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Published on: June 2, 2022
Serum Thyrotropin Elevation and Coronary Artery Calcification in Hemodialysis Patients
Connie M Rhee1, Matthew Budoff2, Gregory Brent3,4
1Harold Simmons Center for Chronic Disease Research and Epidemiology, University of California Irvine School of Medicine, Orange, California, USA.
Insights
Higher serum thyrotropin (TSH) levels are linked to increased coronary artery calcification (CAC) in hemodialysis patients. This finding suggests a potential role for thyroid function in cardiovascular risk for this population.
Area of Science:
- Nephrology
- Endocrinology
- Cardiology
Background:
- Hypothyroidism is common in end-stage kidney disease (ESKD) patients.
- Lower thyroid hormone levels may increase coronary artery calcification (CAC) risk in ESKD.
- The association between serum thyrotropin (TSH) and CAC in hemodialysis patients remains unexamined.
Purpose of the Study:
- To investigate the relationship between serum TSH levels and CAC risk in hemodialysis patients.
- To assess if TSH is an independent predictor of CAC in this population.
Main Methods:
- Secondary analysis of data from the Anti-Inflammatory and Anti-Oxidative Nutrition in Hypoalbuminemic Dialysis Patients trial.
- Serum TSH levels and CAC were assessed using cardiac computed tomography scans.
- Multivariable logistic regression was used to evaluate the association between TSH and CAC Volume (VS) and Agatston score (AS).
Main Results:
- Higher TSH levels (highest tertile) were associated with significantly elevated CAC VS and AS (adjusted ORs 4.26 and 5.53, respectively).
- TSH levels >3.0 mIU/L were also linked to increased CAC VS and AS.
- Lower direct free thyroxine levels showed a trend towards elevated CAC, but did not reach statistical significance.
Conclusions:
- Elevated serum TSH is associated with increased CAC burden in hemodialysis patients.
- Further research is warranted to explore thyroid hormone supplementation as a strategy to reduce CAC in this high-risk group.
Introduction:
Hypothyroidism is highly prevalent in end-stage kidney disease patients, and emerging data show that lower circulating thyroid hormone levels lead to downregulation of vascular calcification inhibitors and coronary artery calcification (CAC) in this population. To date, no studies have examined the association of serum thyrotropin (TSH), the most sensitive and specific single biochemical metric of thyroid function, with CAC risk in hemodialysis patients.
Methods:
In secondary analyses of patients from the Anti-Inflammatory and Anti-Oxidative Nutrition in Hypoalbuminemic Dialysis Patients trial, we examined serum TSH levels and CAC risk assessed by cardiac computed tomography scans collected within a 90-day period. We evaluated the relationship between serum TSH with CAC Volume (VS) and Agatston score (AS) (defined as >100 mm3 and >100 Houndsfield Units, respectively) using multivariable logistic regression.
Results:
Among 104 patients who met eligibility criteria, higher TSH levels in the highest tertile were associated with moderately elevated CAC VS and AS in case-mix-adjusted analyses (ref: lowest tertile): adjusted ORs (95% CIs) 4.26 (1.18, 15.40) and 5.53 (1.44, 21.30), respectively. TSH levels >3.0 mIU/L (ref: ≤3.0 mIU/L) were also associated with moderately elevated CAC VS and AS. In secondary analyses, point estimates of incrementally lower direct free thyroxine levels trended toward elevated CAC VS and AS, although associations did not achieve statistical significance.
Conclusions:
In hemodialysis patients, higher serum TSH was associated with elevated CAC VS and AS. Further studies are needed to determine if thyroid hormone supplementation can attenuate CAC burden in this population.
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