Sclerostin as a new key factor in vascular calcification in chronic kidney disease stages 3 and 4

Lv, Wei; Guan, Lina; Yan, Zhang; Yu, Shengqiang; Cao, Bofeng; Ji, Yongqiang

doi:10.1007/s11255-016-1379-8

Cited by 37 publications

(30 citation statements)

References 30 publications

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“…Animal experiment showed that knockdown of β‐catenin in CKD rats could reduce aortic calcification, while enhanced Wnt5a expression was identified in arteries of CKD patients with VC . Besides, Wnt pathway inhibitor sclerostin was also found to be associated with VC in CKD stage 3‐4 patients . However, it is still unclear how these factors and pathways interplay and contribute to VC in the vascular tissue.…”

Section: Introductionmentioning

confidence: 99%

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Vascular calcification is associated with Wnt‐signaling pathway and blood pressure variability in chronic kidney disease rats

Liao

Wang

et al. 2019

Nephrology

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Aim Vascular calcification (VC) is a common complication in chronic kidney disease (CKD) and has been shown to be associated with increased cardiovascular events and mortality. This study was to explore the role of Wnt‐signaling pathway in CKD VC, and the association between VC and blood pressure variability (BPV) which is a risk factor of cardiovascular events. Methods Adult male Sprague‐Dawley rats were divided into adenine‐induced CKD group (n = 5), 5/6 nephrectomy CKD group (n = 5), sham group (n = 5) and control group (n = 5). Low‐calcium‐high‐phosphate diets were introduced to induce vascular calcification. Both daytime (hour‐to‐hour during the day) and mid‐term (day‐to‐day for 9 days) blood pressure (BP) were collected and analyzed for BPV metrics. At sacrifice, kidney, heart and aorta samples were taken for histological analyses. Calcium deposition in aorta was identified with Alizarin Red stain and graded. Immunohistochemistry stain and western blot were performed for Wnt3a, Wnt5a, β‐catenin, sclerostin, osteopontin, and α‐SMA. Results Compared with control rats, CKD rats suffered from markedly severer VC (Grade 2.6 ± 0.2 and 1.8 ± 0.8 vs 0.0 ± 0.0 and 0.2 ± 0.4, P = .0010). VC was positively correlated with vascular Wnt3a and β‐catenin expression (P = .0032 and .0000), but not significantly associated with Wnta5a or sclerostin. Besides, CKD rats showed increased BPV (P < .001), which was also positively correlated with VC. Conclusion We confirmed that CKD rats had enhanced Wnt‐signaling in vascular tissue and severer aorta calcification together with increased BPV. Wnt pathway may be a potential target in future VC and BPV management in CKD.

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Section: Introductionmentioning

confidence: 99%

“…6 Besides, Wnt pathway inhibitor sclerostin was also found to be associated with VC in CKD stage 3-4 patients. 7 However, it is still unclear how these factors and pathways interplay and contribute to VC in the vascular tissue.…”

Section: Introductionmentioning

confidence: 99%

Vascular calcification is associated with Wnt‐signaling pathway and blood pressure variability in chronic kidney disease rats

Liao

Wang

et al. 2019

Nephrology

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“…Another study by Wei et al on CKD stage 3-4 showed that sclerostin serum concentrations were negatively correlated with renal function, and its increase is positively correlated with the prevalence of vascular calcification. 27 A study by Cejka et al on ESRD patients with dialysis proved that the accumulation of sclerostin contributed to PTH resistance and calcitriol deficiency. 28 This study found that sclerostin and intact parathyroid hormone (iPTH) was negatively correlated on CKD patients with dialysis.…”

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confidence: 99%

Sclerostin Serum Concentration in Patients with Predialysis Ckd Stage 3-5

2018

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Sclerostin is a glycoprotein expressed by osteocytes and plays a role in bone turnover in themetabolism of the bone. Sclerostin blocks the formation of a ligand with its receptor on theWnt/β-catenin pathway, and influences the activity of osteoblasts. Sclerostin also influencesmineral and bone disturbances in CKD via the interaction between kidney, bone and vascularaxis. The concentration of sclerostin will rise especially in patients with ESRD undergoingdialysis. Concentration of sclerostin has not been reported yet in non-dialysis CKD patientstage 3-5 and the aim of this study is to see sclerostin concentration on those population. Methods This is a descriptive and cross-sectional study designed to measure sclerostinconcentration in non dialysis patients with CKD stage 3-5. The sclerostin concentration ismeasured using an enzyme-linked immunosorbent assay kit. CKD stages are diagnosed usingthe KDIGO-2012 criteria which measures the estimated GFR (eGFR) with the formulation of EPICKD. Fifty six patients with CKD stage 3-5 were enrolled in this study and one way ANOVA comparative test followed with a post hoc analysis using Benferroni test to analysethe data. Results The mean concentration level of serum sclerostin in this population is (79.7+ 41.2) pmol/L, and in patients with CKD stage 3, CKD stage 4, and CKD stage 5 are (59.6 +28.5) pmol/L, (71.9 + 42.2) pmol/L and (96.7 + 39.8) pmol/L respectively. The comparativetest of mean concentrations of the serum sclerostin between stages of CKD are statisticallysignificant with a p=0.022. The post hoc analysis of serum sclerostin concentration betweenCKD stage 3 and CKD stage 5 have a significant difference with a mean of 37 pmol/L andp=0.037. Conclusion, The serum sclerostin concentration rise in accordance with the declineof kidney function in patients with pre-dialysis CKD stage 3-5.

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“…This is most likely due to the greatly increased production -it has been proven, that renal elimination of sclerostin increases with declining kidney function [37]. There is evidence that both bone tissue and vasculature participates in enhancement of the SCL production: Presence of the vascular calcification, even in coronary arteries, as seen in computed tomography and in pathology images has been linked to serum sclerostin concentration in numerous research, and the results acquired by both experimental methods were consistent [39,40,41,42]. Another studies may show possible correlation between increased risk of calcification of heart valves and high level of sclerostin in blood serum [50].…”

Section: Sclerostin In Chronic Kidney Disease (Ckd)mentioning

confidence: 84%

Sclerostin - a potential new marker of exercise influence on vascular calcification and mineral and bone disorder in hemodialysed adults

Turoń-Skrzypińska¹,

Dutkiewicz²,

Marchelek-Myśliwiec³

et al. 2019

J Educ Health Sport

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Chronic Kidney Disease (CKD) is defined as abnormalities of kidney structure or function, present for >3 months, with implications for health. Amongst CKD complications the most fatal is cardiovascular disease, which together with Chronic Kidney Disease Mineral and Bone Disorder (CKD-MBD) share a possible origin in Wnt signaling pathway disturbances. Sclerostin, a potent Wnt signaling inhibitor may possibly be used as a potential new marker of exercise influence on vascular calcification and mineral and bone disorder in hemodialysed adults.

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Sclerostin as a new key factor in vascular calcification in chronic kidney disease stages 3 and 4

Abstract: Our data indicate that sclerostin levels are elevated in patients with CKD and are associated with vascular calcification. Therefore, sclerostin may be used as a predictor of vascular calcification in the clinical setting.

Cited by 37 publications

References 30 publications

Vascular calcification is associated with Wnt‐signaling pathway and blood pressure variability in chronic kidney disease rats

Vascular calcification is associated with Wnt‐signaling pathway and blood pressure variability in chronic kidney disease rats

Sclerostin Serum Concentration in Patients with Predialysis Ckd Stage 3-5

Sclerostin - a potential new marker of exercise influence on vascular calcification and mineral and bone disorder in hemodialysed adults

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