Vascular Calcification and Osteoprotegrin in Chronic Kidney Disease

Lenhard, M. James; Maser, Raelene E.

doi:10.1159/000477381

Cited by 7 publications

(3 citation statements)

References 7 publications

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“…The process of VC is similar to that of ossification, as osteogenic proteins accumulate in the arterial wall and promote the differentiation of smooth muscle cells into osteoblasts (Vattikuti and Towler, 2004 ; Lenhard and Maser, 2017 ). VC is a multifactorial process that involves genetic factors, molecular pathway interactions, and environmental factors (Pérezhernández et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

High Mobility Group Box 1 Promotes Aortic Calcification in Chronic Kidney Disease via the Wnt/β-Catenin Pathway

et al. 2018

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Vascular calcification (VC) is common in chronic kidney disease (CKD), where cardiovascular mortality remains the leading cause of death. Here, we examined the role of high-mobility group box1 (HMGB1), a nuclear DNA-binding protein involved in inflammation, in aortic calcification and renal dysfunction induced by high phosphate in a mouse model of CKD induced by 5/6 nephrectomy. HMGB1 and kidney function markers were measured by ELISA in the serum of CKD patients and in CKD mice. Sections of the aortas of mice were analyzed by immunofluorescence and Alizarin red staining, and protein lysates were generated to analyze the expression of related proteins in response to silencing of HMGB1 or β-catenin by western blotting. Our results showed that serum HMGB1 levels were significantly higher in CKD patients than in healthy controls and related to disease stage. High phosphate promoted the translocation of HMGB1 from the nucleus to the cytosol and aortic calcification in CKD mice in vivo, whereas HMGB1 knockdown ameliorated part of renal and vascular function. β-catenin silencing reversed high phosphate-induced calcification and restored renal marker levels. Taken together, our results suggest that HMGB1 is involved in VC associated with CKD via a mechanism involving the β-catenin.

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Section: Introductionmentioning

confidence: 99%

High Mobility Group Box 1 Promotes Aortic Calcification in Chronic Kidney Disease via the Wnt/β-Catenin Pathway

et al. 2018

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“…Paradoxically, although thought to have a protective role against VC, OPG levels increase with CKD progression [ 38 ]. As with sclerostin, this may represent a compensatory mechanism to inhibit cardiovascular calcification [ 39 ]. Nevertheless, it remains to be established to what extent renal impairment contributes to increased OPG concentrations [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Low bone turnover is associated with plain X-ray vascular calcification in predialysis patients

et al. 2021

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Background Vascular calcification (VC) is a common finding in chronic kidney disease (CKD) patients and predicts subsequent cardiovascular morbidity and mortality in this population. Vascular calcification is linked to disordered mineral metabolism and has been associated with bone histomorphometry changes in CKD. However, data on predialysis patients is scarce. Methods A cross-sectional study was conducted on a cohort of 56 CKD patients not yet on dialysis, who underwent a transiliac bone biopsy for histomorphometric evaluation after double tetracycline labeling. Patients had no previous exposure to calcium salts, vitamin D agents, steroids or bisphosphonates. Vascular calcification was assessed at the time of biopsy, using Kauppila (plain X-ray of the lateral lumbar spine) and Adragão (plain X-ray of the pelvis and hands) scores. Results Vascular calcification was seen in two-thirds of the cohort. Subjects with VC were more likely to be male and have diabetes, and had significantly higher sclerostin and osteoprotegerin circulating levels than those without VC. The histomorphometric analysis showed that bone formation rate was significantly lower in VC compared to non-VC patients. In the multivariable logistic regression analysis, bone formation rate was independently associated with the presence of VC. Conclusions Vascular calcification is highly prevalent in predialysis patients, especially in those with diabetes. The independent association between bone formation rate and VC provides evidence of an important interaction between bone and vessel in CKD. Our results suggest that low bone turnover is a non-traditional risk factor for cardiovascular disease in predialysis patients.

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“…OPG is, therefore, believed to inhibit osteoclastogenesis, protect bone volume and bone mass, and inhibit vascular calci cation. 20 Circulating levels of OPG are elevated in patients who require dialysis and may be a strong predictor of vascular calci cation at various stages of kidney disease. [21][22][23] Vascular damage is possibly one of the determinants of high CV risk in patients with CKD and the detection of this damage in the early stages of the disease may contribute to the adoption of strategies with the potential to reduce cardiovascular and renal morbidity and mortality.…”

Section: Introductionmentioning

confidence: 99%

Osteoprotegerin and Vascular Dysfunction in Patients With Stage 3 Chronic Kidney Disease and Those Without Renal Dysfunction: a Case-control Study (Nefrovasc Study)

Matos,

Vitorino,

Orlow

et al. 2023

Preprint

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Background: Osteoprotegerin (OPG) is a marker of vascular calcification and cardiovascular (CV) risk in patients with chronic kidney disease (CKD). The study aimed to compare OPG values with flow-mediated dilation (FMD) and pulse wave velocity (PWV) and to evaluate the correlation between these measures in patients in stage 3 CKD and those without renal dysfunction. Methods: This case-control study was conducted in a specialized hypertension clinic in 2022. A total of 79 patients over 18 years of age participated in the study. The case group consisted of 30 patients who had moderate renal dysfunction (CKD stage 3a and 3b) and the control group included 49 individuals with GFR ≥60 ml/min/1.73 m2. For the comparative analysis between patients with and without renal dysfunction, qualitative variables were analyzed using the chi-square test, while quantitative variables were evaluated using the independent t-test or Mann-Whitney test. The linear correlation between OPG and the other variables was analyzed using Pearson's or Spearman's correlation tests. Results: Central pulse pressure (cPP), PWV, and augmentation index (AIx) were higher in patients with renal dysfunction. The serum OPG level positively correlated with peripheral and central systolic blood pressure (BP), PPc, PWV, and AIx. Conversely, the serum OPG did not correlate with FMD. Conclusions: OPG and PWV are possible biomarkers of vascular dysfunction that are altered in patients with moderate renal dysfunction. This study is has limitations: is a case-control study conducted at a single center with a small number of patients with CKD.

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Vascular Calcification and Osteoprotegrin in Chronic Kidney Disease

Cited by 7 publications

References 7 publications

High Mobility Group Box 1 Promotes Aortic Calcification in Chronic Kidney Disease via the Wnt/β-Catenin Pathway

High Mobility Group Box 1 Promotes Aortic Calcification in Chronic Kidney Disease via the Wnt/β-Catenin Pathway

Low bone turnover is associated with plain X-ray vascular calcification in predialysis patients

Osteoprotegerin and Vascular Dysfunction in Patients With Stage 3 Chronic Kidney Disease and Those Without Renal Dysfunction: a Case-control Study (Nefrovasc Study)

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