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PubMed2004

Natural history of vascular calcification in dialysis and transplant patients.

BACKGROUND: The purpose of the present study was to determine the natural history of coronary artery and aorta calcification by spiral computed tomography (CT) in patients who undergo a renal transplant and patients on haemodialysis. METHODS: Two cohorts were evaluated for the natural history of vascular calcification: (i) 23 patients who underwent a baseline CT scan at the time of renal transplant and a repeat evaluation 15-20 months later; and (ii) 33 chronic kidney disease, stage 5 haemodialysis subjects who underwent a baseline CT scan, all followed for a minimum of 15 months, and 17 of whom underwent a second CT scan. RESULTS: In the patients undergoing a renal transplant, there was no net change in CAC with time, suggesting stabilization of calcification. In the haemodialysis patients, the median CAC increased by 1.27+/-1.88 score/days, P = 0.013. There was a trend towards increasing AoC score in both groups. All patients without calcification at baseline remained calcification free at follow-up. In the 15 months following baseline, the six dialysis patients who died had a significantly greater CAC score at baseline compared with the 24 patients who remained alive. Similarly, those patients who were hospitalized had a greater baseline CAC than patients who were not hospitalized. CONCLUSION: In this preliminary study, renal transplantation appears to slow down or arrest CAC, whereas CAC progresses in haemodialysis patients. In haemodialysis patients, CAC was greater in patients who died or were hospitalized compared with those who remained alive or were not hospitalized.

Adult↗
PubMed2001

Hepatic vascular calcification: an early second trimester sonographic feature of idiopathic infantile arterial calcinosis.

Prenatal sonographic diagnosis of idiopathic infantile arterial calcinosis has been limited to the third trimester. We report a monozygotic twin gestation for which an 18-week ultrasound detected the unique finding of hepatic vascular calcification as the earliest feature of the disorder. In contrast to previous reports, second-trimester ultrasound may permit timely diagnosis of idiopathic infantile arterial calcinosis.

Adult↗
PubMed2006

Volumetric BMD and vascular calcification in middle-aged women: the Study of Women's Health Across the Nation.

UNLABELLED: The association of spine vBMD with AC and CAC was studied in a biracial cohort of 490 middle-aged women in the Study of Women's Health Across the Nation. Lower vBMD was related to high AC, but not to CAC, independent of age and shared risk factors between osteoporosis and cardiovascular disease. INTRODUCTION: This analysis studied the association of spine volumetric BMD (vBMD) with aortic (AC) and coronary artery (CAC) calcification in middle-aged women and evaluated whether such associations were independent of age and shared risk factors between osteoporosis and cardiovascular disease (CVD) or explained by endogenous estradiol levels. MATERIALS AND METHODS: Vascular calcification and trabecular vBMD of the spine were measured using electron-beam CT in 490 women free from clinical CVD in the Study of Women's Health Across the Nation. Women were 45-58 years of age, 61% were white, and 64% were perimenopausal. Calcification scores were categorized into three levels (no AC, N = 146; moderate AC, scores = 1-74, N = 221; high AC, N = 123; no CAC, N = 256; moderate CAC, score = 1-7.54, N = 111; high CAC, N = 123). The highest categories were set at the 75th percentiles. Multinomial logistic regression was used to assess the association between vBMD (per SD) and the AC and CAC levels, with no calcification as the reference group. RESULTS: AC and CAC were detected in 70% and 48% of the population, respectively. Mean vBMD was 161.6 +/- 37.2 (SD) mg/ml. vBMD was associated with high AC in unadjusted, age-adjusted, and risk factor-adjusted analysis. Per 1 SD decrease in vBMD, the adjusted odds of high AC compared with no AC was significantly increased by 68% (95% CI, 1.06-2.68). Estradiol did not influence this association. vBMD was related to high CAC in unadjusted (OR = 1.35; 95% CI, 1.08-1.70) but not adjusted models. No associations of vBMD with moderate AC or CAC were observed. CONCLUSION: Lower vBMD was related to high AC, but not to CAC, in a biracial cohort of healthy middle-aged women independent of age and shared risk factors between osteoporosis and CVD. Further research should study possible pathophysiological links between the two conditions and the potential for common preventive and therapeutic interventions.

Bone Density↗
PubMed2006

Vascular calcification in patients with chronic kidney disease.

Chronic kidney disease (CKD) represents an extremely common condition, and cardiovascular diseases are frequently reported in this patient population. Traditional risk factors are not accurate prognostic predictors in CKD patients, and new potential markers to predict the cardiovascular involvement in uremic patients need to be identified. Vascular calcification (VC) represents a hallmark of the atherosclerotic process in CKD. This review summarizes the processes responsible for VC (particularly focusing on the mechanisms operative in the presence of renal dysfunction), discusses the utility of computer tomography modalities in the detection of VC in patients with CKD, and reports the potential role of VC as pathophysiological link between kidney disease and cardiovascular events.

Atherosclerosis↗
PubMed1985

Vascular calcification in types II and IV hyperlipoproteinemia: radiographic appearance and clinical significance.

Nearly 90% of patients with clear-cut hyperlipidemia seen in clinical practice have type II or IV hyperlipoproteinemia. Previous studies have shown that these syndromes have different distributions of coronary artery atherosclerosis and different outcomes after coronary bypass grafting. A characteristic pattern of vascular calcification on chest films might have some prognostic value. Therefore, to determine the location and extent of aortic root and coronary artery calcification seen on chest films, 33 consecutive patients with type II and 17 with type IV hyperlipoproteinemia were studied who were admitted for coronary arteriography between 1970 and 1982. Among the 33 patients with type II disease, 21 women and 12 men, 22 had radiographically visible calcification that was different in distribution from that usually found in atherosclerotic disease. The ascending aorta was involved in 21 and the arch in 12. In eight patients, the calcium outlined a distinctive narrowing of the ascending aorta. Six patients had significant left ventricular obstruction; in five it was from aortic valve stenosis. Of the 17 type IV patients, 16 men and one woman, none had aortic calcification or left ventricular outflow obstruction, and only one had coronary artery calcification. These data demonstrate that patients with type II hyperlipoproteinemia have severe calcific atherosclerosis of the aortic root that often is visible on chest films. Such calcification may alert physicians to the presence of type II hyperlipoproteinemia and the high probability of severe coronary artery disease.

Adolescent↗
PubMed2003

Slowing the progression of vascular calcification in hemodialysis.

Hyperphosphatemia and secondary hyperparathyroidism are common complications of ESRD (chronic kidney disease stage 5) that, when untreated, may result in increased morbidity and mortality. Hyperphosphatemia and hypercalcemia have been associated with increased coronary artery calcification. Achieving control of serum phosphorus without increasing serum calcium is an important goal for patients with ESRD. Although calcium-based phosphate binders effectively reduce serum phosphorus and parathyroid hormone concentrations, these agents can lead to hypercalcemia and have been associated with increased vascular calcification. The phosphorus binder sevelamer was developed to overcome the limitations associated with the usual management of hyperphosphatemia and secondary hyperparathyroidism (i.e., mineral salts). Sevelamer, a nonabsorbable hydrogel, is as efficacious as calcium-based phosphate binders for reducing serum phosphorus but does not cause hypercalcemia or other adverse metabolic effects. Sevelamer also exhibits beneficial effects on lipids, consistently and significantly decreasing LDL cholesterol and increasing HDL cholesterol in most studies. In a head-to-head randomized clinical trial, sevelamer and calcium-based binders achieved similarly excellent phosphorus control, but the use of calcium-based binders led to significantly higher serum calcium concentrations and an increased incidence of hypercalcemia and unintended suppression of parathyroid hormone. Treatment with calcium-based binders also led to the progression of coronary artery and aortic calcification, whereas sevelamer attenuated or arrested progression. Strategies that use oral calcium and vitamin D in patients with ESRD should be reexamined, and the potential advantages of sevelamer should be considered when selecting a primary agent to reduce serum phosphorus in hemodialysis patients.

Aortic Diseases↗
PubMed2005

Modeling the implications of changes in vascular calcification in patients on hemodialysis.

BACKGROUND: The Treat-to-Goal Study found that sevelamer slowed the progression of coronary calcification in patients on hemodialysis compared to calcium-based phosphate binders. To understand the implications of this effect for cardiovascular events, risk equations are needed. METHODS: Data on 179 patients on hemodialysis treated at one center in France included biochemical values during the year prior to study entry, patient characteristics, and cardiovascular events over an average of 4 years. As arterial calcification was evaluated ultrasonographically and quantified using a 0 to 4 score, an equation relating this to the electron-beam tomography (EBT)-based calcification score used in the trial was developed and applied to all patients. The estimated scores were then used in survival and Cox proportional hazards analyses of cardiovascular events in relation to the degree of calcification, controlling for other characteristics. RESULTS: Mean age at inclusion was 54 years, dialysis vintage 70 months, average follow-up 49 months; 32% suffered an event. The calcification score, diabetes, C-reactive protein (CRP), diastolic blood pressure, gender, smoking and hypertension are independent predictors of cardiovascular risk. The resulting equation indicates that, relative to a calcification score below 400, the risk of an initial event increases 44% for a score of 600, and more than doubles for a score of 1000. CONCLUSION: In the absence of long-term follow-up studies, these equations permit quantification of the expected long-term clinical consequences of the impact of various phosphate binders on vascular calcification. Together with resource use and cost information, these equations are key inputs for formal cost-effectiveness analyses.

Blood Pressure↗
PubMed2004

Inhibitory effects of etidronate on the progression of vascular calcification in hemodialysis patients.

The present study was designed to determine if etidronate inhibits the development of aortic calcification in hemodialysis (HD) patients. Eighteen Japanese HD patients were divided randomly into etidronate-treated or control groups. Etidronate was given orally at the dose of 200 mg just before sleep on the day of dialysis, which was performed three times per week. In the control group, the aortic calcification area (ACA) increased after 6 months. In the patients who received etidronate, however, when compared to the control group, increases in ACA were significantly suppressed. Serum Ca, P, and the Ca x P product did not change during etidronate treatment. These results suggest that etidronate inhibits the progression of vascular calcification without changes in serum Ca and P levels.

Aged↗
PubMed2002

[Suppressive effects of bisphosphonates on the vascular calcification in ESRD patients].

The progress of aortic calcification is associated with the incidence of cardiac and cerebrovascular diseases in hemodialysis patients. The present study was designed to determine whether etidronate can affect the development of aortic calcification in hemodialysis patients. Etidronate was given orally just before sleep on the day of dialysis, which was performed 2 or 3 sessions per week. Aortic calcification area (ACA), bone mineral density (BMD), and biochemical parameters were measured 6 months after the start of etidronate treatment to them compare with control. ACA in the control group showed a statistically significant increase after 6 months. However, the patients who received etidronate had no significant changes in ACA. Clinical and biochemical parameters and BMD were not influenced by etidronate treatment except serum alkaline phosphatase. These results suggest that etidronate has a potential ability to inhibit the progression of vascular calcification in hemodialysis patients, and that this beneficial effect of etidronate may prevent cardiovascular and cerebrovascular diseases that are major causes of death in hemodialysis patients.

English Abstract↗
PubMed2006

Atherosclerosis and vascular calcification in chronic renal failure.

Cardiovascular complications are a major clinical problem in patients with chronic kidney disease and end-stage renal failure; cardiac death accounts for approximately 40-50% of all deaths in these patients. Death from cardiovascular causes is up to 20 times more common in uremic patients than in the general population with the risk being even higher than in patients with diabetes mellitus. A high rate of myocardial infarction and excessive cardiac mortality have repeatedly been documented in patients with kidney disease and renal failure. Not only is the prevalence of myocardial infarction high, but also the case fatality rate is significantly higher in uremic patients with and without diabetes, respectively, compared to nonuremic patients. This is of particular interest since the prevalence of coronary atheroma in uremic patients was shown to be approximately 30% by autopsy and coronary angiography studies. Thus, coronary factors, i.e. atherosclerosis, and non-coronary factors may play an important role in the genesis of cardiac complications in the renal patient. In addition, renal failure recently has also be identified as a predictor of mortality in different stages of peripheral vascular disease. In particular, marked differences in the pathogenesis, morphology and course of atherosclerosis and arteriosclerosis under the conditions of renal failure have been documented. Among others increased plaque formation and particularly higher proportion and intensity of vascular calcification have been found in clinical and autopsy studies. In addition to the so-called classical or traditional risk factors, an important role for nonclassical risk factors such as microinflammation, hyperphosphatemia and oxidative stress has been documented in patients with renal failure and is discussed in detail.

Animals↗
PubMed2005

Association of vascular 18F-FDG uptake with vascular calcification.

UNLABELLED: Both calcification and FDG uptake have been advocated as indicators of atheroma. Atheromas calcify as cells in the lesion undergo apoptosis and necrosis during evolution of the lesion and at the end stage of the lesion. FDG concentrates in lesions due to the relatively dense cellularity in regions of inflammation of active atheromas. This investigation examines the geographic relationship of focal vascular (18)F-FDG uptake, as a marker of atherosclerotic inflammation, to arterial calcification detected by contemporaneous CT. METHODS: We reviewed PET/CT images from 78 patients who were referred for tumor staging for the presence of vascular (18)F-FDG uptake and vascular calcification. Arterial wall (18)F-FDG accumulation greater than adjacent blood-pool activity was considered inflammation. Arterial attenuation of >130 Hounsfield units was considered calcification. Sites in the ascending and descending aorta, the carotid and iliac arteries, and the coronary territories were examined on the emission, CT, and fusion images on a point-by-point basis. When lesions were seen, we evaluated whether they were overlapping or discrete. RESULTS: The (18)F-FDG arterial distribution was consistent with established atherosclerotic topography, with increased uptake in the thoracic aorta, at the carotid bifurcation, and in the proximal coronary vessels. Arteries typically displayed a patchwork of normal vessel, focal inflammation, or calcification; inflammation and calcification overlapped in <2% of cases. Arterial inflammation preceded calcification, in terms of mean patient age. Coronary inflammation was more prevalent in patients with more cardiovascular risk factors. CONCLUSION: Vascular calcification and vascular metabolic activity rarely overlap, suggesting these findings represent different stages in the evolution of atheroma.

Adolescent↗
PubMed2005

Novel conformation-specific antibodies against matrix gamma-carboxyglutamic acid (Gla) protein: undercarboxylated matrix Gla protein as marker for vascular calcification.

OBJECTIVE: Matrix gamma-carboxyglutamic acid (Gla) protein (MGP), a vitamin K-dependent protein, is a potent in vivo inhibitor of arterial calcification. We hypothesized that low endogenous production of MGP and impaired carboxylation of MGP may contribute to the development or the progression of vascular disease. METHODS AND RESULTS: Novel conformation-specific antibodies against MGP were used for immunohistochemistry of healthy and sclerotic arteries. In healthy arteries, MGP was mainly displayed around the elastin fibers in the tunica media. The staining colocalized with that for carboxylated MGP, whereas undercarboxylated MGP (ucMGP) was not detected. In atherosclerotic arteries, ucMGP was found in the intima, where it was associated with vesicular structures. In Mönckeberg's sclerosis of the media, ucMGP was localized around all areas of calcification. The results indicate that ucMGP is strongly associated with vascular calcification of different etiologies. In a separate study, serum MGP concentrations in a cohort of 172 subjects who had undergone percutaneous coronary intervention were significantly reduced compared with an apparently healthy population. CONCLUSIONS: These data show that impaired carboxylation of MGP is associated with intimal and medial vascular calcification and suggest the essentiality of the vitamin K modification to the function of MGP as an inhibitor of ectopic calcification.

Antibody Specificity↗
PubMed2004

Pathophysiology of vascular calcification in chronic kidney disease.

Patients with chronic kidney disease (CKD) on dialysis have 2- to 5-fold more coronary artery calcification than age-matched individuals with angiographically proven coronary artery disease. In addition to increased traditional risk factors, CKD patients also have a number of nontraditional cardiovascular risk factors that may play a prominent role in the pathogenesis of arterial calcification, including duration of dialysis and disorders of mineral metabolism. In histological specimens from the inferior epigastric artery of dialysis patients, we have found expression of the osteoblast differentiation factor core binding factor alpha-1 (Cbfa1) and several bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, type I collagen) in both the intima and medial layers when calcification was present. In cultured vascular smooth muscle cells, the addition of pooled serum from dialysis patients (versus normal healthy controls) accelerated mineralization and increased expression of Cbfa1, osteopontin, and alkaline phosphatase to a similar magnitude as does beta-glycerophosphate alone. However, a lack of inhibitors of calcification may also be important. Dialysis patients with low levels of serum fetuin-A, a circulating inhibitor of mineralization, have increased coronary artery calcification and fetuin-A can inhibit mineralization of vascular smooth muscle cells in vitro. These data support that elevated levels of phosphorus and/or other potential uremic toxins may play an important role by transforming vascular smooth muscle cells into osteoblast-like cells, which can produce a matrix of bone collagen and noncollagenous proteins. This nidus can then mineralize if the balance of pro-mineralizing factors outweighs inhibitory factors.

Animals↗
PubMed2003

Helical computed tomography angiography is the most efficient test to assess vascular calcifications in the iliac arterial sector in renal transplant candidates.

UNLABELLED: The increased scope of renal transplant indications has lead to a larger number of recipients with vascular problems due to arterial calcifications in the iliac region. Compared to magnetic resonance and conventional arteriography, helical computed tomography angiography (HCTA) accurately depicts arterial diseases, including the location and extent of arterial calcification. The objective of this study was to assess the value of HCTA with maximum-intensity-projection (MIP) reconstruction to evaluate iliac arterial calcifications and stenosis among candidates for renal transplantation. MATERIAL AND METHODS: From December 1997 to March 2002, 114 HCTA scans with MIP reconstruction were performed in candidates for renal transplantation. Included patients fulfilled some of the following conditions: (a) older than 55 years, (b) diabetic, (c) second transplants, and (d) obvious vascular calcifications on plain abdominal x-ray. RESULTS: Among the 114 patients, 33 (29%) were excluded for transplantation due to universal calcification of the iliac arterial sector, and 81 (71%) were included on the waiting list due to the presence of calcium-free areas for the vascular anastomosis. Transplantation, which was attempted in 28 of the 81 patients, was successful in 25 using the area programmed after HCTA analysis. The transplants failed in three cases because no calcium-free area could be found upon surgical examination. CONCLUSION: HCTA with MIP reconstruction makes it possible to draw an exact map of the arterial calcifications of the iliac arterial sector, allowing better recipient selection and accurate planning for the vascular anastomosis and placement of the renal graft.

Angiography↗
PubMed2003

Vascular calcification: in vitro evidence for the role of inorganic phosphate.

Uremic patients are prone to widespread ectopic extraskeletal calcification resulting from an imbalance of systemic inorganic phosphate (Pi). There can be serious consequences of this process, particularly when it results in the calcification of the vasculature. A recent study examined the response of cultured human aortic smooth muscle cells to varying levels of extracellular Pi. Cells that were exposed to Pi levels similar to those seen in uremic patients (>1.4 mmol/L) showed dose-dependent increases in cell culture calcium deposition. The results of this study also defined the role of elevated phosphate in transforming the vascular phenotype of these cells to an osteogenic phenotype, such that a predisposition for calcification was created. Pi-induced changes included increased expression of the osteogenic markers osteocalcin and core-binding factor-1 genes, the latter of which is considered a "master gene" critical for osteoblast differentiation. These changes occur early after exposure to high phosphate levels and seem to be mediated by a sodium-dependent phosphate co-transporter, Pit-1 (Glvr-1). Calcification of vascular cells also seems to occur in the absence of a mineral imbalance but in the presence of platelet-derived growth factor, a potent atherogenic factor. Taken together, these data suggest that calcification of vascular cells can occur early in a phosphate-rich environment similar to that seen in patients with renal failure and in a platelet-derived growth factor-rich atherosclerotic region under normal phosphorus conditions. From a clinical viewpoint, it seems that early control or prevention of hyperphosphatemia may reduce coronary calcification and its associated morbidity and mortality for patients on dialysis.

Calcinosis↗
PubMed1997

Intracranial vascular calcifications, glioblastoma multiforme, and lead poisoning.

A 72-year-man with previous lead poisoning presented with raised intracranial pressure and localizing neurologic signs. CT scans showed a high-grade glioma and extensive intracranial calcifications, which proved to be vascular in distribution on postmortem examination. The latter findings support the concept of dystrophic calcification following lead-induced cerebrovascular injury. Lead poisoning should be considered in the differential diagnosis of unexplained intracranial calcifications. There is also evidence from previous studies to suggest a causative relationship between lead poisoning and development of glioma.

Aged↗