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PubMed2002

[Inhibitory effects of bisphosphonate on vascular calcification].

Recently, it has been hypothesized that vascular calcification is an actively regulated process in which vascular smooth muscle cells (VSMCs) acquire osteoblast-like functions. Bisphosphonates prevent in vitro calcification of VSMCs and probably inhibit phosphate transport by sodium dependent phosphate transporter which plays a key role in VSMCs calcification. The effects of bisphosphonate on VSMCs have important implications for the future management of patients with vascular calcification.

English Abstract↗
PubMed2004

Left ventricular hypertrophy is associated with arterial stiffness and vascular calcification in hemodialysis patients.

Left ventricular hypertrophy (LVH) is the most frequent cardiac abnormality in patients with end-stage renal disease (ESRD). Recent studies have shown that arterial stiffness is associated with mediacalcinosis in these patients. However, whether arterial stiffness and vascular calcification are associated with the LVH in patients with ESRD has not been well established. Forty-nine patients on chronic hemodialysis participated in this study. 1) To better understand the mechanism underlying the increased incidence of LVH, we studied the relation between LVH and each of arterial wall stiffness, aortic calcification, and numerous clinical parameters in 49 patients on chronic hemodialysis. 2) To evaluate the contribution of arterial stiffness and arterial calcification to LVH in hemodialysis patients, we performed the present clinical analysis on 49 patients on chronic hemodialysis. We used an automatic device to measure arterial pulse wave velocity (PWV) as an index of arterial wall stiffness. The aortic calcification index (ACI) was quantified morphometrically by CT scan. The left ventricular mass index (LVMI) was estimated by M-mode echocardiography. To understand the mechanism underlying the increased incidence of LVH, we examined the factors contributing to LVMI in these patients. The correlation between each of the study parameters and LVMI as an indicator of LVH was then examined. The LVMI value was correlated positively with PWV (r=0.439, p=0.0014), systolic blood pressure (r=0.421, p=0.0023), and ACI (r=0.467, p=0.0006). A stepwise linear regression analysis showed that PWV, systolic blood pressure, and ACI were independently associated with LVH in our subjects. These results suggest that LVH is associated with hypertension, increased arterial stiffness, and the extent of vascular calcification in hemodialysis patients, with vascular calcification being the most important contributor to the development of LVH. Alteration of pulsatile dynamics contributes to an increase in left ventricular load and thus is also related to the LVH in these patients. These results suggest that LVH is associated with hypertension, increased arterial stiffness, and the extent of vascular calcification in hemodialysis patients. Vascular calcification, which alters the pulsatile dynamics and thereby contributes to an increase in left ventricular load, is the most important contributor to the development of LVH in patients undergoing hemodialysis.

Aortic Diseases↗
PubMed2006

High-resolution X-ray microtomography is a sensitive method to detect vascular calcification in living rats with chronic renal failure.

OBJECTIVE: Chronic renal failure (CRF) is associated with a 10- to 20-fold increase in cardiovascular risk. Vascular calcification is a prominent feature of cardiovascular disease in patients with end-stage renal failure and contributes to the excess mortality in this population. In this study, we explored in vivo X-ray microtomography (micro-CT) as a tool to detect and follow-up vascular calcifications in the aorta of living rats with adenine-induced CRF. METHODS AND RESULTS: With in vivo micro-CT, calcification of the aorta in uremic rats was clearly discernible on transversal virtual cross-sections. Micro-CT findings correlated well with tissue calcium content and histology. Repetitive scans in animals with light, moderate, and severe vascular calcification showed good reproducibility with minimal interference of motion artifacts. Moreover, both calcified volume and area could be quantified with this method. CONCLUSIONS: In vivo micro-CT scanning is a sensitive method to detect vascular calcifications in CRF rats, allowing follow-up and quantification of the development, and potential reversal during treatment, of vascular calcifications in living animals.

Animals↗
PubMedDate not supplied

Bone metabolism, vascular calcifications and mortality: associations beyond mere coincidence.

Bone and cardiovascular disorders are common age-related disorders in the general population and also in patients suffering from chronic kidney disease (CKD). Recent studies have shown an association between these two disorders and the rate of mortality. This article addresses some limitations of the concept of osteoporosis in CKD and compares bone and vascular disorders and mortality between non-selected general population and dialysis patients from the same geographic area. In the general population, all metabolic disorders increase with age, as well as vascular calcifications. The progression of vascular calcification was associated with a higher prevalence and incidence of bone fractures. In addition, both vascular calcifications and vertebral fractures were associated with higher mortality. A similar pattern was observed in dialysis patients with no increments in vertebral fractures, although with higher prevalence of vascular calcifications also both associated with higher mortality. Age was the strongest variable associated with all the analysed parameters, but some of the associations remained significant after age adjustment indicating the likely role of other common factors in the pathogenesis of bone and vascular disorders.

Bone Density↗
PubMed2003

BMP-7 is an efficacious treatment of vascular calcification in a murine model of atherosclerosis and chronic renal failure.

Chronic renal failure is complicated by high cardiovascular mortality. One key contributor to this mortality is vascular calcification, for which no therapy currently exists. Bone morphogenetic protein 7 is an essential renal morphogen that maintains renal tubular differentiation in the adult and is downregulated in renal failure. Several studies have demonstrated its efficacy in treating various renal diseases in rodents, and it was hypothesized that it would also be an effective treatment of vascular calcification in this setting. Uremia was imposed on LDL receptor null mice (a model of atherosclerosis), which were then treated with bone morphogenetic protein 7 for 15 wk. Uremic animals had increased vascular calcification by histology and chemical analysis. Calcification in treated animals was similar to or less than non-uremic control animals. Cells exhibiting an osteoblast-like phenotype in the vessel wall may be important in the etiology of vascular calcification. Expression of osteocalcin was assessed as a marker of osteoblastic function, and it is shown that it is increased in untreated uremic animals but downregulated to levels similar to non-uremic control animals with treatment. The data are compatible with bone morphogenetic protein 7 deficiency as a pathophysiologic factor in chronic renal failure, and they demonstrate its efficacy as a potential treatment of vascular calcification.

Animals↗
PubMed2003

[Significance of vascular calcification in diabetic patients with increased risks of cardiovascular disease and stroke].

Patients with diabetes have greatly elevated risks of atherosclerotic diseases such as coronary artery disease (CAD) and stroke. Vascular calcification in advanced atherosclerosis is a common feature in diabetic patients. In vitro and in vivo studies suggest that apoptosis and chondro/osteogenic differentiation of vascular wall cells such as smooth muscle cells may play important roles in the progression of vascular calcification. Diabetes may promote vascular calcification through the action of various factors including hyperglycemia, oxidative stress, tumor necrosis factor-alpha, and advanced glycation end products. Detection of coronary calcium by electron-beam computed tomography (EBCT) revealed clinical significance of vascular calcification and this technique may be a useful method to identify diabetic patients with increased risks of cardiovascular disease and stroke.

English Abstract↗
PubMed2006

Vascular calcification: pathobiological mechanisms and clinical implications.

Once thought to result from passive precipitation of calcium and phosphate, it now appears that vascular calcification is a consequence of tightly regulated processes that culminate in organized extracellular matrix deposition by osteoblast-like cells. These cells may be derived from stem cells (circulating or within the vessel wall) or differentiation of existing cells, such as smooth muscle cells (SMCs) or pericytes. Several factors induce this transition, including bone morphogenetic proteins, oxidant stress, high phosphate levels, parathyroid hormone fragments, and vitamin D. Once the osteogenic phenotype is induced, cells gain a distinctive molecular fingerprint, marked by the transcription factor core binding factor alpha1. Alternatively, loss of inhibitors of mineralization, such as matrix gamma-carboxyglutamic acid Gla protein, fetuin, and osteopontin, also contribute to vascular calcification. The normal balance between promotion and inhibition of calcification becomes dysregulated in chronic kidney disease, diabetes mellitus, atherosclerosis, and as a consequence of aging. Once the physiological determinants of calcification are perturbed, calcification may occur at several sites in the cardiovascular system, including the intima and media of vessels and cardiac valves. Here, calcification may occur through overlapping yet distinct molecular mechanisms, each with different clinical ramifications. A variety of imaging techniques are available to visualize vascular calcification, including fluoroscopy, echocardiography, intravascular ultrasound, and electron beam computed tomography. These imaging modalities vary in sensitivity and specificity, as well as clinical application. Through greater understanding of both the mechanism and clinical consequences of vascular calcification, future therapeutic strategies may be more effectively designed and applied.

Animals↗
PubMed2006

Measurement of vascular calcification using CT fistulograms.

BACKGROUND: Vascular calcification (VC), precipitated by calcium and phosphate imbalance, is a major contributor to cardiovascular disease (CVD) in chronic kidney disease (CKD). Electron-beam computed tomography (EBCT) quantitatively assesses coronary artery calcification (CAC), with VC scores predictive of atherosclerosis and cardiac events in the general and CKD population. EBCT is not readily available but spiral CT can also provide quantitative assessment of the extent of VC. CT fistulograms can be used as initial investigation for arterio-venous fistula (AVF) problems in haemodialysis (HD). The images obtained include thoracic aorta, brachio-cephalic, subclavian and common carotid arteries which allow assessment of the extent of VC in these vessels. No study to date has combined the CT fistulogram with concurrent determination of VC. METHODS: We hypothesize that a single investigation for AVF management may also provide information on VC. We retrospectively analysed CT fistulograms on 28 HD patients determining VC scores (in Hounsfield units) in AVF, subclavian and carotid arteries and aorta. We correlated these scores with patient demographics, serum markers of mineral metabolism (time averaged for the period 6 months prior to CT) and calcium-based phosphate binders. RESULTS: Patients (60.7% male) had a median age of 59 years and 46.4% were diabetic. The mean duration of dialysis was 17.5 months. CT fistulograms showed predominantly aortic (75% of patients) and subclavian (75%) calcifications, with only 21.4% having carotid VC and minimal VC at the level of AVF. Median VC scores were 619.8 (0-1481.4) for aorta and 521.7 (0-1139.6) for subclavian (scores of >400 indicate severe atherosclerotic disease), but there was no significant correlation with serum markers or duration of HD. Increasing age correlated significantly with greater VC in aortic (R = 0.53, P = 0.003) and subclavian (R = 0.40, P = 0.03) vessels, as well as with the number of VC sites involved. CAC was present in most patients (89.3%) but CAC scores were not able to be determined because of cardiac movement. CONCLUSION: Concurrent determination of the degree of calcification in certain vessels may be possible from CT studies assessing AVF structure. VC scores provided by CT fistulograms could contribute to HD patient CVD risk assessment but studies with larger patient numbers are required to determine their relevance.

Adult↗
PubMed2001

Soluble osteopontin and vascular calcification in hemodialysis patients.

BACKGROUND: Vascular calcification often occurs in patients with uremia. As osteopontin (OPN) is not only involved in the physiological but also the pathological calcification of tissues, OPN may be associated with the pathogenesis of aortic calcification in hemodialysis (HD) patients. METHODS: We examined the expression of OPN in atherosclerotic aortas of HD patients. In addition, we performed a prospective longitudinal study by using CT scans to detect aortic calcifications and by measuring the plasma OPN concentration by ELISA in HD patients (20 men, 16 women; mean age 55.2 +/- 21.3 years) and in healthy volunteers (18 men, 17 women; mean age 54.0 +/- 13.2 years). RESULTS: By immunohistochemical staining, OPN was abundantly localized in atherosclerotic plaques of HD patients. The macrophages surrounding the atheromatous plaques were identified as the OPN-expressing cells. We furthermore found that the concentration of soluble plasma OPN was significantly higher in HD patients as compared with the concentrations in age-matched healthy volunteers (837.3 +/- 443.2 vs. 315.1 +/- 117.4 ng/ml, p < 0.01). The OPN concentration was positively correlated with the aortic calcification index in HD patients (r = 0.749, p < 0.01). CONCLUSION: These data suggest that OPN, secreted by macrophages, plays a role in the calcification of atheromatous plaques in HD patients.

Adult↗
PubMed2001

Regulation of vascular calcification in atherosclerosis.

Over a century ago it was recognized that the vessel wall is a predominant site for ectopic calcification which is a hallmark of clinically significant atherosclerotic lesions. Old observational studies, which characterized vascular calcification as osteogenesis, and recent identification of common molecular mechanisms in bone and vascular calcification have led to the new recognition that atherosclerotic calcification is an actively regulated process similar to osteogenesis and distinct from a metastatic passive mineralization. Since the atherosclerotic lesion is composed of a multitude of cells and inflammatory mediators, elucidation of the role of these components in induction and acceleration of calcification is of fundamental importance in better understanding its pathogenesis and identifying possible interventional targets. This article will focus on four important mediators of vascular calcification: 1) calcifying vascular cells, 2) oxidized lipids, 3) cytokines, and 4) leptin.

Arteriosclerosis↗
PubMed1996

Extensive vascular calcification in a patient with perinatally acquired AIDS.

Extensive vascular calcification in an 8-year-old girl with perinatally acquired AIDS is reported. Complicating factors included cardiomyopathy, chronic lung disease, disseminated Mycobacterium avium complex (MAC), and wasting syndrome with total nutrition dependence. Plain abdominal films and CT of the abdomen immediately prior to her death revealed dense calcification of major vessels. Autopsy revealed calcification in the media of most major vessels typical of HIV arteriopathy. A review of the literature failed to reveal a description of similar vascular calcifications in pediatric AIDS.

AIDS-Related Opportunistic Infections↗
PubMed2000

Dramatic worsening of vascular calcifications after kidney transplantation in spite of early parathyroidectomy.

Vascular calcification is a common feature in chronic dialysis patients, but their clinical significance is debated and the role of kidney transplantation (TP) in the natural history of their development has received scanty attention. We will describe a case of dramatic worsening of vascular calcifications during TP in a young patient in spite of early and successful parathyroidectomy (PTX), and will discuss other causes which might be putatively linked to vascular damage during the time of TP. A 37-year-old man on regular dialytic treatment (RDT) for 11 years, received his first cadaveric transplantation in January 1993. He underwent PTX 6 months after TP because of the lack of decreasing in parathyroid hormone values despite normal graft function. Although PTX was effective, a dramatic worsening was evident in large as well as in medium and small-sized arteries during the following three years of TP. In February 1997, few months after starting dialysis again because of the recurrence of his primary membranoproliferative glomerulonephritis (MPGN), the patient experienced myocardial infarction followed by aorto-coronary bypass (right coronary artery and anterior descending coronary artery) and leg "claudicatio". Though a role for parathyroid hormone in vascular disease has been commonly accepted, the case here reported clearly shows that blunting parathyroid gland activity may be unable to avoid the worsening of a process of vascular disease during the time of TP. Many other factors--linked to the time of TP--may be involved in vascular diseases, such as nephrotic syndrome, dyslipidemia, hypertension and drugs. In the case of our patient, a clear cut risk factor for his progressive atherosclerosis can be designated hyperlipidema and other disturbancies secondary to a nephrotic syndrome due to relapse of MPGN, together with persistent hypertension. This is the first case report in the English literature which clearly demonstrates that TP may add fuel to the fire of vascular disease also in young people and even in the absence of parathyroid hyperactivity, perhaps on the basis of a favorable genetic background. Furthermore, the history of our patient demonstrates that vascular calcifcation heralds major cardiovascular diseases.

Adult↗
PubMed2005

Biology of vascular calcification in renal disease.

The high rates of atherosclerotic vascular disease in patients with end-stage renal disease (ESRD) cannot be fully explained by the excess of traditional risk factors. Interest has therefore arisen in the possible role of vascular calcification, which is increased in these patients and may effect plaque stability and have detrimental hemodynamic consequences. Considerable evidence has accumulated recently pointing to the regulated nature of the calcification process. The initiation of calcium crystal formation appears to require the presence of small membrane bound vesicles released by living or apoptotic cells. The cellular release, content and phagocytosis of these vesicles appear to be important regulatory pathways in vascular calcification. Better understanding of these mechanisms may have therapeutic potential in reducing the adverse cardiovascular event rates in patients with (ESRD).

Atherosclerosis↗
PubMed2005

[Vascular calcification in advanced secondary hyperparathyroidism].

Cardiovascular disease is one of the largest cause of mortality in maintenance hemodialysis patients. Vascular calcifications frequently encountered in hemodialysis patients. In advanced uremic secondary hyperparathyroidism model mice, vascular calcifications were observed in their aorta, by Kossa staining. This mouse model may be a useful model to study vascular calcification in maintenance hemodialysis patients.

Animals↗
PubMedDate not supplied

Relationship between serum magnesium, parathyroid hormone, and vascular calcification in patients on dialysis: a literature review.

Secondary hyperparathyroidism is present in most patients with end-stage renal disease and has been linked to uremic bone disease, vascular calcification, and mortality. Current literature suggests an association between hypomagnesemia and cardiovascular disease in the general population. We reviewed all published studies on the relationship between serum magnesium and parathyroid hormone and the relationship between serum Mg and vascular calcification in dialysis patients. Of these, 10 of 12 studies of patients on hemodialysis and 4 of 5 studies of patients on peritoneal dialysis showed a significantinverse relationship between serum Mg and serum intact parathyroid hormone. Hyperparathyroidism develops in peritoneal dialysis patients dialyzed with a solution containing normal calcium (1.25 mmol/L) and low Mg (0.25 mmol/L), even though serum calcium is maintained at a normal level. Four of the hemodialysis studies and one of the peritoneal dialysis studies indicated that there is an inverse relationship between serum Mg and vascular calcification in these patients. Potential benefits have been attributed to magnesium carbonate as a phosphate binder and it may possibly be an effective, less toxic, less expensive phosphate binder. We believe that the role of Mg in secondary hyperparathyroidism and vascular calcification merits further investigation.

Calcinosis↗
PubMed2006

Vascular calcification and osteoporosis--from clinical observation towards molecular understanding.

Patients with osteoporosis frequently suffer from vascular calcification, which was shown to predict both cardiovascular morbidity/mortality and osteoporotic fractures. Various common risk factors and mechanisms have been suggested to cause both bone loss and vascular calcification, including aging, estrogen deficiency, vitamin D and K abnormalities, chronic inflammation and oxidative stress. Major breakthroughs in molecular and cellular biology of bone metabolism and the characterization of knockout animals with deletion of bone-related genes have led to the concept that common signaling pathways, transcription factors and extracellular matrix interactions may account for both skeletal and vascular abnormalities. For example, mice that lack the cytokine decoy receptor osteoprotegerin or the hormone Klotho display a combined osteoporosis-arterial calcification phenotype. In this review, we summarize the current data and evaluate potential mechanisms of the osteoporosis-arterial calcification syndrome. We propose a unifying hypothesis of vascular calcification that combines both active and passive mechanisms of vascular mineralization with aspects of bone resorption and age-related changes.

Animals↗
PubMed2005

Vascular calcification in dialysis patients.

UNLABELLED: The risk factors for vascular calcification (VC) in dialysis patients include duration of dialysis, diabetes mellitus, aging, hyperphosphatemia, hyperparathyroidism, and calcium or vitamin D supplementation. This study was performed to evaluate the prevalence of and risk factors for VC in our dialysis population. METHODS: One hundred twenty-nine chronic dialysis patients underwent plain x-rays of the hands for VC. Patients were grouped as either positive (PVC) or negative (NVC) for VC. Age, gender, duration of dialysis, presence of non-insulin-dependent diabetes mellitus (NIDDM), oral calcium, and 1alpha-hydroxyvitamin D3 supplement, serum levels of calcium (Ca), phosphorus (P), calcium phosphorus product (CaxP), alkaline phosphates (ALP) and intact parathyroid hormone (iPTH) were compared between the two groups. RESULTS: Thirty-four patients (26.35%) showed VC. There were no differences between PVC and NVC patients for duration of dialysis (38.4 +/- 27.7 for PVC and 34.6 +/- 31.2 months for NVC, P = .80), levels of serum Ca (P = .26), P (P = .19), CaxP (P = .33), ALP (P = .89), or iPTH (P = .24). Similarly, oral calcium and 1alpha-hydroxyvitamin D3 intake were not different between the two groups (P = .971 and P = .3710 respectively). Compared to NVC patients, PVC patients were older (56.3 +/- 10.4 versus 47.5 +/- 16.1 years, P = .008) and had a greater incidence of NIDDM (17/34 PVC and diabetic versus 20/95 NVC, P = .001). In conclusion, for patients with a medium length of dialysis, the duration of dialysis as well as the doses of calcium salts and of 1alpha-hydroxyvitamin D3 were not significantly associated with vascular calcifications, but it was not possible to exclude a role for these and other factors in patients with longer dialysis.

Alkaline Phosphatase↗
PubMedDate not supplied

Determinants of coronary vascular calcification in patients with chronic kidney disease and end-stage renal disease: a systematic review.

BACKGROUND: Vascular calcification (VC) is a recognized process involved in senescence and atherosclerosis. Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are conditions associated with metabolic disorders related to soft tissue calcification. METHODS: We performed a systematic review of the literature confined to patients with CKD or ESRD with clinical observations of VC. Case reports of calciphylaxis were excluded. We identified 30 studies over 20 years: 11 prospective cohort, 7 cross-sectional, 11 case-control, and 1 retrospective cohort; n = 2918 subjects, mean age 51 years, 59% men and 41% women. Imaging methods used included: x-ray 43%, computed tomography 30%, ultrasound 17%, and other methods 10%. RESULTS: The most consistent determinants of VC were older age and dialysis vintage. Eight analyses determined a relationship between VC and measures of calcium-phosphate balance while 20 analyses specifically did not find such a relationship. Three studies suggested the degree of calcium loading, treatment with phosphate binders, or treatment with vitamin D analogues were related to VC. When taken into consideration, the lipid profile (primarily low high-density lipoprotein cholesterol, elevated triglycerides, elevated low-density lipoprotein, and elevated total cholesterol) were predictive factors in four analyses. CONCLUSIONS: VC is a common observation in CKD and ESRD and is mainly related to age, length of time on dialysis therapy, and possibly dyslipidemia. The calcium-phosphorus balance and its related treatments are likely not related to this unique form of vascular calcification. Further research into the determinants and potential treatments for vascular calcification is warranted.

Age Factors↗