Kidney Week

Abstract: SA-OR022

Large Secondary Calciprotein Particles Are Associated with Vascular Calcification

Session Information

• Mineral Disease: Bones, Vessels, Stones
  November 04, 2017 | Location: Room 273, Morial Convention Center
  Abstract Time: 04:42 PM - 04:54 PM

Category: Mineral Disease

• 1205 Vascular Calcification

Authors

• Chen, Wei, University of Rochester School of Medicine , Rochester, New York, United States

Wei Chen, MD, MS

https://www.urmc.rochester.edu/people/28958017-wei-chen/researchers

• Anokhina, Viktoriya, University of Rochester School of Medicine , Rochester, New York, United States

Viktoriya Anokhina,

• Miller, Benjamin L., University of Rochester School of Medicine , Rochester, New York, United States

Benjamin L. Miller,

• Dieudonne, Gregory, University of Rochester School of Medicine , Rochester, New York, United States

Gregory Dieudonne,

• Abramowitz, Matthew K., Albert Einstein College of Medicine, Bronx, New York, United States

Matthew K. Abramowitz,

• Kashyap, Randeep, University of Rochester School of Medicine , Rochester, New York, United States

Randeep Kashyap,

• Yan, Chen, University of Rochester School of Medicine , Rochester, New York, United States

Chen Yan,

• Wu, Tong tong, University of Rochester School of Medicine , Rochester, New York, United States

Tong tong Wu,

• Bushinsky, David A., University of Rochester School of Medicine , Rochester, New York, United States

David A. Bushinsky,

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