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At least 37 records · Page 2Linked to original sources
PubMed2005

Role of calcification inhibitors in the pathogenesis of vascular calcification in chronic kidney disease (CKD).

BACKGROUND: The majority of patients with chronic kidney disease (CKD) have excessive vascular calcification; however, most studies demonstrate that a subset of CKD patients do not have, nor develop, vascular calcification despite similar exposure to the uremic environment. This suggests protective mechanisms, or naturally occurring inhibitors, of calcification may be important. METHODS: In order to determine the role of three inhibitors, fetuin-A, matrix gla protein (MGP), and osteoprotegerin (OPG) in the vascular calcification observed in patients with CKD-5, we (1) measured serum levels of these inhibitors and compared the levels to calcification assessed by computed tomography (CT); (2) examined arteries from CKD-5 patients by immunostaining for these inhibitors; and (3) examined the expression and effect of these inhibitors in cultured bovine vascular smooth muscle cells (BVSMCs) incubated in serum pooled from uremic patients compared to healthy controls. RESULTS: There was a negative correlation of coronary artery calcification scores with serum fetuin-A levels (r=-0.30, P= 0.034) and a positive association with OPG levels (r= 0.29, P= 0.045). There was increasing immunostaining for both fetuin-A and MGP in arteries with increasing calcification graded semiquantitatively (P < 0.003). In vitro, fetuin-A added to mineralizing BVSMCs inhibited mineralization (P < 0.001). Compared to normal serum, BVSMCs incubated with uremic serum had a progressive increase in MGP expression with mineralization (P < 0.001) and increased expression of OPG in BVSMCs (P < 0.04). CONCLUSION: These data demonstrate that fetuin-A, OPG, and MGP play an important role in the pathogenesis of uremic vascular calcification.

Animals↗
PubMed2002

Stroke is associated with coronary calcification as detected by electron-beam CT: the Rotterdam Coronary Calcification Study.

BACKGROUND AND PURPOSE: Coronary calcification as detected by electron-beam CT measures the atherosclerotic plaque burden and has been reported to predict coronary events. Because atherosclerosis is a generalized process, coronary calcification may also be associated with manifest atherosclerotic disease at other sites of the vascular tree. We examined whether coronary calcification as detected by electron-beam CT is related to the presence of stroke. METHODS: From 1997 onward, subjects were invited to participate in the prospective Rotterdam Coronary Calcification Study and undergo electron-beam CT to detect coronary calcification. The study was embedded in the population-based Rotterdam Study. Calcifications were quantified in a calcium score according to Agatston's method. Calcium scores were available for 2013 subjects (mean age [SD], 71 [5.7] years). Fifty subjects had experienced stroke before scanning. RESULTS: Subjects were 2 times more likely to have experienced stroke when their calcium score was between 101 and 500 (odds ratio [OR], 2.1; 95% CI, 0.9 to 4.7) and 3 times more likely when their calcium score was above 500 (OR, 3.3; 95% CI, 1.5 to 7.2), compared with subjects in the lowest calcium score category (0 to 100). Additional adjustment for cardiovascular risk factors did not materially alter the risk estimates. CONCLUSIONS: In this population-based study, a markedly graded association was found between coronary calcification and stroke. The results suggest that coronary calcification as detected by electron-beam CT may be useful to identify subjects at high risk of stroke.

Aged↗
PubMed2006

Physiologic calcification of the pineal gland in children on computed tomography: prevalence, observer reliability and association with choroid plexus calcification.

RATIONALE AND OBJECTIVES: To evaluate the prevalence of physiologic pineal calcification, estimate observer variability, and examine the association with choroid plexus calcification. MATERIALS AND METHODS: A retrospective review of hard copy head computed tomography films of 242 patients age younger than 16 years by two independent observers. RESULTS: Physiologic pineal calcification was present in 20% of the whole group, in 39% of those 8-14 years age, in 8% of those younger than 10 years age, and in 1% of those younger than age 6 years. Observer agreement was very good (kappa = 0.72). Choroid plexus calcification was present in 16% and was four times as common in those with pineal calcification (38% versus 10%, P = .005), with very good observer agreement (kappa = 0.74). CONCLUSION: Physiologic pineal calcification is more common in children than previously reported, mostly because of improving computed tomography technology. There is an association with choroid plexus calcification.

Adolescent↗
PubMed2005

Cerebellopontine calcification: a new entity of idiopathic intracranial calcification?

We report the autopsy case of a 40-year-old woman with severe intellectual and motor disabilities, who showed calcification in the cerebellum and pons but not in the basal ganglia on CT scan, and died of intracranial hemorrhage due to intractable hypertension. At autopsy, numerous calcium deposits were noted in the cerebellar cortex, the dentate nucleus, the cerebellar white matter and the ventral pons. These deposits were distributed both in the neuropil and the white matter, but rarely within the arterial walls or in contact with capillaries. This weak relationship between calcification and the blood vessels, in addition to the paucity of basal ganglia calcification, is in contrast to the findings with other disorders involving intracranial calcification, including Fahr's disease and calcium metabolism disorders. Immunohistochemistry revealed intense staining of calbindin-D28K and parvalbumin at sites of calcium deposits both in the present case and in a case of pseudohypoparathyroidism, whereas these proteins were not localized to calcium deposits in the cerebellum of a Fahr's disease brain. We propose that the present case may represent a distinct entity among diseases characterized by idiopathic intracranial calcification. In addition, calcium-binding proteins may be involved in the calcification process in some cases with intracranial calcification.

Adult↗
PubMed2004

The association of Rose questionnaire angina pectoris and coronary calcification in a general population: the Rotterdam Coronary Calcification Study.

PURPOSE: The Rose questionnaire is a standardized method of measuring angina pectoris in general populations. Electron-beam computed tomography (CT) is a non-invasive technique to quantify the amount of coronary calcification. In a population-based study, we investigated the association between Rose questionnaire angina pectoris and coronary calcification. METHODS: The Rotterdam Coronary Calcification Study is embedded in the Rotterdam Study, a population-based study in subjects aged > or = 55 years. Participants of the Rotterdam Coronary Calcification Study underwent an electron-beam CT scan between 1997 and 2000. Coronary calcification was quantified in a calcium score according to Agatston's method. Rose questionnaire angina pectoris was assessed during a home interview. The first 2013 participants were included in the present analyses. RESULTS: In men, the presence of Rose questionnaire angina pectoris was associated with a 12.9-fold (95% confidence interval: 3.8-43.7) increased risk of a calcium score >1000 (reference: calcium score 0-100). The corresponding relative risk in women was 4.8 (2.0-11.3). Similar results were found when we computed sex-specific quartiles of the calcium score. CONCLUSIONS: Rose questionnaire angina pectoris is strongly associated with the amount of coronary calcification. Rose questionnaire angina pectoris corresponds better with the amount of coronary calcification in men than in women.

Aged↗
PubMed2003

Endothelin-1 is a potent regulator in vivo in vascular calcification and in vitro in calcification of vascular smooth muscle cells.

We observed changes of endothelin content and endothelin mRNA in vivo in vascular calcification and in vitro in calcification of vascular smooth muscle cells to explore the role of endothelin in vascular calcification. Calcification model in vivo was induced by administration of Vitamin D(3) plus nicotine. Calcification of vascular smooth muscle cells (VSMCs) was induced by beta-glycerophosphate. Endothelin content was measured by using radioimmunoassay. Endothelin mRNA amount was determined by using competitive quantitative RT-PCR. The results showed that calcium content, 45Ca(2+) uptake and alkaline phosphatase (ALP) activity were increased in calcified VSMCs, compared with controls, but were decreased, compared with calcified VSMCs plus BQ123 group. The endothelin content in the medium and endothelin mRNA in VSMCs were elevated by 35 and 120% (P<0.05), respectively, compared with those normal VSMCs. Calcium content, 45Ca(2+) accumulation and ALP activity in calcified arteries increased by 5.0-, 1.4-, and 1.4-fold. The endothelin levels in plasma and aorta as well as the amount of endothelin mRNA in calcified aorta were increased by 102, 103, and 22%, respectively, compared with control group. However, calcium content, 45Ca(2+) uptake and ALP activity in VDN plus bosentan group was 33, 36.7, and 40.4% lower than those in VDN group. These results indicated an upregulated endothelin gene expression as well as an increased production of endothelin in calcified aorta and VSMCs with BQ123 and bosentan significantly reducing vascular calcification. This suggested that endothelin might be involved in pathogenesis of vascular calcification.

Animals↗
PubMedDate not supplied

Mechanism of dystrophic calcification in rabbit aortas: temporal and spatial distributions of calcifying vesicles and calcification-related structural proteins.

INTRODUCTION: We have previously demonstrated the accumulation of calcifying vesicles in the thoracic aorta undergoing dystrophic calcification. Whether the distributions of other structural proteins related to calcification such as collagen and elastin fibers undergo coordinated modifications has not been established. METHODS: Young rabbits with various degrees of aortic calcification induced by cholesterol dietary interventions were used as an animal model to study the correlations. RESULTS: Rabbits fed a diet enriched in cholesterol for 3 months accumulated calcifying vesicles in the ascending thoracic aortas but did not develop histologically identifiable calcification. There were concomitant marked thickenings of the intima with focal deposition of collagen and disruption of the internal elastic fibers at this stage. By the 6th month, calcification was predominantly present in the intimal area adjacent to the media. At this calcified stage, calcifying activity of vesicles was higher than earlier stages. Concomitantly, collagen deposition in the lesions was intensified and the internal elastic fibers were completely disintegrated. These changes were found to be more profound in the proximal than in the distal portion of the aortas. CONCLUSION: The coordinated changes in the accumulation of collagen, disintegration of internal elastic fibers, and the appearance of calcifying vesicles in the lesions before calcification may set the stage for aortic calcification.

Animals↗
PubMed2003

Mobile components associated with rapidly developing mitral annulus calcification in patients with chronic renal failure: review of mobile elements associated with mitral annulus calcification.

Mitral annulus calcification may directly cause cerebrovascular accidents by serving as a source of calcific or thrombotic emboli. This hypothesis has been supported by recent reports of mobile components associated with mitral annulus calcification detected by echocardiography. Cardiovascular calcifications, including mitral annulus calcification, are common in end-stage renal disease and may develop and progress over a short period of time. We report two patients with mobile components associated with mitral annulus calcification and end-stage renal disease. Serial echocardiography documented that the mitral annulus calcification in these two patients had developed rapidly. Follow-up echocardiography in one patient demonstrated resolution of the mobile elements.

Calcinosis↗
PubMed2005

Association of conjunctival and corneal calcification with vascular calcification in dialysis patients.

BACKGROUND: Conjunctival and corneal calcification (CCC) is a well-known and easily detectable extraskeletal calcification, but its association with vascular calcification was not investigated previously. The aim of this study is to investigate the relationship of CCC with vascular calcification and bone metabolism parameters in dialysis patients. METHODS: We evaluated 63 patients (30 men, 33 women; mean age, 43.5 +/- 13.4 years) who were on dialysis therapy for more than 6 months. Forty-four patients were on peritoneal dialysis and 19 patients were on hemodialysis therapy. The same observer evaluated the presence of CCC by using a slit-lamp microscope, and a total CCC score was recorded for each patient. Fifty-two age- and sex-matched healthy controls also were evaluated by using the same method. Biochemical data were collected from patient files. Bone mineral density (BMD) of the lumbar spine and femoral neck was measured, and the presence of vascular calcification was assessed by using x-ray examinations of the pelvis and hands. RESULTS: Mean CCC score in patients was significantly higher than that in controls (6.2 +/- 5.1 versus 1.3 +/- 1.8; P = 0.001). CCC score correlated significantly with duration of renal replacement therapy ( r s = 0.392; P = 0.002), serum phosphorus level ( r s = 0.259; P = 0.042), and calcium x phosphorus product ( r s = 0.337; P = 0.007). However, we did not find a significant correlation with calcium, parathyroid hormone, alkaline phosphatase, albumin, or C-reactive protein level or BMD. The frequency of vascular calcification was significantly greater in patients with a high CCC score (CCC score > or = 10) compared with a low CCC score (< or =3; 56.3% versus 5.6%; P = 0.002). CONCLUSION: Evaluation of CCC score is an easy, fast, and noninvasive method. It seems that CCC score can be used as an additional tool to assess the status of extraskeletal calcification in dialysis patients.

Adult↗
PubMed2003

Parallels between arterial and cartilage calcification: what understanding artery calcification can teach us about chondrocalcinosis.

The pathogenesis of arterial calcification and chondrocalcinosis has become concurrently illuminated in recent years. For example, both processes occur in chronic inflammation-mediated degenerative diseases associated with aging (including atherosclerosis and osteoarthritis). Both processes are also modulated by altered gene expression by resident cells and by the release of mineralization-competent cell fragments (matrix vesicles and apoptotic bodies). Among the variety of genetic diseases associated with artery calcification are disorders that also promote cartilage calcification and/or dysregulated bone formation. Our discussion highlights that pathologic arterial and articular cartilage calcification both can be owing to genetic deficiencies of calcification inhibitors such as the inorganic pyrophosphate-generating ectoenzyme PC-1/nucleotide pyrophosphatase phosphodiesterase 1. Conversely, pathologic arterial and articular cartilage calcification also can primarily arise as a consequence of active processes driven by inflammatory cytokines and by disordered calcium and inorganic phosphate homeostasis. As discussed in this review, recent developments in the pathogenesis of arterial calcification provide valuable information pertinent to potential future advances in controlling chondrocalcinosis.

Animals↗
PubMed2001

Control of serum phosphorus: implications for coronary artery calcification and calcific uremic arteriolopathy (calciphylaxis).

There is mounting evidence that elevated serum phosphorus is an important cardiovascular risk factor in patients with end stage renal disease. Recent work has shown that vascular smooth muscle cells have the ability to undergo osteoblastic differentiation and produce an environment conducive to mineralization. Serum phosphorus is an important stimulator of this process and the adverse cardiovascular effects of hyperphosphatemia are most likely mediated via its ability to enhance the development of vascular calcification. Arterial calcification, whether it is intimal or medial in location, is a strong independent risk factor for cardiovascular morbidity and mortality. Both coronary artery calcification and calciphylaxis are prototypical examples of arterial calcification that have been associated with poor phosphate control. Furthermore, several investigators have recently suggested that the prescription of large doses of calcium to achieve phosphate control may augment, rather than diminish, the risk of vascular calcification. This is more likely to be true in the presence of low turnover bone disease, a diagnosis difficult to make with routine laboratory testing. A brief review of the molecular biology of vascular calcification supports the concept that warfarin administration may exacerbate the calcific process, particularly in the setting of hyperphosphatemia, as has been reported in patients with calciphylaxis. Recognizing the consequences of poor phosphate control, it is time to adopt strict target levels that aim to normalize serum phosphorus levels. The available evidence supports that this control should not be achieved through the use of supraphysiologic doses of supplemental calcium.

Arterioles↗
PubMed2004

Human vascular smooth muscle cells undergo vesicle-mediated calcification in response to changes in extracellular calcium and phosphate concentrations: a potential mechanism for accelerated vascular calcification in ESRD.

Patients with ESRD have a high circulating calcium (Ca) x phosphate (P) product and develop extensive vascular calcification that may contribute to their high cardiovascular morbidity. However, the cellular mechanisms underlying vascular calcification in this context are poorly understood. In an in vitro model, elevated Ca or P induced human vascular smooth muscle cell (VSMC) calcification independently and synergistically, a process that was potently inhibited by serum. Calcification was initiated by release from living VSMC of membrane-bound matrix vesicles (MV) and also by apoptotic bodies from dying cells. Vesicles released by VSMC after prolonged exposure to Ca and P contained preformed basic calcium phosphate and calcified extensively. However, vesicles released in the presence of serum did not contain basic calcium phosphate, co-purified with the mineralization inhibitor fetuin-A and calcified minimally. Importantly, MV released under normal physiologic conditions did not calcify, and VSMC were also able to inhibit the spontaneous precipitation of Ca and P in solution. The potent mineralization inhibitor matrix Gla protein was found to be present in MV, and pretreatment of VSMC with warfarin markedly enhanced vesicle calcification. These data suggest that in the context of raised Ca and P, vascular calcification is a modifiable, cell-mediated process regulated by vesicle release. These vesicles contain mineralization inhibitors derived from VSMC and serum, and perturbation of the production or function of these inhibitors would lead to accelerated vascular calcification.

Adolescent↗
PubMed2000

Apoptosis regulates human vascular calcification in vitro: evidence for initiation of vascular calcification by apoptotic bodies.

The mechanisms involved in the initiation of vascular calcification are not known, but matrix vesicles, the nucleation sites for calcium crystal formation in bone, are likely candidates, because similar structures have been found in calcified arteries. The regulation of matrix vesicle production is poorly understood but is thought to be associated with apoptotic cell death. In the present study, we investigated the role of apoptosis in vascular calcification. We report that apoptosis occurs in a human vascular calcification model in which postconfluent vascular smooth muscle cell (VSMC) cultures form nodules spontaneously and calcify after approximately 28 days. Apoptosis occurred before the onset of calcification in VSMC nodules and was detected by several methods, including nuclear morphology, the TUNEL technique, and external display of phosphatidyl serine. Inhibition of apoptosis with the caspase inhibitor ZVAD.fmk reduced calcification in nodules by approximately 40%, as measured by the cresolphthalein method and alizarin red staining. In addition, when apoptosis was stimulated in nodular cultures with anti-Fas IgM, there was a 10-fold increase in calcification. Furthermore, incubation of VSMC-derived apoptotic bodies with (45)Ca demonstrated that, like matrix vesicles, they can concentrate calcium. These observations provide evidence that apoptosis precedes VSMC calcification and that apoptotic bodies derived from VSMCs may act as nucleating structures for calcium crystal formation.

Amino Acid Chloromethyl Ketones↗
PubMed2004

Association of mitral annulus calcification, aortic valve calcification with carotid intima media thickness.

BACKGROUND: Mitral annular calcification (MAC) and aortic annular calcification (AVC) may represent a manifestation of generalized atherosclerosis in the elderly. Alterations in vascular structure, as indexed by the intima media thickness (IMT), are also recognized as independent predictors of adverse cardiovascular outcomes. AIM: To examine the relationship between the degree of calcification at mitral and/or aortic valve annulus and large artery structure (thickness). METHODS: We evaluated 102 consecutive patients who underwent transthoracic echocardiography and carotid artery echoDoppler for various indications; variables measured were: systemic blood pressure (BP), pulse pressure (PP=SBP-DBP), body mass index (BMI), fasting glucose, total, HDL, LDL chlolesterol, triglycerides, cIMT. The patients were divided according to a grading of valvular/annular lesions independent scores based on acoustic densitometry: 1 = annular/valvular sclerosis/calcification absence; 2 = annular/valvular sclerosis; 3 = annular calcification; 4 = annular-valvular calcification; 5 = valvular calcification with no recognition of the leaflets. RESULTS: Patient score was the highest observed for either valvular/annulus. Mean cIMT increased linearly with increasing valvular calcification score, ranging from 3.9 +/- 0.48 mm in controls to 12.9 +/- 1.8 mm in those subjects scored 5 (p < 0.0001). In the first to fourth quartile of cIMT values the respective maximal percentual of score were: score 1: 76.1%, score 2: 70.1%, score 4: 54.3% and score 5: 69.5% (p > 0.0001). CONCLUSION: MAC and AVC score can identify subgroups of patients with different cIMT values which indicate different incidence and prevalence of systemic artery diseases. This data may confirm MAC-AVC as a useful important diagnostic parameter of systemic atherosclerotic disease.

Aged↗
PubMed2006

Calcification inhibitors and Wnt signaling proteins are implicated in bovine artery smooth muscle cell calcification in the presence of phosphate and vitamin D sterols.

Administration of active vitamin D sterols to treat secondary hyperparathyroidism in patients with chronic kidney disease receiving dialysis has been associated with elevated serum calcium and phosphorus levels, which may lead to increased risk of vascular calcification. However, calcimimetics, by binding to the parathyroid gland calcium-sensing receptors, reduce serum parathyroid hormone, calcium, phosphorus, and the calcium-phosphorus product. Using cultured bovine aorta vascular smooth muscle cells (BASMCs), an in vitro model of vascular calcification, we compared calcification levels and gene expression profiles after exposure to the phosphate source ss-glycerolphosphate (BGP), the active vitamin D sterols calcitriol and paricalcitol, the calcimimetic R-568, or BGP with the active vitamin D sterols or R-568. Cells exposed to BGP (10 mM) alone or with calcitriol or paricalcitol showed dose-dependent BASMC calcification. No change in calcification was observed in cultures exposed to BGP with R-568, consistent with the observed lack of calcium-sensing receptor expression. Microarray analysis using total cellular RNA from cultures exposed to vehicle or BGP in the absence and presence of 10(-8) M calcitriol or paricalcitol for 7 days showed that cells exposed to BGP with calcitriol or BGP with paricalcitol had virtually identical gene expression profiles, which differed from those of cells treated with BGP or vehicle alone. Several osteoblast- and chondrocyte-associated genes were modulated by BGP and vitamin D exposure. In this study, exposure of BASMCs to phosphate and active vitamin D sterols induced calcification and changes in expression of genes associated with mineralized tissue.

Alkaline Phosphatase↗
PubMed1995

Aorto-pulmonary calcification: an unusual manifestation of idiopathic calcification of infancy evident antenatally.

BACKGROUND: Idiopathic arterial calcification of infancy represents a clinical spectrum involving calcification of large and medium-sized blood vessels with an unknown etiology. Its complications include severe systemic hypertension and cardiomyopathy. CASE: A twin infant with a variant of idiopathic arterial calcification was diagnosed antenatally by the detection of hyperechogenicity of the proximal aorta and central pulmonary vessels. The calcification was apparently isolated to these vessels and was associated with polyhydramnios and hypertrophic cardiomyopathy. CONCLUSION: Because antenatal diagnosis is possible, we suggest that there should be a high index of suspicion for idiopathic arterial calcification when there is sonographic hyperechogenicity of vessel walls, evidence of polyhydramnios, cardiomyopathy, or a family history of idiopathic arterial calcification.

Adult↗
PubMed2005

The association between angiotensin-converting enzyme gene polymorphism and coronary calcification. The Rotterdam Coronary Calcification Study.

BACKGROUND: An insertion/deletion (I/D) polymorphism in the gene encoding angiotensin-converting enzyme (ACE) has been associated with serum ACE levels. The association between the ACE I/D polymorphism and coronary heart disease is unclear. Electron-beam-computed tomography (EBT) is a technique to non-invasively quantify the amount of coronary calcification. We investigated the association between the ACE I/D polymorphism and coronary calcification. METHODS AND RESULTS: The Rotterdam Coronary Calcification Study is a population-based study in subjects aged 55 years and over. EBT scanning was performed in 2013 participants. Coronary calcification was quantified according to the Agatston score. The ACE I/D polymorphism was available for 1976 subjects. Geometric mean calcium scores in men with the II, ID and DD genotype were 167, 207 and 219, respectively. However, the difference in calcium score (p=0.19 for ID versus II; p=0.15 for DD versus II) and the trend (ptrend=0.17) were not significant. Calcium scores in women with the II, ID and DD genotype were 44, 42 and 36, respectively. There were no significant differences in calcium score (p=0.78 for ID versus II; p=0.29 for DD versus II), neither was the trend (ptrend=0.27). After we stratified on cardiovascular risk factors, no associations were present. CONCLUSION: The present study failed to show an association between the ACE I/D polymorphism and coronary calcification in the general population. Also, no significant associations were present between the ACE I/D polymorphism and coronary calcification in strata of cardiovascular risk factors.

Aged↗