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Abstract: FR-PO145

Associations of Calciprotein Particle Transformation with Arterial Calcification, Arterial Stiffness, and All-Cause Mortality in Hemodialysis Patients

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical


  • Chen, Wei, Albert Einstein College of Medicine, Bronx, New York, United States
  • Fitzpatrick, Jessica, The Hospital for Sick Children, Toronto, Ontario, Canada
  • Monroy-Trujillo, Jose Manuel, Johns Hopkins University, Baltimore, Maryland, United States
  • Sozio, Stephen M., Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Jaar, Bernard G., Johns Hopkins University and Nephrology Center of Maryland, Baltimore, Maryland, United States
  • Estrella, Michelle M., University of California, San Francisco and San Francisco VA Medical Center, San Francisco, California, United States
  • Serrano, Jishyra V., University of Rochester Medical Center, Rochester, New York, United States
  • Melamed, Michal L., Albert Einstein College of Medicine, Bronx, New York, United States
  • Bushinsky, David A., University of Rochester Medical Center, Rochester, New York, United States
  • Parekh, Rulan S., The Hospital For Sick Children, Toronto, Ontario, Canada

Group or Team Name

  • PACE

Transformation of primary to secondary calciprotein particles (CPP) in the serum may be a marker for arterial calcification as suggested by in vitro studies. Using dynamic light scattering, we can measure the size of secondary CPP aggregates (CPP2) and time of transformation (T50). We hypothesized that a higher ratio of CPP2 to T50 (CPP2:T50) is associated with greater arterial calcification, arterial stiffness, and mortality among hemodialysis (HD) patients.


We measured baseline CPP2:T50 in 387 incident HD patients enrolled in the Predictors of Arrhythmic and Cardiovascular Risk in ESRD (PACE) cohort. We examined cross-sectional associations of CPP2:T50 with serum markers of arterial calcification (fetuin-A, matrix Gla protein and osteoprotegerin), coronary arterial calcification (CAC), thoracic aortic calcification (TAC) and pulse wave velocity (PWV), as well as its longitudinal associations with PWV and all-cause mortality. Models were adjusted for demographics, co-morbidities, smoking history, body mass index, serum calcium and phosphorous.


Mean age was 55 ± 13 years; 41% were female; 71% were black and 58% had diabetes mellitus. Median CPP2 was 295 nm (IQR 208-382); T50 was 303 min (IQR 229-387); CPP2:T50 was 1.01 nm/min (IQR 0.57-1.66) and follow up length was 3.5 years (IQR 1.7-6.2). Per 0.1 nm/min higher CPP2:T50, fetuin-A level was 9 mg/L lower (95% CI: -10 to -7) and matrix Gla protein level was 1.0% higher (95% CI: 0.1-2.0%). CPP2:T50 was not associated with osteoprotegerin, baseline CAC, TAC and PWV, or with changes in PWV. Higher CPP2:T50 was associated with greater all-cause mortality [HR 1.02 (95% CI 1.00-1.04) per 0.1 nm/min higher CPP2:T50, p=0.02].


In incident HD patients, higher serum CPP2:T50 was associated with lower fetuin-A, higher matrix Gla protein levels, and higher risk of all-cause mortality, but not with arterial calcification or arterial stiffness. These findings support CPP transformation as a marker for calcification inhibitors and mortality, but not for arterial calcification.


  • NIDDK Support