Abstract: FR-PO137
Relationship Between Parathyroid Hormone and Renin Angiotensin Aldosterone System in Hyperparathyroidism
Session Information
- Bone and Mineral Metabolism: Phosphorus, FGF23, Vascular Calcification
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 402 Bone and Mineral Metabolism: Clinical
Authors
- Kono, Keiji, Kobe University Graduate School of Medicine, Kobe, Japan
- Fujii, Hideki, Kobe University Graduate School of Medicine, Kobe, Japan
- Watanabe, Shuhei, Kobe University Graduate School of Medicine, Kobe, Japan
- Goto, Shunsuke, Kobe University Graduate School of Medicine, Kobe, Japan
- Nishi, Shinichi, Kobe University Graduate School of Medicine, Kobe, Japan
Background
Parathyroid hormone (PTH) is known to be one of the regulators for calcium and phosphate metabolism. On the other hand, it has been reported that PTH has several effects on the cardiovascular system. However, its mechanism remains to be not fully elucidated. As a possible mechanism, PTH is thought to be associated with the renin angiotensin aldosterone system (RAS). Therefore, we investigated their hormonal interaction in patients with primary and secondary hyperparathyroidism (HPT).
Methods
Twenty-seven HPT patients (primary HPT: N=10, secondary HPT: N=17) were included in this study. All the study patients underwent parathyroidectomy (PTx) in our institution. We measured serum intact PTH, plasma renin activity (PRA) and plasma aldosterone levels (ALD) before and after PTx. In addition, we evaluated blood pressure before and after PTx.
Results
Baseline estimated glomerular filtration rate (eGFR) was 44.3±35.4 ml/min/1.73m2 in the primary HPT group. All patients in the secondary HPT group received maintenance hemodialysis. Pre-operative serum intact PTH levels were positively correlated with pre-operative ALD and PRA in both HPT groups (primary HPT group (ALD: r= 0.685, p< 0.05, PRA: r= 0.661, p< 0.05), secondary HPT group (ALD: r=0.493, p< 0.05, PRA: r=0.446, p= 0.072)). Along with changes of serum intact PTH levels after PTx, both PRA and ALD were also significantly decreased after PTx in both HPT groups. In addition, changes of serum intact PTH levels were positively correlated with changes of PRA and ALD in both groups (primary HPT group (ALD: r= 0.774, p< 0.05, PRA: r=0.815, p<0.05), secondary HPT group (ALD; r= 0.451, p= 0.069, PRA; r= 0.466 p= 0.059)). Although blood pressure was significantly decreased after PTx in the primary HPT group, it did not change in the secondary HPT group.
Conclusion
Our findings suggest that the effects of HPT on the cardiovascular system could be partially mediated by RAS in secondary and primary HPT.