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Clinical Summary

High-sensitivity C-reactive protein as a marker for adverse renal outcomes post-MI

Takeaway

  • Elevated levels of high-sensitivity C-reactive protein (hsCRP) are associated with subsequent risk for acute kidney injury (AKI) and progression of chronic kidney disease (CKD) in patients after myocardial infarction (MI).

Why this matters

  • Findings support the hypothesis that inflammation may be one of the pathways connecting cardiac and kidney dysfunction, and this association may help in implementing preventive therapies and lifestyle changes.

Study design

  • 12,905 MI survivors who underwent hsCRP testing >30 days with available information on estimated glomerular filtration rate (eGFR) were included.
  • Main outcomes included CKD progression (composite of doubling plasma creatinine, renal replacement therapy or renal death) and AKI (plasma creatinine level >26.5 μmol/L according to the Kidney Disease: Improving Global Outcomes criteria).
  • Funding: None disclosed.

Key results

  • During a median follow-up of 3.2 years, 1019 CKD progressions (incident rate, 2.7%) and 1481 AKI events (incident rate, 3.95%) were reported.
  • After adjustment for confounders, patients with hsCRP ≥2 mg/L vs those with hsCRP <2 mg/L were at an increased risk for CKD progression (HR, 1.42; 95% CI, 1.21-1.66) and AKI events (HR, 1.29; 95% CI, 1.13-1.47).
  • Compared to those with hsCRP ≤1 mg/L, HRs for patients with 1-3, 3-10 and >10 mg/L, respectively, were:
  • CKD progression
  • 1.26 (95% CI, 1.03-1.53),
  • 1.55 (95% CI, 1.29-1.86) and
  • 1.62 (95% CI, 1.31-2.01).
  • AKI
  • 1.22 (95% CI, 1.04-1.43),
  • 1.43 (95% CI, 1.22-1.66) and
  • 1.51 (95% CI, 1.27-1.81).
  • The association between hsCRP and AKI was weakened in a sub-analysis of patients with eGFR 30-44 mL/min/1.73 m2 and eGFR ≤30 mL/min/1.73 m2.

Limitations

  • Results have limited generalisability.
  • Potential risk for residual and unknown confounding

References


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