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Published on: May 31, 2016
Gla-Rich Protein Across the Chronic Kidney Disease Spectrum: Association with Vascular Calcification Burden and
Antun Lončarić1, Marlena Išek Lončarić2, Diana Balenović1
1Department of Cardiology, General Hospital Dr. Ivo Pedišić Sisak, 44000 Sisak, Croatia.
Insights
Serum Gla-rich protein (GRP) is linked to chronic kidney disease mineral and bone disorder (CKD-MBD) markers like FGF-23 and β-Klotho. Its association with vascular calcification and stiffness in CKD patients was modest.
Area of Science:
- Nephrology
- Cardiovascular Biology
- Biochemistry
Background:
- Vascular calcification and arterial stiffness are prevalent in chronic kidney disease (CKD).
- Gla-rich protein (GRP) is a vitamin K-dependent protein involved in mineral metabolism.
- Limited clinical data exists on GRP's role across various CKD stages.
Purpose of the Study:
- To investigate the association between serum GRP levels and vascular calcification (VC) burden.
- To evaluate the relationship between serum GRP and arterial stiffness in individuals across the CKD spectrum.
- To compare these associations in controls, non-dialysis CKD patients, and hemodialysis patients.
Main Methods:
- Prospective observational study with 185 adult participants (controls, CKD IIIb-IV, CKD V on hemodialysis).
- Assessment of abdominal aortic calcification using the Kauppila score and arterial stiffness via pulse wave velocity (PWV).
- Measurement of serum GRP, FGF-23, and β-Klotho (KLb) using ELISA; statistical analysis included non-parametric comparisons and Bonferroni-corrected Spearman correlations.
Main Results:
- Serum GRP levels exhibited a non-linear pattern across CKD stages, being lowest in CKD IIIb-IV (p < 0.001).
- Pulse wave velocity (PWV) and Kauppila scores increased progressively with CKD stage (p < 0.001).
- Serum GRP strongly correlated with KLb (ρ = 0.720) and FGF-23 (ρ = 0.625) but not directly with PWV or Kauppila score. Multivariable analysis showed modest associations between GRP, PWV, and Kauppila score.
Conclusions:
- Serum GRP is more strongly associated with CKD-MBD biochemical markers (KLb, FGF-23) than with vascular phenotypes in the CKD spectrum.
- The associations of GRP with vascular calcification burden and arterial stiffness are modest.
- GRP may serve as a marker for the CKD-MBD biochemical profile rather than a direct surrogate for vascular disease in CKD.
Abstract:
Background/Objectives: Vascular calcification and arterial stiffness are common in chronic kidney disease (CKD). Gla-rich protein (GRP) is a vitamin K-dependent protein implicated in mineral biology, but clinical evidence across CKD stages is limited. We evaluated associations of serum GRP with vascular calcification (VC) burden and arterial stiffness across CKD stages, including hemodialysis, compared with controls. Methods: In this prospective observational study, 185 adults were enrolled: controls (n = 61), individuals with CKD stage IIIb-IV (n = 61), and individuals with CKD stage V on hemodialysis (HD) (n = 63). Abdominal aortic calcification was assessed by the Kauppila score, and arterial stiffness was assessed by oscillometric pulse wave velocity (PWV). Serum GRP, FGF-23, and β-Klotho (KLb) were measured by ELISA. Non-parametric group comparisons and Bonferroni-corrected Spearman correlations were used. Results: GRP differed across groups (p < 0.001), showing a non-linear pattern with the lowest values in CKD IIIb-IV. PWV and Kauppila score increased across CKD stages (both p < 0.001). After Bonferroni correction, GRP correlated with KLb (ρ = 0.720) and FGF-23 (ρ = 0.625), but not with PWV or Kauppila score. In multivariable analyses, GRP showed a statistically significant but modest association with PWV and Kauppila score. Conclusions: In this CKD spectrum cohort, serum GRP was associated with CKD-MBD biochemical markers (KLb and FGF-23) much more strongly than with vascular phenotypes; its associations with vascular calcification burden and arterial stiffness were modest in multivariable modelling, supporting GRP as a marker of the CKD-MBD biochemical profile rather than a strong surrogate of vascular phenotype.
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