Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Hou, Yi‐Chou; Lu, Cheng Wei; Zheng, Cai Mei; Chen, Ruei Ming; Lin, Yuh‐Feng; Liu, Wen-Chih; Yen, Tzung‐Hai; Chen, Remy; Lu, Kuo‐Cheng

doi:10.3390/nu11010152

Cited by 30 publications

(62 citation statements)

References 83 publications

(98 reference statements)

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“…Protein-bound uremic toxin can further aggravate this active calcification process in endothelial and medial layers of the vessel [7]. New concepts indicated that calciprotein particles (CPPs) and matrix vesicles (MVs) participate in passive calcification, which can be triggered by hyperphosphatemia and protein-bound uremic toxin-related inflammatory reactions, and lead to calcification within the medial layer of vessel [8][9][10]. In addition to the medial layer, VC can also occur in the intimal layer of the vessel wall.…”

Section: Introductionmentioning

confidence: 99%

Sirtuin-1 and Its Relevance in Vascular Calcification

Liao

Hou

et al. 2020

IJMS

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Vascular calcification (VC) is highly associated with cardiovascular disease and all-cause mortality in patients with chronic kidney disease. Dysregulation of endothelial cells and vascular smooth muscle cells (VSMCs) is related to VC. Sirtuin-1 (Sirt1) deacetylase encompasses a broad range of transcription factors that are linked to an extended lifespan. Sirt1 enhances endothelial NO synthase and upregulates FoxOs to activate its antioxidant properties and delay cell senescence. Sirt1 reverses osteogenic phenotypic transdifferentiation by influencing RUNX2 expression in VSMCs. Low Sirt1 hardly prevents acetylation by p300 and phosphorylation of β-catenin that, following the facilitation of β-catenin translocation, drives osteogenic phenotypic transdifferentiation. Hyperphosphatemia induces VC by osteogenic conversion, apoptosis, and senescence of VSMCs through the Pit-1 cotransporter, which can be retarded by the sirt1 activator resveratrol. Proinflammatory adipocytokines released from dysfunctional perivascular adipose tissue (PVAT) mediate medial calcification and arterial stiffness. Sirt1 ameliorates release of PVAT adipokines and increases adiponectin secretion, which interact with FoxO 1 against oxidative stress and inflammatory arterial insult. Conclusively, Sirt1 decelerates VC by means of influencing endothelial NO bioavailability, senescence of ECs and VSMCs, osteogenic phenotypic transdifferentiation, apoptosis of VSMCs, ECM deposition, and the inflammatory response of PVAT. Factors that aggravate VC include vitamin D deficiency-related macrophage recruitment and further inflammation responses. Supplementation with vitamin D to adequate levels is beneficial in improving PVAT macrophage infiltration and local inflammation, which further prevents VC.

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Section: Introductionmentioning

confidence: 99%

Sirtuin-1 and Its Relevance in Vascular Calcification

Liao

Hou

et al. 2020

IJMS

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“…37 Hyperphosphatemia elevates the blood concentration of fibroblast growth factor 23, reduction in active vitamin D synthesis, and the tendency toward hypocalcemia -all are potent stimuli for secondary hyperparathyroidism. [38][39][40] Hyperparathyroidism depletes cortical bone and stimulate formation of cancellous bone, resulting in changes in the contour of the affected bony structure. The preferential loss of cortical bone and increased formation of trabecular bone, particularly in the oral cavity, are usually the early signs of renal osteodystrophy.…”

Section: Discussionmentioning

confidence: 99%

<p>Torus Palatinus in Taiwan Patients Receiving Peritoneal Dialysis and Hemodialysis: A Prospective Observational Study</p>

Chang

Hsu

Tai

et al. 2020

JMDH

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Purpose: A consensus about the pathogenesis of torus palatinus (TP) in patients receiving dialysis still eludes the scientific community. This prospective observational study investigated the epidemiology of TP in peritoneal dialysis and hemodialysis patients and analyzed the influences of multiple pathogenic factors such as mineral and bone disorders, genetic, environmental or nutritional triggers, progression of age, heredity, climatologic or biomechanical causes, and hyperparathyroidism on the formation of TP. Methods: Between 2013 and 2016, a total of 575 chronic dialysis patients (441 on hemodialysis and 134 on peritoneal dialysis) were recruited from Chang Gung Memorial Hospital, Taiwan. Patients were stratified into two groups based on the presence (n = 179) or absence (n = 396) of TP. Demographic, oral examination, laboratory, and dialysis data were collected for analysis. Student's t-test was used to analyze the quantitative variables and Chisquare or Fisher's exact test for categorical variables. Univariate binary logistic regression analysis was conducted to determine the predictors for TP and multivariate binary logistic regression analysis to identify significant associated factors. Results: The prevalence of TP in dialysis patients in this study was 31.1% (28.3% for hemodialysis and 40.3% for peritoneal dialysis). Patients with TP were younger (54.6 ± 13.4 versus 58.9 ± 14.7 years, P = 0.001) and mostly female (60.3 versus 41.2%, P < 0.001). Most TP cases (55.3%) were small in size (<2 cm), with the flat shape (56.4%) being the most common followed by the spindle (17.9%), nodular (17.3%), and lobular (8.4%) shapes. A longer duration of dialysis was associated with TP ≥2 cm than with TP <2 cm (94.4 ± 85.9 versus 72.8 ± 59.1 months, P = 0.048). Multivariate logistic regression revealed that female gender (odds ratio 2.108, 95% confidence interval 1.455-3.055, P < 0.001) and younger age (odds ratio 0.982; 95% confidence interval 0.969-0.994, P = 0.005) were significant predictors for TP. Conclusion: The prevalence of TP in chronic dialysis patients is 31.1%, higher in patients receiving peritoneal dialysis (40.3%) than hemodialysis (28.3%). Female gender and younger age are significant predictors associated with TP.

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“…Vitamin K supplementation increases MGP carboxylation. What is more, VD supplementation upregulates MGP synthesis, whereas vitamin K suppressed 1,25VD-associated calcinosis [101,102].…”

Section: Vitamin Kmentioning

confidence: 99%

Vitamin D Deficiency in Renal Disease

Filipov¹,

Dimitrov²

2020

Vitamin D Deficiency

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Vitamin D deficiency is highly prevalent in patients with renal disease. The abnormal vitamin D (VD) metabolism in chronic kidney disease (CKD) is a key factor for developing CKD-related mineral bone disease (CKD-MBD), which directly influences the survival of the CKD patients. The importance of VD is perhaps of greater value due to its pleiotropic effects that span beyond calcium-phosphorus metabolism (cancer protection, diabetes prevention, and renal protection). The aim of our chapter is to depict the clinical implications of VD deficiency in the setting of CKD, including VD pleiotropy in renal disease, and to propose the most adequate treatment suggested in the literature. Keywords: vitamin D deficiency, chronic kidney disease, mineral bone disease, vitamin D pleiotropy, vitamin D supplementationVitamin D Deficiency 2 the ratio between free and total 25VD remained unchained; therefore, total 25VD is the indicator of VD status in CKD [3].Generally, 25VD level has reverse association with parathyroid hormone (PTH) levels. In addition, higher 25VD is associated with higher calcium intestinal reabsorption. However, at 25VD ≥ 75 nmol/l, no reduction in PTH levels and no increase in calcium intestinal reabsorption occurs [4, 5]. Therefore, 25VD ≥ 75 nmol/l is regarded as a cut-off value for vitamin D sufficiency.No generally accepted definition for VD deficiency exists, as authors choose cut-off value either serum 25VD of 25 nmol/L [6] or serum 25VD of 50 nmol/L [7]. However, target levels of 75 nmol/L are recommended, taking into consideration the clinical importance of mild VD insufficiency (25VD between 50 and 74.9 nmol/L) [7,8].Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, present for more than 3 months, with implications for health [one of the following: estimated glomerular filtration rate (eGFR) less than 60 ml/ min/1.73 m 2 ,presence of proteinuria, structural abnormalities of the kidney detected on imaging, pathological findings detected on kidney biopsy, urine sediment pathology, electrolyte abnormalities due to tubular disorders, history of kidney transplantation] [9]. CKD patients are at increased risk for VD deficiency; therefore, they require VD screening [7]. Vitamin D metabolism in health and renal disease VD metabolism in healthy subjectsVD is synthesized predominantly endogenously (approx. to 90% of the total VD in human body). In the skin, the ultraviolet light transforms 7-dehydroxycholesterol (provitamin D) to pre-vitamin D, which under the influence of body temperature spontaneously isomerizes to cholecalciferol (vitamin D3). Approximately, 10% of total body VD is taken orally (vitamin D2, ergocalciferol, and cholecalciferol). VD is transported via VD-binding protein to the liver, where it is hydroxylated to 25VD. The next step in VD activation is hydroxylation of 25VD by the enzyme 1α-hydroxylase (CYP27B1) to 1,25VD, which is the active VD metabolite. The process occurs predominantly in the renal tubules. In addition, non-renal CYP27B1 was detected...

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Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Cited by 30 publications

References 83 publications

Sirtuin-1 and Its Relevance in Vascular Calcification

Sirtuin-1 and Its Relevance in Vascular Calcification

<p>Torus Palatinus in Taiwan Patients Receiving Peritoneal Dialysis and Hemodialysis: A Prospective Observational Study</p>

Vitamin D Deficiency in Renal Disease

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