CKD: inflammation tied to treatment-resistant HTN in CRIC

  • Chen J & al.
  • Hypertension
  • 19 Feb 2019

  • curated by Yael Waknine
  • Clinical Essentials
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Takeaway

  • Higher levels of interleukin (IL)-6 and tumor necrosis factor-α (TNF-α) are associated with higher odds of apparent treatment-resistant hypertension (ATRH) in chronic kidney disease (CKD).
  • Lower levels of transforming growth factor-β (TGF-β) are tied to lower ATRH risk.

Why this matters

  • ATRH prevalence in CKD is 40.4% (vs general population, 8.9%).
  • Targeting specific inflammatory pathways may improve BP control.

    Key results

    • ATRH risk was elevated with highest vs lowest tertiles of IL-6 (aOR=1.29; 95% CI, 1.05-1.59) and TNF-α (aOR=1.49; 95% CI, 1.20-1.85).
      • IL-6: risk/1 standard deviation (SD) increase (0.89 pg/mL: aOR=1.09; P=.05).
      • TNF-α: risk/1SD increase (0.69 mg/dL: aOR=1.12; P=.009).
    • ATRH risk was lowered with highest vs lowest tertiles of TGF-β (aOR=0.77; 95% CI, 0.63-0.95).
      • Risk/1SD increase (0.67 ng/mL: aOR=0.88; P=.004).
    • No significant associations with high-sensitivity C-reactive protein, fibrinogen, IL-1β, or IL-1 receptor antagonist.
    • ATRH was tied to increased risks for cardiovascular disease (aHR=1.49; P<.001 and all-cause mortality p=".002).</li">

    Study design

    • Chronic Renal Insufficiency Cohort (CRIC) participants with CKD and hypertension (HTN): 1359 with ATRH and 2008 without.
    • ATRH: BP ≥140/90 mmHg on ≥3 antihypertensives or
    • Funding: National Institute of Diabetes and Digestive and Kidney Diseases, Perelman School of Medicine, Johns Hopkins University, others.

    Limitations

    • Observational design.