Abstract
BackgroundPatients with end-stage renal disease have a higher risk of death from cardiovascular events, which can be mainly attributed to coronary artery calcification (CAC). Wnt signaling is involved in vascular development and may play a role in vascular calcification. This study aimed to evaluate CAC prevalence in patients on dialysis with severe secondary hyperparathyroidism (SHPT) and identify CAC risk factors.MethodsThe study is a retrospective analysis of the severe hyperparathyroidism registration study that prospectively recruited patients on dialysis with severe SHPT who were candidates for parathyroidectomy, from October 2013 to May 2015. CAC and bone mineral density (BMD) were measured. Demographic and clinical data including calcium, phosphorus, alkaline phosphatase, intact parathyroid hormone, Dickkopf-related protein 1 (DKK1), and sclerostin levels were analyzed. CAC scores were reported in Agatston units (AU).ResultsA total of 61 patients were included in this study. No CAC, mild CAC (<100 AU), moderate CAC (>100 AU), and severe CAC (>400 AU) were observed in 4.9%, 11.4%, 14.8%, and 68.9% of patients, respectively. DKK1 and sclerostin were not associated with CAC. In univariate analysis, CAC was significantly correlated with age, sex (male), total cholesterol, and intravenous pulse calcitriol (p<0.05). CAC was not inversely correlated with the BMD, T scores, or Z scores of the femoral neck (p>0.05). In multivariate analysis, the stepwise forward multiple linear regression revealed that CAC was associated with age, male sex and intravenous pulse calcitriol (p<0.05). Furthermore, serum sclerostin was positively correlated with the BMD of the femoral neck but negatively associated with intact parathyroid hormone (p<0.05). Serum sclerostin was significantly associated with severely low bone mass with Z-scores<-2.5 of the femoral neck, even when adjusted for serum intact parathyroid hormone, vitamin D status, dialysis pattern, sex, and DKK-1 (p<0.05).ConclusionsThe patients on dialysis with severe SHPT have a high prevalence of vascular calcification. Although the Wnt signaling pathway could play a role in hyperparathyroid bone disease, CAC may be mainly due to the treatment modality rather than the Wnt signaling pathway associated bone metabolism in patients on dialysis with severe SHPT.
Highlights
Patients with end-stage renal disease have a higher risk of death from cardiovascular events, which can be mainly attributed to coronary artery calcification (CAC)
The levels of serum sclerostin have been reported to negatively correlate with parathyroid hormone (PTH) levels [18]. These results suggest that the Wnt signaling pathway may provide a causal link between hyperparathyroidism, low bone mineral density, and possible vascular calcification via Wnt signaling pathway
A total of 61 patients with severe secondary hyperparathyroidism (SHPT) were referred to our outpatient department for parathyroidectomy
Summary
Patients with end-stage renal disease have a higher risk of death from cardiovascular events, which can be mainly attributed to coronary artery calcification (CAC). The major cause of cardiovascular mortality in patients on dialysis with end-stage renal disease (ESRD) can be mainly attributed to vascular calcification [1, 2]. Patients with ESRD have a high prevalence of traditional coronary artery disease (CAD) risk factors such as hypertension and diabetes mellitus and non-traditional, uremiarelated CAD risk factors, such as oxidative stress, inflammation and abnormal calcium-phosphorus metabolism [3,4,5]. The calcium paradox is likely caused by the differential responses of osteoblasts and osteoclasts to oxidative stress between the bone and artery. Many studies have highlighted the importance of the bone-vascular axis in the regulation of calcification between the two tissues [8,9,10,11]
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