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      Effect of Intensive Blood Pressure Lowering on Kidney Tubule Injury: Findings From the ACCORD Trial Study Participants

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          Abstract

          Rationale & Objective:

          Randomization to intensive blood pressure lowering (SBP<120 mm Hg) compared to a less intensive BP target (SBP <140 mm Hg) in the ACCORD-BP trial resulted in a more rapid decline in the estimated glomerular filtration rate (eGFR). Whether this reflects hemodynamic effects or intrinsic kidney damage is unknown.

          Study Design:

          Longitudinal analysis of a sub-group of clinical trial participants.

          Settings & Participants:

          A subgroup of 529 participants in ACCORD-BP.

          Exposures:

          Urine biomarkers of tubular injury (kidney injury molecule 1 [KIM-1], interleukin 18 [IL-18]), repair (YKL-40) and inflammation (monocyte chemoattractant protein 1 [MCP-1]) at baseline and year 2.

          Outcomes:

          Changes in eGFR from baseline to 2 years.

          Analytical Approach:

          We compared changes in biomarkers and changes in eGFR across participants treated to an intensive vs. less intensive BP goal using analysis of covariance.

          Results:

          Of the 529 participants, 260 had been randomized to the intensive and 269 to the standard blood pressure arm. Mean age was 62 ± 6.5 and eGFR 90 ml/min/1.73m 2. Baseline clinical characteristics, eGFR, urinary albumin-to-creatinine ratio (ACR), and urinary biomarkers were similar across BP treatment groups. Compared to less intensive BP treatment, eGFR was 9.2 ml/min/1.73m 2 lower in the intensive BP treatment group at year 2. Despite the eGFR reduction, within this treatment group ACR was 30% lower and 4 urinary biomarkers were unchanged or lower at year 2. Also within this group, participants with largest declines in eGFR had greater reductions in urinary IL-18 and YKL-40. In a subgroup analysis of participants developing incident CKD (sustained 30% decline and eGFR < 60 ml/min/1.73 m 2, n=77), neither ACR nor 4 biomarkers increased in the intensive treatment group, whereas one biomarker, IL-18, increased in the less intensive treatment group.

          Limitations:

          Few participants with advanced baseline CKD. Comparisons across treatment groups do not represent comparisons of treatment arms created solely through randomization.

          Conclusions:

          Among a subset of ACCORD-BP trial participants, intensive BP control was associated reductions of eGFR but not with an increase in injury markers. These findings support that eGFR decline observed with intensive BP goals in ACCORD participants may predominantly reflect hemodynamic alterations.

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          Author and article information

          Journal
          8110075
          423
          Am J Kidney Dis
          Am. J. Kidney Dis.
          American journal of kidney diseases : the official journal of the National Kidney Foundation
          0272-6386
          1523-6838
          24 August 2018
          02 October 2018
          January 2019
          01 January 2020
          : 73
          : 1
          : 31-38
          Affiliations
          [1. ]Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai
          [2. ]Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, CT.
          [3. ]Division of Nephrology-Hypertension, Department of Medicine, University of California San Diego, San Diego, CA
          [4. ]Nephrology Section, Veterans Affairs San Diego Healthcare System, San Diego, California.
          [5. ]Division of Preventive Medicine, Department of Family Medicine and Public Health, University of California San Diego, San Diego, California;
          [6. ]Kidney Health Research Collaborative, University of California San Francisco, San Francisco, CA.
          [7. ]Department of Medicine, San Francisco VA Medical Center and University of California, San Francisco,
          [8. ]Program of Applied Translational Research, Section of Nephrology, Department of Medicine, Yale University School of Medicine, New Haven, CT; Veterans Affairs Connecticut Healthcare System, New Haven, CT
          Author notes

          Authors’ Contributions: Study concept and design: GNN, SGC, CRP; acquisition, analysis, or interpretation of data: KC, VR, JHI, MGS, CRP, SGC; statistical analysis: GNN, VR, KC; obtained funding: CRP, SGC. Each author contributed important intellectual content during manuscript drafting or revision and accepts accountability for the overall work by ensuring that questions pertaining to the accuracy or integrity of any portion of the work are appropriately investigated and resolved.

          Corresponding author: Girish N. Nadkarni, MD, MPH, CPH or Steven Coca DO, MS, Icahn School of Medicine at Mount Sinai, One Gustave L Levy Place, Box 1243, New York, NY 10029, Telephone number: (212) 241-1385 / (212) 241-6633, Fax number: (212) 849-2643, girish.nadkarni@ 123456mountsinai.org or steven.coca@ 123456mssm.edu
          Article
          PMC6309631 PMC6309631 6309631 nihpa1504909
          10.1053/j.ajkd.2018.07.016
          6309631
          30291011
          04deda88-6b2d-4540-83b3-1cac3f890d0a
          History
          Categories
          Article

          urine,chronic kidney disease (CKD),renal perfusion,hypertension,urinary biomarkers,CKD progression,eGFR decline,kidney tubule,hemodynamics,estimated glomerular filtration rate (eGFR),tubular injury,blood pressure (BP),intensive BP control

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