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Identifying early pathogenic events during vascular calcification in uremic rats
Luis Hortells1, Cecilia Sosa1, Natalia Guillén1
1Laboratory of Molecular Toxicology, University of Zaragoza, Spain.
Kidney International
|August 29, 2017
Summary
In chronic kidney disease, vascular calcification begins with increased Dkk1 and tissue non-specific alkaline phosphatase (TNAP) in the aorta, preceded by elevated FGF23 and activin A. Other factors emerge later in this complex process.
Area of Science:
- Nephrology
- Biochemistry
- Pathology
Background:
- Vascular calcification is a complex complication of chronic kidney disease (CKD).
- Traditional explanations involve multiple factors.
- Distinguishing initiating from complicating factors in CKD-related vascular calcification is crucial.
Purpose of the Study:
- To clarify the roles of diverse agents in vascular calcification in uremic rats.
- To differentiate between initiating and complicating factors in the process.
Main Methods:
- 5/6 nephrectomy in rats followed by a high-phosphorus diet.
- Analysis of aortic tissue and plasma at various time points post-nephrectomy.
- Measurement of gene expression, protein activity, and plasma analyte concentrations.
Main Results:
- Early aortic changes (11 weeks) included increased Dkk1 mRNA and tissue non-specific alkaline phosphatase (TNAP) expression/activity.
- Initial aortic calcium deposits appeared at 12 weeks, correlating with TNAP expression.
- Elevated plasma FGF23 and activin A were observed at 11 weeks, preceding increases in PTH and phosphorus (20 weeks).
Conclusions:
- Increased aortic TNAP and Dkk1 expression precede initial vascular calcification in this CKD model.
- Elevated circulating FGF23 and activin A are early events.
- Other calcification-related factors are altered at later disease stages.
