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Updated: Jul 9, 2025
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Plasma activin A rises with declining kidney function and is independently associated with mortality in patients with
Anders Nordholm1,2, Ida M H Sørensen1, Sasha S Bjergfelt1,3
1Department of Nephrology, Rigshospitalet, Copenhagen, Denmark.
Insights
Plasma activin A is elevated in chronic kidney disease (CKD) and linked to higher mortality risk. This study found activin A levels increase with declining kidney function and independently predict death in CKD patients.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Endocrinology
Background:
- Plasma activin A is elevated in chronic kidney disease-mineral and bone disorder (CKD-MBD).
- Activin A inhibition ameliorates CKD-MBD complications in rodent models.
- The role of plasma activin A in CKD patient outcomes requires investigation.
Purpose of the Study:
- To examine the association of plasma activin A with major adverse cardiovascular events (MACE), all-cause mortality, and CKD-MBD complications in CKD patients.
Main Methods:
- Prospective cohort study of 916 participants (741 CKD patients, 175 controls).
- Evaluated plasma activin A levels against estimated glomerular filtration rate (eGFR), vascular calcification (Agatston scores), and bone mineral density (BMD).
- Assessed association with MACE and all-cause mortality using survival analysis (Aalen-Johansen/Kaplan-Meier) and Cox regression.
Main Results:
- Plasma activin A increased with CKD stage and inversely correlated with eGFR (r = -0.53, P < .01).
- Plasma activin A was associated with all-cause mortality (HR 1.55, P < .05) independently of age, sex, diabetes mellitus (DM), and eGFR.
- No significant association was found between plasma activin A and MACE, vascular calcification, or BMD after eGFR adjustment.
Conclusions:
- Plasma activin A levels rise with decreasing kidney function.
- Elevated plasma activin A is an independent predictor of all-cause mortality in CKD patients.
- Plasma activin A is not significantly associated with MACE, vascular calcification, or BMD in this cohort.
Background:
Plasma (p-)activin A is elevated in chronic kidney disease-mineral and bone disorder (CKD-MBD). Activin A inhibition ameliorates CKD-MBD complications (vascular calcification and bone disease) in rodent CKD models. We examined whether p-activin A was associated with major adverse cardiovascular events (MACE), all-cause mortality and CKD-MBD complications in CKD patients.
Methods:
The study included 916 participants (741 patients and 175 controls) from the prospective Copenhagen CKD cohort. Comparisons of p-activin A with estimated glomerular filtration rate (eGFR), coronary and thoracic aorta Agatston scores, and bone mineral density (BMD) were evaluated by univariable linear regression using Spearman's rank correlation, analysis of covariance and ordinal logistic regression with adjustments. Association of p-activin A with rates of MACE and all-cause mortality was evaluated by the Aalen-Johansen or Kaplan-Meier estimator, with subsequent multiple Cox regression analyses.
Results:
P-activin A was increased by CKD stage 3 (124-225 pg/mL, P < .001) and correlated inversely with eGFR (r = -0.53, P < 0.01). P-activin A was associated with all-cause mortality [97 events, hazard ratio 1.55 (95% confidence interval 1.04; 2.32), P < 0.05] after adjusting for age, sex, diabetes mellitus (DM) and eGFR. Median follow-up was 4.36 (interquartile range 3.64-4.75) years. The association with MACE was not significant after eGFR adjustment. Agatston scores and BMD were not associated with p-activin A.
Conclusion:
P-activin A increased with declining kidney function and was associated with all-cause mortality independently of age, sex, DM and eGFR. No association with MACE, vascular calcification or BMD was demonstrated.
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