Low serum intact parathyroid hormone level is an independent risk factor for overall mortality and major adverse cardiac and cerebrovascular events in incident dialysis patients

Lee, Sul A; Lee, Mi Jung; Ryu, Geun Woo; Jhee, Jong Hyun; Kim, Hyung Woo; Park, Seohyun; Jung, Su Young; Oh, Hyung Jung; Park, Sun-Hee; Han, Seung Hyeok; Kang, Shin Wook; Yoo, Tae‐Hyun

doi:10.1007/s00198-016-3636-1

Cited by 25 publications

(20 citation statements)

References 35 publications

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“…However, the role of PTH as a risk factor of calcification is not well understood. Low PTH levels have also been reported to be associated with severe arterial calcification (23). Additionally, PTH is known to be a crucial regulator of the cardiovascular system (24).…”

Section: Discussionmentioning

confidence: 99%

Parathyroid hormone promotes osteoblastic differentiation of endothelial cells via the extracellular signal‑regulated protein kinase 1/2 and nuclear factor‑κB signaling pathways

Cheng

Ling³

et al. 2017

Exp Ther Med

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Abstract. Vascular calcification (VC) occurs in patients with chronic kidney disease (CKD) and contributes to cardiovascular dysfunction and mortality. Parathyroid hormone (PTH) is a crucial regulator of VC. High PTH serum levels constitute as a major risk factor for patients with CKD. However, the effect and mechanism of PTH on osteoblastic differentiation in endothelial cells have not been fully elucidated. In the present study, the role of PTH in VC was investigated using an in vitro calcification model. Endothelial cells were stimulated with PTH in the femto-to picomolar range. As determined by western blot analysis and ELISA, osteoblastic differentiation, as indicated by the BMP2 marker, occurred with maximum effect at 1x10 -10 mmol/l PTH. The results indicate that PTH promotes osteoblastic differentiation of endothelial cells, as demonstrated by the increased expression of bone morphogenetic protein (BMP) 2 and BMP4. In addition, western blot analysis revealed that PTH activated the extracellular signal-regulated protein kinase (Erk)1/2 and nuclear factor (NF)-κB signaling pathways. However, reverse transcription-quantitative polymerase chain reaction demonstrated that inhibitors specific to Erk1/2 and NF-κB eradicated the effect of PTH treatment on BMP2, BMP4, ALP and RUNX2 expression. These results demonstrate that PTH promotes the osteoblastic differentiation of endothelial cells via the Erk1/2 and NF-κB signaling pathways, which suggests a potential role of PTH in the promotion of VC. These findings provide an insight into the association between PTH and cardiovascular disease.

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Section: Discussionmentioning

confidence: 99%

Parathyroid hormone promotes osteoblastic differentiation of endothelial cells via the extracellular signal‑regulated protein kinase 1/2 and nuclear factor‑κB signaling pathways

Cheng

Ling³

et al. 2017

Exp Ther Med

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“…This constellation of findings was thought to be the best predictor of LTBD rather than iPTH alone. As previously discussed, LTBD predisposes to increased risk of vascular calcification and arterial stiffness due to inability of bone to buffer excess calcium and phosphorus salts …”

Section: Management Of Vascular Calcificationmentioning

confidence: 94%

“…Notably, several studies have shown that LTBD associated with low iPTH levels predict progression of vascular calcification and has been correlated with increased morbidity and mortality in ESRD patients. [31][32][33][34][35] Since the bone is the primary storehouse for calcium and phosphorus, inactivity of the bone predisposes to ectopic deposition of calcium and phosphorus within tissues such as vasculature.…”

Section: Role Of Pth In Vascular Calcificationmentioning

confidence: 99%

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Pathogenesis and management of vascular calcification in CKD and dialysis patients

Kakani

Elyamny

Ayach

et al. 2019

Seminars in Dialysis

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Patients with chronic kidney disease (CKD) have a predisposition to develop vascular calcification due to dysregulated homeostatic mechanisms, which lead to an imbalance in the circulatory promoters and inhibitors of vascular calcification, leading to a net calcification stress. These factors promote ectopic calcification and induce vascular smooth muscle cells to undergo osteogenic differentiation and actively calcify the vascular media. The article summarizes clinically relevant pathogenic mechanisms of vascular calcification in patients with CKD and in dialysis patients and summarizes novel therapeutic interventions. In addition to the management of traditional cardiovascular risk factors, patients with CKD‐mineral and bone disorder need close attention in the management of the mineral metabolism to prevent adverse effects on the bone and vascular compartments. This article reviews current evidence and therapeutic guidelines in the management of mineral metabolism in CKD and dialysis.

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“…Furthermore, significantly lower iPTH levels were observed in the stroke group than in the non-stroke group, and a notable inverse correlation of iPTH levels was observed between stroke and non-stroke patients during follow-up. Low iPTH levels are also significantly correlated with vascular calcification, cardiovascular disease and mortality in dialysis patients [30,31,17,18]. However, whether the decreased iPTH level is a cause or just a phenomenon associated with stroke in CAPD patients is still unclear.…”

Section: Discussionmentioning

confidence: 99%

Effects of parathyroid hormone and vitamin D supplementation on stroke among patients receiving peritoneal dialysis

You

Zhou

Zhang

et al. 2020

Preprint

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Background: Continuous ambulatory peritoneal dialysis (CAPD) patients have a high incidence of stroke and commonly have increased parathyroid hormone levels and vitamin D insufficiency. We seek to investigate the incidence of stroke and the role of parathyroid hormone and vitamin D supplementation in stroke risk among CAPD patients.Methods: This study employed a retrospective design. We enrolled a Chinese cohort of 980 CAPD patients who were routinely followed in our department. The demographic and clinical data were recorded at the time of initial CAPD and during follow-up. The included patients were separated into non-stroke and stroke groups. The effects of parathyroid hormone and vitamin D supplementation on stroke in CAPD patients was evaluated. The primary endpoint is defined as the first occurrence of stroke, and composite endpoint events are defined as death or switch to hemodialysis during follow-up.Results: A total of 757 eligible CAPD patients with a mean follow-up time of 54.7 (standard deviation, 33) months were included in the study. The median incidence of stroke among our CAPD patients was 18.9 (interquartile range, 15.7 - 22.1) per 1000 person-years. A significant nonlinear correlation between baseline iPTH and hazard of stroke (p-value of linear association = 0.2 and nonlinear association = 0.002) was observed in our univariate Cox regression analysis, and low baseline iPTH levels (≤150 pg/ml) were associated with an increased cumulative hazard of stroke. Multivariate Cox regression analysis indicated a significant interaction effect between age and iPTH after adjusting for other confounders. Vitamin D supplementation during follow-up was a predictive factor for stroke in our cohort.Conclusions: CAPD patients suffered a high risk of stroke, and lower iPTH levels were significantly correlated with an increased risk of stroke. Nevertheless, vitamin D supplementation may reduce the risk of stroke in these patients.

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Low serum intact parathyroid hormone level is an independent risk factor for overall mortality and major adverse cardiac and cerebrovascular events in incident dialysis patients

Abstract: Low serum TA-iPTH is a useful clinical marker of both overall mortality and MACCEs in patients undergoing incident dialysis, mediated by vascular calcification.

Cited by 25 publications

References 35 publications

Parathyroid hormone promotes osteoblastic differentiation of endothelial cells via the extracellular signal‑regulated protein kinase 1/2 and nuclear factor‑κB signaling pathways

Parathyroid hormone promotes osteoblastic differentiation of endothelial cells via the extracellular signal‑regulated protein kinase 1/2 and nuclear factor‑κB signaling pathways

Pathogenesis and management of vascular calcification in CKD and dialysis patients

Effects of parathyroid hormone and vitamin D supplementation on stroke among patients receiving peritoneal dialysis

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