Abstract: FR-PO0260
Size of Secondary Calciprotein Particle Aggregates in Serum and Coronary Artery Calcification Among Patients with CKD: The CRIC Study
Session Information
- Bone and Mineral Metabolism: Clinical Epidemiology and Outcomes
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Chen, Wei, Albert Einstein College of Medicine, Bronx, New York, United States
- Graham, Garry Anthony, Albert Einstein College of Medicine, Bronx, New York, United States
- Hanna, David B., Albert Einstein College of Medicine, Bronx, New York, United States
- Eiwaz, Mahaba B, Albert Einstein College of Medicine, Bronx, New York, United States
- Sibinga, Nicholas, Albert Einstein College of Medicine, Bronx, New York, United States
- Saini, Sara, Albert Einstein College of Medicine, Bronx, New York, United States
- Jaar, Bernard G., Johns Hopkins University, Baltimore, Maryland, United States
- Srivastava, Anand, University of Illinois Chicago, Chicago, Illinois, United States
- Rincon-Choles, Hernan, Cleveland Clinic, Cleveland, Ohio, United States
- Kuro-o, Makoto, Jichi Ika Daigaku, Shimotsuke, Tochigi Prefecture, Japan
- Isakova, Tamara, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States
- Mowrey, Wenzhu, Albert Einstein College of Medicine, Bronx, New York, United States
Group or Team Name
- CRIC.
Background
Calciprotein particles (CPPs) are nanoparticles of calcium phosphate crystals and calcification inhibitors. In patients with end stage kidney disease, large size of secondary CPP aggregates (CPP2) have been linked with high mortality. We hypothesized that CPP2 size is associated with coronary artery calcification (CAC) in patients with CKD stage 2 to 4.
Methods
CPP2 size was measured in stored serum of 1,403 participants from the Chronic Renal Insufficiency Cohort (CRIC) Study. We conducted cross-sectional and longitudinal analyses to examine associations of CPP2 size with CAC prevalence, incidence and progression. CAC was quantified using Agatston units, with a score>0 indicating CAC. Multivariable generalized linear mixed models were used and adjusted for demographics, clinical site, eGFR, proteinuria, diabetes, systolic blood pressure, number of antihypertensive medications, smoking, history of cardiovascular disease, total cholesterol, and statin use.
Results
Mean CPP2 size was 153 ± 48 nm. At baseline, 915 (65%) participants had prevalent CAC. CPP2 size was not associated with CAC prevalence. Among participants with prevalent CAC, larger CPP2 was associated with CAC severity after adjusting for demographics and clinical site: 1-SD larger CPP2 was associated with 20% (95% CI: 4-41%) greater CAC severity (Table). Among 886 participants who had repeat CAC scans after an average of 3 years follow-up, 90 (26%) without baseline CAC developed incident CAC, while 39 (7%) with baseline CAC had progression defined as annual increase ≥200 Agatston units. In fully adjusted models, CPP2 size was not associated with incident CAC, but significantly associated with CAC progression among those with baseline CAC: 1-SD larger CPP2 was associated with 49% (95% CI: 15-94%) higher risk of CAC progression.
Conclusion
Among patients with CKD stages 2 to 4 and prevalent CAC, larger CPP2 is associated with more severe CAC and CAC progression.
Funding
- NIDDK Support