Systemic Inflammation Is Associated With Coronary Artery Calcification and All-Cause Mortality in Chronic Kidney

In-Chang Hwang1, Hyo Eun Park, Hack-Lyoung Kim

  • 1Department of Internal Medicine, Seoul National University College of Medicine.

Insights

Systemic inflammation in chronic kidney disease (CKD) worsens coronary artery calcification (CAC) and mortality risk. Coronary evaluation is advised for CKD patients with elevated hsCRP and significant CAC.

Area of Science:

  • Cardiology
  • Nephrology
  • Public Health

Background:

  • Systemic inflammation is linked to coronary artery calcification (CAC) in chronic kidney disease (CKD).
  • The prognostic impact of this association on mortality remains unclear.
  • Evaluating the interplay between CAC, kidney function, and inflammation is crucial.

Purpose of the Study:

  • To investigate the association between CAC, estimated glomerular filtration rate (eGFR), and all-cause mortality.
  • To determine if systemic inflammation modifies these associations.
  • To identify high-risk CKD patients who may benefit from coronary evaluation.

Main Methods:

  • A cohort of 30,703 individuals with CAC measurements was followed for a median of 79 months.
  • Patients were stratified by CAC score, eGFR categories, and hsCRP levels (≥2.0 mg/L indicating inflammation).
  • Statistical analyses adjusted for potential confounders.

Main Results:

  • Lower eGFR and higher hsCRP were independently associated with increased CAC prevalence and extent.
  • The association between lower eGFR and high CAC score (≥400) was more pronounced with higher hsCRP.
  • In CKD patients (eGFR <60 ml/min/1.73 m²), greater CAC burden predicted worse outcomes only in those with elevated hsCRP.

Conclusions:

  • Reduced eGFR and extensive CAC increase mortality risk in CKD patients.
  • Systemic inflammation significantly influences the relationship between CAC, kidney function, and mortality.
  • Coronary evaluation should be considered for CKD patients with elevated hsCRP and significant CAC.
Abstract

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