Patients with advanced chronic kidney disease and vascular calcification have a large hydrodynamic radius of secondary calciprotein particles.


Journal

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
ISSN: 1460-2385
Titre abrégé: Nephrol Dial Transplant
Pays: England
ID NLM: 8706402

Informations de publication

Date de publication:
01 06 2019
Historique:
received: 16 02 2018
pubmed: 23 5 2018
medline: 15 4 2020
entrez: 23 5 2018
Statut: ppublish

Résumé

The size of secondary calciprotein particles (CPP2) and the speed of transformation (T50) from primary calciprotein particles (CPP1) to CPP2 in serum may be associated with vascular calcification (VC) in patients with chronic kidney disease (CKD). We developed a high throughput, microplate-based assay using dynamic light scattering (DLS) to measure the transformation of CPP1 to CPP2, hydrodynamic radius (Rh) of CPP1 and CPP2, T50 and aggregation of CPP2. We used this DLS assay to test the hypothesis that a large Rh of CPP2 and/or a fast T50 are associated with VC in 45 participants with CKD Stages 4-5 (22 without VC and 23 with VC) and 17 healthy volunteers (HV). VC was defined as a Kauppila score >6 or an Adragao score ≥3. CKD participants with VC had larger cumulants Rh of CPP2 {370 nm [interquartile range (IQR) 272-566]} compared with CKD participants without VC [212 nm (IQR 169-315)] and compared with HV [168 nm (IQR 145-352), P < 0.01 for each]. More CPP2 were in aggregates in CKD participants with VC than those without VC (70% versus 36%). The odds of having VC increased by 9% with every 10 nm increase in the Rh of CPP2, after adjusting for age, diabetes, serum calcium and phosphate [odds ratio 1.09, 95% confidence interval (CI) 1.03, 1.16, P = 0.005]. The area under the receiver operating characteristic curve for VC of CPP2 size was 0.75 (95% CI 0.60, 0.90). T50 was similar in CKD participants with and without VC, although both groups had a lower T50 than HV. Rh of CPP2, but not T50, is independently associated with VC in patients with CKD Stages 4-5.

Sections du résumé

BACKGROUND
The size of secondary calciprotein particles (CPP2) and the speed of transformation (T50) from primary calciprotein particles (CPP1) to CPP2 in serum may be associated with vascular calcification (VC) in patients with chronic kidney disease (CKD).
METHODS
We developed a high throughput, microplate-based assay using dynamic light scattering (DLS) to measure the transformation of CPP1 to CPP2, hydrodynamic radius (Rh) of CPP1 and CPP2, T50 and aggregation of CPP2. We used this DLS assay to test the hypothesis that a large Rh of CPP2 and/or a fast T50 are associated with VC in 45 participants with CKD Stages 4-5 (22 without VC and 23 with VC) and 17 healthy volunteers (HV). VC was defined as a Kauppila score >6 or an Adragao score ≥3.
RESULTS
CKD participants with VC had larger cumulants Rh of CPP2 {370 nm [interquartile range (IQR) 272-566]} compared with CKD participants without VC [212 nm (IQR 169-315)] and compared with HV [168 nm (IQR 145-352), P < 0.01 for each]. More CPP2 were in aggregates in CKD participants with VC than those without VC (70% versus 36%). The odds of having VC increased by 9% with every 10 nm increase in the Rh of CPP2, after adjusting for age, diabetes, serum calcium and phosphate [odds ratio 1.09, 95% confidence interval (CI) 1.03, 1.16, P = 0.005]. The area under the receiver operating characteristic curve for VC of CPP2 size was 0.75 (95% CI 0.60, 0.90). T50 was similar in CKD participants with and without VC, although both groups had a lower T50 than HV.
CONCLUSIONS
Rh of CPP2, but not T50, is independently associated with VC in patients with CKD Stages 4-5.

Identifiants

pubmed: 29788425
pii: 4996711
doi: 10.1093/ndt/gfy117
pmc: PMC6545469
doi:

Substances chimiques

Phosphates 0
Calcium SY7Q814VUP

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

992-1000

Subventions

Organisme : NCATS NIH HHS
ID : KL2 TR001999
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK075462
Pays : United States
Organisme : NCRR NIH HHS
ID : S10 RR026501
Pays : United States
Organisme : NCRR NIH HHS
ID : S10 RR027241
Pays : United States

Informations de copyright

© The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

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Auteurs

Wei Chen (W)

Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

Viktoriya Anokhina (V)

Department of Biochemistry and Biophysics, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

Gregory Dieudonne (G)

Department of Radiology, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

Matthew K Abramowitz (MK)

Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA.

Randeep Kashyap (R)

Department of Surgery, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

Chen Yan (C)

Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

Tong Tong Wu (TT)

Department of Biostatistics and Computational Biology, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

Karen L de Mesy Bentley (KL)

Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

Benjamin L Miller (BL)

Department of Biochemistry and Biophysics, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.
Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.
Department of Biomedical Engineering, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

David A Bushinsky (DA)

Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

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