Abstract: SA-OR022

Large Secondary Calciprotein Particles Are Associated with Vascular Calcification

Session Information

Category: Mineral Disease

  • 1205 Vascular Calcification

Authors

  • Chen, Wei, University of Rochester School of Medicine , Rochester, New York, United States
  • Anokhina, Viktoriya, University of Rochester School of Medicine , Rochester, New York, United States
  • Miller, Benjamin L., University of Rochester School of Medicine , Rochester, New York, United States
  • Dieudonne, Gregory, University of Rochester School of Medicine , Rochester, New York, United States
  • Abramowitz, Matthew K., Albert Einstein College of Medicine, Bronx, New York, United States
  • Kashyap, Randeep, University of Rochester School of Medicine , Rochester, New York, United States
  • Yan, Chen, University of Rochester School of Medicine , Rochester, New York, United States
  • Wu, Tong tong, University of Rochester School of Medicine , Rochester, New York, United States
  • Bushinsky, David A., University of Rochester School of Medicine , Rochester, New York, United States
Background

Vascular calcification (VC) is common and contributes to cardiovascular mortality in patients with CKD. Calcification propensity as measured by the serum assay of Pasch et al. using nephelometry is associated with cardiovascular events; however, whether it is a biomarker for VC is unknown. We modified this assay through the use of microplate-based dynamic light scattering, which allowed us to measure both time for half-maximal transformation (T50) of 1° to 2° calciprotein particles (CPPs) and size of 2°CPPs (CPP2) (instead of only T50 with nephelometry). A fast T50 and/or a large CPP2 appears to reflect a procalcific milieu. Here we tested the hypothesis that a fast T50 and/or a large CPP2 would be associated with VC.

Methods

We measured T50 and CPP2 in 46 subjects with stage 4-5 CKD and 17 healthy volunteers. T50 and CPP2 were examined as continuous and categorical variables (dichotomized at the median). VC was measured on plain radiographs and defined as a Kauppila score >6 (lumbar aorta) or Adragao score ≥3 (iliac, femoral, radial and digital arteries). Logistic regression was used to examine the association of T50 and CPP2 size with VC, adjusting for age, gender, eGFR and diabetes.

Results

Compared to healthy volunteers (age 24±5 yr, eGFR 114±13ml/min/1.73m2), CKD patients (age 65±12 yr, eGFR 19±8ml/min/1.73m2) had lower mean T50 (191±40 vs. 221±31 min, p=0.008) and higher median CPP2 [305 (187-477) vs. 168 (145-352) nm, p=0.02]. T50 was correlated inversely with CPP2 (r=-0.50, p<0.001). No healthy volunteers had VC, while 51% of CKD patients did. In all subjects, compared to those without VC, those with VC had a higher median CPP2 [370 (272-566) vs. 195 (153-327) nm, p=0.001] with no difference in mean T50 (191±39 vs. 203±41 min, p=0.27). Compared to those with CPP2 in the lower half (median=305nm), those with CPP2 in the upper half had 10.7 times higher odds of having VC (95% CI 1.4, 79.1, p=0.02). Similar results were obtained when analysis was limited to CKD patients.

Conclusion

CKD patients had larger CPP2 and faster T50 indicating greater calcification propensity compared with healthy volunteers. While a faster T50 was associated with larger CPP2, only a large CPP2 was associated with VC suggesting that CPP2 may be a useful biomarker for VC.

Funding

  • Other NIH Support