The Strategy to Prevent and Regress the Vascular Calcification in Dialysis Patients.

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Term Occurence Count Dictionary
calciphylaxis 6 endocrinologydiseases
diabetes mellitus 3 endocrinologydiseases
hyperphosphatemia 3 endocrinologydiseases
secondary hyperparathyroidism 4 endocrinologydiseases
metabolic syndrome 2 endocrinologydiseases
paricalcitol 1 endocrinologydiseasesdrugs
vitamin K deficiency 1 endocrinologydiseases
calcinosis 2 endocrinologydiseases
calcitriol 2 endocrinologydiseasesdrugs
hyperglycemia 1 endocrinologydiseases
hyperhomocysteinemia 1 endocrinologydiseases
hypercalcemia 1 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
hyperparathyroidism 10 endocrinologydiseases
obesity 2 endocrinologydiseases
Denosumab 3 endocrinologydiseasesdrugs
Sevelamer 3 endocrinologydiseasesdrugs
vascular calcification 40 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Denosumab 26233 patients in current trials be reduced.5.6. Other Antiresorption Therapies5.6.1. Bisphosphonates and Denosumab Bisphosphonates are synthetic analogues of inorganic pyrophosphate that have the ability to inhibit osteoclast-mediated
Denosumab 26765 production may represent a therapeutic strategy to preventing bone loss and vascular calcification. Denosumab is considered as OPG mimicker. Bisphosphonates and denosumab could reduce vascular calcification in
Denosumab 27538 disease. The decision to use a bisphosphonates in a CKD patient should be individualized per patient. Denosumab , as bisphosphonates, inhibits osteoclast-mediated bone resorption, but because it is not cleared by
Sevelamer 24080 binder treatments should be considered. Calcium-free-based phosphate binder could decrease mortality. Sevelamer has pleiotropic effects on lipid profiles, fibroblast growth factor 23, inflammation, uremic toxins,
Sevelamer 32850 carbonate1.0HighNoVascular and soft tissue calcificationLowCalcium acetate1.0HighNoVascular and soft tissue calcificationLow Sevelamer carbonate/Sevelamer hydrochloride0.75HighPleiotropic effects (lipid profiles, fibroblast growth factor
Sevelamer 32870 calcificationLowCalcium acetate1.0HighNoVascular and soft tissue calcificationLowSevelamer carbonate/ Sevelamer hydrochloride0.75HighPleiotropic effects (lipid profiles, fibroblast growth factor 23, inflammation,
calcitriol 5287 difficult to mobilize the calcium deposits. However, vascular and soft tissue calcifications induced by calcitriol administration to rats partially revert after withdrawal of calcitriol treatment [[10]]. An active cellular
calcitriol 5358 tissue calcifications induced by calcitriol administration to rats partially revert after withdrawal of calcitriol treatment [[10]]. An active cellular process seems to be involved in regression of vascular calcification.
paricalcitol 23033 limiting or discontinuing activated vitamin D therapy. Activated vitamin D analogues, particularly paricalcitol , appear to be less phosphatemic. Cinacalcet improves the attainment of KDOQI bone metabolism serum phosphate
Select Disease Character Offset Disease Term Instance
calcinosis 5790 calcification inhibitor [[11]]. Furthermore, in clinical practice, extraosseous calcification such as tumor calcinosis and uremia-related vascular calcification such as calciphylaxis were considered controllable, at least
calcinosis 6463 (Figure 1(a)), cardiac valve calcification (Figure 1(b)), calciphylaxis (Figures 1(c)–1(e)), and tumor calcinosis (Figure 1(f)). These four types are the consequence of distinct yet overlapping pathological mechanisms,
calciphylaxis 5851 extraosseous calcification such as tumor calcinosis and uremia-related vascular calcification such as calciphylaxis were considered controllable, at least partially, by parathyroidectomy and multiple intervention treatments
calciphylaxis 6416 calcification or medial artery calcification (Figure 1(a)), cardiac valve calcification (Figure 1(b)), calciphylaxis (Figures 1(c)–1(e)), and tumor calcinosis (Figure 1(f)). These four types are the consequence of distinct
calciphylaxis 28712 to form a highly soluble calcium thiosulfate salt. The use of sodium thiosulfate in the treatment of calciphylaxis has been described primarily in case reports with partial-to-complete resolution of skin lesions. Sodium
calciphylaxis 29082 intravenously over 1 h). The most common adverse effects during sodium thiosulfate treatment for calciphylaxis were nausea, vomiting, and increased anion gap acidosis [[98]–[101]]. However, the current bicarbonate
calciphylaxis 30398 can be seen on the mitral valve (arrow) in computed tomography studies. (c) Macroscopic evidence of calciphylaxis , (d) skin biopsy showing fat necrosis, composed of necrotic adipocytes, minimal inflammatory cell infiltration,
calciphylaxis 30797 branches as shown by the so-called tram track phenomenon were found in a hemodialysis patient with calciphylaxis . (f) Left hip radiographs show a large radiopaque lesion on the soft tissue around the hip joint comprising
diabetes mellitus 1034 persons with chronic renal failure. In addition to traditional cardiovascular risk factors such as diabetes mellitus and blood pressure control, other ESRD-related risks such as phosphate retention, excess calcium, and
diabetes mellitus 3265 morbidity and mortality. Recent evidence suggests that the interaction of traditional (i.e., age, smoking, diabetes mellitus [DM], hypertension, and dyslipidemia) and uremia-related so-called cardiovascular risk factors (e.g.,
diabetes mellitus 11348 considering the bone-vascular axis. In addition to traditional cardiovascular risk factors such as diabetes mellitus and blood pressure control, the strategies are as follows.5.1. Minimize InflammationRecent evidence
hypercalcemia 20230 should be considered if a high blood PTH level (>800 pg/mL) remains resistant to medical treatment and hypercalcemia or hyperphosphatemia is also noted.5.3. Avoid Calcium Positive BalanceThe related concept that Ca concentrations
hyperglycemia 2680 heart disease outcomes in the general population and include hypertension, smoking, hyperlipidemia, hyperglycemia , and obesity. Nontraditional risk factors (i.e., anemia, abnormal calcium/phosphorus metabolism, hyperhomocysteinemia,
hyperhomocysteinemia 2791 hyperglycemia, and obesity. Nontraditional risk factors (i.e., anemia, abnormal calcium/phosphorus metabolism, hyperhomocysteinemia , and malnutrition) are uremia-related factors that increase in prevalence as kidney function declines
hyperlipidemia 2664 predict coronary heart disease outcomes in the general population and include hypertension, smoking, hyperlipidemia , hyperglycemia, and obesity. Nontraditional risk factors (i.e., anemia, abnormal calcium/phosphorus
hyperparathyroidism 1717 balance such as correction of vitamin D and K deficiency; parathyroid intervention is reserved for severe hyperparathyroidism . The role of bone antiresorption therapy such as bisphosphonates and denosumab in vascular calcification
hyperparathyroidism 15017 current option for noninvasive assessment of bone turnover. Medical or surgical treatments to control hyperparathyroidism should be emphasized, and low-bone-turnover diseases should be avoided to maintain the intermediate
hyperparathyroidism 17635 high-bone-turnover disease, according to the KDIGO guidelines [[46]]. Bone biopsy should always be performed before hyperparathyroidism treatment if there is a marked difference between the bone metabolism marker values and the serum P,
hyperparathyroidism 18617 including the KDOQI American commentary and the 2009 KDIGO guideline, suggest that the primary choice of a hyperparathyroidism treatment may be based on serum calcium and phosphate. Cinacalcet could markedly improve the achievement
hyperparathyroidism 18786 phosphate. Cinacalcet could markedly improve the achievement of target levels in patients with secondary hyperparathyroidism [[60]]. Furthermore, the efficacy of cinacalcet in preventing the progression of CV calcifications (ADVANCE)
hyperparathyroidism 19175 percutaneous ethanol parathyroid injection and parathyroidectomy, which is reserved for severe secondary hyperparathyroidism , could increase serum osteoprotegerin and fetuin A levels to restore anticalcification factor balance
hyperparathyroidism 19518 [62]].Treatment of High-Bone-Turnover Disease [[44], [46], [58]] Always consider bone biopsy before hyperparathyroidism treatment if there is a marked difference between the bone metabolism marker values and the serum P,
hyperparathyroidism 23216 KDOQI bone metabolism serum phosphate levels in dialysis patients with various stages of secondary hyperparathyroidism [[73]]. The use of certain high-protein low-phosphate foods such as whey protein and egg whites can
hyperparathyroidism 23815 color of food products [[72]–[74]]. The other positive vascular phosphate balance concerns including hyperparathyroidism leading to phosphate efflux from bone [[73]]. In addition to adequate dialysis clearance and phosphate
hyperparathyroidism 25063 [[44]]. There is some evidence that 25(OH) D supplementation can assist with the management of secondary hyperparathyroidism and possibly prevent vascular calcification [[52], [81]].Vitamin K (K1 and K2) is involved in the production
hyperphosphatemia 3385 [DM], hypertension, and dyslipidemia) and uremia-related so-called cardiovascular risk factors (e.g., hyperphosphatemia , high calcium × phosphorus product, oxidative stress, systemic inflammation, protein energy wasting,
hyperphosphatemia 20247 if a high blood PTH level (>800 pg/mL) remains resistant to medical treatment and hypercalcemia or hyperphosphatemia is also noted.5.3. Avoid Calcium Positive BalanceThe related concept that Ca concentrations do not reflect
hyperphosphatemia 22155 function deteriorates, positive phosphate balance is inevitable. Based on epidemiological data linking hyperphosphatemia to reduced survival, the KDOQI guidelines suggested that P levels should be maintained between 3.5 and
metabolic syndrome 31360 calcification; patch or striped calcification on X-ray examination. Risk factors include hypercholesterolemia, metabolic syndrome , diabetes, and hypertension.Ischemia/infarctionArterial medial calcificationCalcification of the media
metabolic syndrome 31987 metabolism, inflammation, and traditional cardiovascular risk factors such as hypercholesterolemia, metabolic syndrome , diabetes, and hypertension.Heart failureCalcific uremic arteriolopathyDermal arteriolar medial calcification
obesity 2699 outcomes in the general population and include hypertension, smoking, hyperlipidemia, hyperglycemia, and obesity . Nontraditional risk factors (i.e., anemia, abnormal calcium/phosphorus metabolism, hyperhomocysteinemia,
obesity 32348 hands and feet reveals calcified artery in the absence of thrombosis. Risk factors include diabetes, obesity , vitamin K antagonist, and steroid.Painful nodule and subcutaneous skin/fat necrosis woundTable 2How
secondary hyperparathyroidism 18776 and phosphate. Cinacalcet could markedly improve the achievement of target levels in patients with secondary hyperparathyroidism [[60]]. Furthermore, the efficacy of cinacalcet in preventing the progression of CV calcifications (ADVANCE)
secondary hyperparathyroidism 19165 including percutaneous ethanol parathyroid injection and parathyroidectomy, which is reserved for severe secondary hyperparathyroidism , could increase serum osteoprotegerin and fetuin A levels to restore anticalcification factor balance
secondary hyperparathyroidism 23206 attainment of KDOQI bone metabolism serum phosphate levels in dialysis patients with various stages of secondary hyperparathyroidism [[73]]. The use of certain high-protein low-phosphate foods such as whey protein and egg whites can
secondary hyperparathyroidism 25053 <20 ng/mL) [[44]]. There is some evidence that 25(OH) D supplementation can assist with the management of secondary hyperparathyroidism and possibly prevent vascular calcification [[52], [81]].Vitamin K (K1 and K2) is involved in the production
vascular calcification 1216 phosphate retention, excess calcium, and prolonged dialysis time also contribute to the development of vascular calcification . The strategies are to reverse “calcium paradox” and lower vascular calcification by decreasing
vascular calcification 1302 development of vascular calcification. The strategies are to reverse “calcium paradox” and lower vascular calcification by decreasing procalcific factors including minimization of inflammation (through adequate dialysis
vascular calcification 1819 hyperparathyroidism. The role of bone antiresorption therapy such as bisphosphonates and denosumab in vascular calcification in high-bone-turnover disease remains unclear. The limited data on sodium thiosulfate are promising.
vascular calcification 3665 activator of NF-κB (RANK)/RANK ligand system, and osteopontin) contributes to excessive and accelerated vascular calcification in CKD patients [[5]]. Intervention for these risk factors may delay the progression of vascular calcification.
vascular calcification 3776 calcification in CKD patients [[5]]. Intervention for these risk factors may delay the progression of vascular calcification . Cinacalcet with low-dose active vitamin D attenuated the progression of vascular and aortic valve calcification
vascular calcification 4386 progression of coronary artery calcification at a rate of 11% per year [[7], [8]].These data suggested that vascular calcification , once it occurs, is unlikely to be reversed. Thus, therapeutic interventions that stop and reverse calcification
vascular calcification 4692 Currently, no definite therapy has emerged. Hence, we reviewed the current strategy and treatments for vascular calcification in CKD patients.2. Could the Extraosseous Calcification Be Reversed?Can it reverse calcification? The
vascular calcification 4847 Extraosseous Calcification Be Reversed?Can it reverse calcification? The answer is yes. Uremia-related vascular calcification s contain poor crystalline insoluble whitlockite and soluble amorphous calcium phosphate [[9]]. Although
vascular calcification 5051 phosphate [[9]]. Although there was a portion of soluble amorphous calcium-phosphate in uremic related vascular calcification , the majority of the calcification is extremely insoluble whitlockite under physiological conditions
vascular calcification 5452 withdrawal of calcitriol treatment [[10]]. An active cellular process seems to be involved in regression of vascular calcification . High intake of vitamin K1 supplementation can result in regression of vascular calcification and restore
vascular calcification 5546 regression of vascular calcification. High intake of vitamin K1 supplementation can result in regression of vascular calcification and restore the artery elasticity by virtue of its ability to activate matrix Gla protein, a local intravascular
vascular calcification 5673 restore the artery elasticity by virtue of its ability to activate matrix Gla protein, a local intra vascular calcification inhibitor [[11]]. Furthermore, in clinical practice, extraosseous calcification such as tumor calcinosis
vascular calcification 5820 Furthermore, in clinical practice, extraosseous calcification such as tumor calcinosis and uremia-related vascular calcification such as calciphylaxis were considered controllable, at least partially, by parathyroidectomy and multiple
vascular calcification 6215 [[12]–[16]].3. Clinical Presentation of Calcification in CKD PatientsThere are four different types of vascular calcification (Table 1) [[17]] and one type of soft tissue calcification: intimal artery calcification or medial artery
vascular calcification 8331 infiltration of inflammatory cells, calcium deposits, and bone matrix proteins, suggesting that valvular and vascular calcification s are likely associated syndromes [[24]–[26]]. Medial calcification develops concurrently with valve
vascular calcification 8706 increase cardiovascular mortality.4. How to Measure and Monitor Vascular CalcificationThe evaluation of vascular calcification therapies is problematic because of lack of good methods to quantify it. Computed tomography of the
vascular calcification 9332 or chest (aortic arch) [[29]] and the hand [[30]] can be used to detect the presence or absence of vascular calcification , and an echocardiogram can be used as a reasonable alternative to computed tomography-based imaging
vascular calcification 9733 calcification may be of great value to patients with ESRD. Bone tissue has been detected in areas of vascular calcification , including osteoblast- and osteoclast-like cells, and in various bone-related extracellular matrix proteins,
vascular calcification 10619 inflammatory cytokines are also involved [[32]].Although there was disappearance of a portion of uremic vascular calcification , the majority of vascular calcification that is composed of highly insoluble apatite is difficult to
vascular calcification 10659 [[32]].Although there was disappearance of a portion of uremic vascular calcification, the majority of vascular calcification that is composed of highly insoluble apatite is difficult to mobilize the calcium deposits in a short-time
vascular calcification 11128 blood vessels makes them more rigid [[33]]. Specific interventions in CKD patients without or with vascular calcification are aimed at restoring a new balance between pro- and anticalcification factors, at the same time considering
vascular calcification 11953 interleukin 1 (IL-1), IL-6, C-reactive protein, and tumor necrosis factor alpha (TNFα) are found to promote vascular calcification in CKD patients [[32], [34], [35]]. The switch from cuprophane dialyzers to more biocompatible materials
vascular calcification 12573 demonstrated that dietary phosphorus increased serum TNFα and malnutrition accelerated the progression of vascular calcification in uremic rats [[39]]. Furthermore, the introduction of high-dose iron preparations raises the future
vascular calcification 13631 bone mineralization releases excessive calcium and phosphate into the extracellular fluid and causes vascular calcification [[43]]. Hence, how to keep appropriate bone turnover is very important. As mentioned earlier, bone biopsy
vascular calcification 15840 it is easy to reverse with deferoxamine (5 mg/kg/week), which facilitates removal by dialysis. The vascular calcification of adynamic bone disease could be attributed to the low capacity of bones to accommodate a phosphate
vascular calcification 18234 selective ability to result in less positive calcium and phosphate balance, which are key mediators of vascular calcification [[59]]. Further basic and clinical investigations are needed to determine the optimal doses and type
vascular calcification 19008 (ADVANCE) trial suggested that cinacalcet plus low doses of vitamin D may attenuate the progression of vascular calcification [[6]]. Parathyroid treatment including percutaneous ethanol parathyroid injection and parathyroidectomy,
vascular calcification 19385 factor balance and negative extraosseous calcium and phosphate balance in order to reduce or stabilize vascular calcification [[61], [62]].Treatment of High-Bone-Turnover Disease [[44], [46], [58]] Always consider bone biopsy
vascular calcification 21630 avoid inappropriate calcium loading in adults [[67], [68]]. The increased acceptable idea is that the vascular calcification of chronic kidney disease patients should influence the choice of the negative calcium balance by non-calcium
vascular calcification 25104 supplementation can assist with the management of secondary hyperparathyroidism and possibly prevent vascular calcification [[52], [81]].Vitamin K (K1 and K2) is involved in the production of bone and matrix amino acid γ-carboxyglutamic
vascular calcification 25371 anticalcification, and bone-forming molecule. Low vitamin K concentrations increase the risks of bone fracture and vascular calcification . Experimental data suggest that vitamin K antagonist may decrease the activity of matrix-g-carboxyglutamic
vascular calcification 25935 the controls [[85]]. Vitamin K supplementation may be a simple means to prevent the progression of vascular calcification in hemodialysis patients, a population characterized by severe functional vitamin K deficiency [[86]].
vascular calcification 26526 the bone and vessels. In the search for a common mediator capable of influencing bone remodeling and vascular calcification , the OPG/RANK/RANK ligand system has received recent attention. Restoring a balanced RANKL-to-OPG by
vascular calcification 26741 RANKL-to-OPG by modulating OPG production may represent a therapeutic strategy to preventing bone loss and vascular calcification . Denosumab is considered as OPG mimicker. Bisphosphonates and denosumab could reduce vascular calcification
vascular calcification 26849 calcification. Denosumab is considered as OPG mimicker. Bisphosphonates and denosumab could reduce vascular calcification in chronic kidney failure animal models and some case reports [[87]–[90]]. Antiresorption therapy
vascular calcification 27980 required [[93]–[95]]. In view of the potential role of the OPG-RANK-RANKL axis in the development of vascular calcification , whether this therapeutic compound can regress vascular calcifications is worth investigating. However,
vascular calcification 28050 OPG-RANK-RANKL axis in the development of vascular calcification, whether this therapeutic compound can regress vascular calcification s is worth investigating. However, well-controlled trials are needed to confirm the benefit.5.6.2. Sodium
vascular calcification 29417 involved in calcium deposition are emerging, no intervention has been described to reliably reverse vascular calcification . Consistent implementation of a systematic multi-interventional treatment strategy is suggested, consisting
vascular calcification 30035 keep extraosseous calcium and phosphate negative balance as much as possible may alter the course of vascular calcification . Further studies are needed to confirm clinical effects.Figure 1(a) Radial artery of a patient with
vascular calcification 30967 on the soft tissue around the hip joint comprising multiple round calcified masses.Table 1Types of vascular calcification .TypeCharacteristics/risk factorsComplicationAtherosclerotic intimal calcificationCalcification of atherosclerotic
vitamin K deficiency 26032 of vascular calcification in hemodialysis patients, a population characterized by severe functional vitamin K deficiency [[86]]. It is hoped that the existing coronary artery calcification in dialysis patients in current

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