to the standard arm, eGFR was 9.2 ml/min/1.73m2 lower in the intensive arm at year 2. Despite the reduction in eGFR, ACR was 30% lower in the intensive arm and 4 urinary biomarkers were unchanged or lower at year 2 in the intensive arm (Figure). Moreover, participants in the intensive arm with the largest declines in eGFR had greater reductions in urine IL-18 and YKL-40. In a subgroup analysis stratified by incident CKD development (sustained 30% decline and eGFR < 60 ml/min/1.73 m2, n=77), ACR and 4 biomarkers were flat to decreased in the intensive arm, whereas the urinary biomarkers were unchanged or increased in those that developed CKD in standard arm.


Among a subgrop from the ACCORD trial, randomization to intensive BP control reduced eGFR but did not increase injury markers. These findings support the hypothesis that eGFR decline in intensive BP arm of ACCORD predominantly reflect hemodynamic alterations.


  • NIDDK Support