High parathyroid hormone levels and bone loss may predict progression of coronary artery calcification (CAC) in patients receiving dialysis, according to a study published online April 2 in the Journal of the American Society of Nephrology.
"We discovered that high parathyroid hormone and the consequential bone loss are major risk factors for progression of vascular calcifications," Hartmut H. Malluche, MD, from the Division of Nephrology, Bone and Mineral Metabolism, University of Kentucky, Lexington, commented in a news release.
"These two factors were heretofore not appreciated and were independent from traditional known risk factors," he added.
Elevated parathyroid hormone levels cause the release of calcium from bone, leading to bone loss and thinning. Most patients receiving dialysis for chronic kidney disease have CAC. CAC increases the risk for cardiovascular events, which in turn cause the majority of deaths in patients with CKD, the authors note.
Therefore, Dr Malluche and colleagues recommend monitoring bone loss with measurements of parathyroid hormone or bone mineral density (BMD) as a way to predict progression of CAC in patients receiving dialysis.
Between August 2009 and April 2013, the researchers enrolled 213 participants from 38 dialysis centers in Kentucky. Participants underwent measurement of routine laboratory tests, serum markers of bone metabolism, and CAC at baseline and 1 year. The researchers also evaluated BMD at both points using dual-energy X-ray absorptiometry scans and quantitative computed tomography. They assessed CAC using multislide computed tomography of the heart and CAC square root of coronary artery calcification volume, an analytic technique that accounts for variability in scanning.
About 80% of participants had CAC at baseline, and almost 50% of these had measurements suggesting high risk for cardiovascular events. One third of participants had osteoporosis.
Independent positive predictors of baseline CAC included coronary artery disease, diabetes, length of time receiving dialysis, age, and concentration of fibroblast growth factor 23, which regulates serum phosphate levels and helps maintain bone strength. In contrast, BMD of the spine inversely predicted baseline CAC.
CAC progression at 1 year occurred among three quarters of the 122 patients who completed the study. Independent risk factors for CAC progression included age, osteoporosis (β = 4.6; 95% confidence interval, 1.8 - 7.5; P = .002), and baseline total or whole parathyroid hormone more than nine times the normal value, after adjusting for age (β = 6.9; 95% confidence interval, 2.4 - 11.4; P = .003).
The researchers note several limitations for the study, including exclusion of about 20% of screened patients because of severe comorbidities or impaired mental status. In addition, the prospective, short-term nature of the study precluded determination of disease mechanisms and long-term relationships.
Dr Malluche noted in the press release that important links may exist between the level of calcification in bones and calcifications in blood vessels.
"Studies need to be done to find out whether prevention of bone loss will reduce progression of vascular calcifications," he emphasized.
The authors have disclosed no relevant financial relationships.
J Am Soc Nephrol. Published online April 2, 2015. Abstract
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