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PubMed2005

Pathophysiological aspects of vascular calcification in chronic renal failure.

The nephrology community has progressively recognized that vascular calcification in patients with chronic renal failure is a major problem in terms of morbidity and mortality. This type of soft tissue calcification is not only passive, as thought previously, but implies active processes as well. It results from disturbances of the normal balance between calcification inhibitors and promoters, acting both at the systemic and the local level, and from the phenotypic change of smooth muscle cells towards osteoblast-like calcifying cells in the vessel wall. The recognition of the main factors involved will allow in the future a more appropriate prophylactic and therapeutic approach of this clinically important complication of chronic renal failure.

Adult↗
PubMed2003

Assessment of vascular calcification in ESRD patients using spiral CT.

BACKGROUND: Dialysis patients have increased vascular calcification of the coronary arteries and aorta by electron beam CT scan. The purpose of the present study was to utilize an alternative machine, spiral CT, to assess calcification in end-stage renal disease (ESRD) patients. METHODS: Two groups of patients with ESRD were evaluated: group 1, those receiving a renal transplant (n=38); and group 2, those remaining on dialysis (n=33). All patients underwent quad-slice spiral CT with retrospective gating to evaluate coronary artery and aorta calcification scores. Both area (Agatston method) and volume calculations were utilized, with retrospective gating in all but 16 subjects. Laboratory tests, medications and clinical characteristics were analysed. RESULTS: Using spiral CT, the intra-reader variability for coronary artery calcification (after correction for very low scores) was 0.9% mean / 0% median using the area (Agatston method) and 2.9% mean / 0% median using volume calculations. Group 1 patients were younger, more likely to be Caucasian and on peritoneal dialysis, had lower serum calcium and higher C-reactive protein levels than group 2. In patients without vs those with coronary artery calcification, only longer duration of dialysis (34+/-64 vs 55+/-50 months, P=0.004; r=0.39, P=0.005) and increasing age (39+/-13 vs 54+/-10 years, P<0.001; r=0.29, P=0.039) were associated, whereas only increasing age was associated with aorta calcification. CONCLUSION: In ESRD patients, the factors correlating with coronary calcification were duration of dialysis and advancing age, whereas only age correlated with aorta calcification. Spiral CT offers an alternative technique for the assessment of these changes.

Adult↗
PubMed1997

Vascular calcification in long-term haemodialysis patients in a single unit: a retrospective analysis.

Vascular calcification (VC), which is described in the elderly and in diabetics, is frequently seen in uraemia. It is usually regarded as having little significance. We studied the roentgenological appearance of VC in a homogeneous group of 38 long-hours haemodialysis patients whose longevity on dialysis allowed sustained (10-25 years) follow-up, including annual skeletal surveys and thrice-yearly clinical examinations and biochemical profiles. We compiled a dossier of clinical and laboratory parameters from the start of dialysis to the present day. We were able to analyze the natural history of VC and to determine which clinical parameters were linked with progression. We found that VC became steadily more prevalent-at dialysis onset present in 39% of the patients, but in 92% after an average dialysis duration of 16 years, with a mean onset 9.7 years after starting dialysis. As well as becoming more prevalent, the calcification became progressively more severe in most patients. There were two patterns of VC: axial (aorta and iliac and femoral arteries), seen alone in 32% of the patients, and peripheral (digital arteries), seen alone in 3% of patients. Most patients (65%) had evidence of both types. Calcification was scored for site and severity. Patient age (r = 0.57, p < 0.001), systolic blood pressure (r = 0.54, p < 0.001), hyperparathyroidism (reduced progression after parathyroidectomy), plasma phosphate (r = 0.34, p = 0.042), and vitamin D concentrations (r = 0.53, p < 0.001) were the principal determinants of severity and rate of progression of VC in this population. There was a weak negative association between progression and serum ferritin (r = -0.33, p = 0.046). The reduced vessel compliance that results from VC is likely to be cardiovascularly deleterious. In severe cases, tissue perfusion or vascular access for haemodialysis can be compromised. VC and accelerated cardiovascular mortality are common to uraemia, diabetes, and systolic hypertension in the elderly. Better understanding of these pathological processes may permit intervention and possibly lead to a reduction in cardiovascular mortality.

Calcinosis↗
PubMed2007

Clinical assessment of vascular calcification.

Cardiovascular calcification poses an increased risk for cardiovascular events in advanced phases of chronic kidney disease. This evidence has brought many investigators to focus their attention on the importance of detection of calcification and avoidance of further development of it with appropriate therapeutic choices. Physicians can use a variety of noninvasive imaging tools to identify cardiovascular calcification, some with merely qualitative and others with both qualitative and quantitative capabilities. Plain x-rays and ultrasonography can be used to identify macroscopic calcification of aorta and peripheral arteries, echocardiography is helpful for assessment of valvular calcification, and computed tomography technologies constitute the gold standard for quantification of cardiovascular calcification. The latter is also useful to monitor calcification progression and to assess the effect of different therapeutic strategies directed at modifying calcification progression. In this article, we review the clinical significance of vascular calcification and some of the evidence surrounding the most commonly employed noninvasive imaging techniques.

Calcinosis↗
PubMed1986

Progressive vascular calcification with necrosis of extremities in hemodialysis patients: a possible role of iron overload.

Progressive vascular calcification with ischemia and gangrene of the extremities occurs rarely in uremic patients, patients undergoing maintenance dialysis, and following renal transplantation. In this paper we present two additional patients on chronic hemodialysis who developed this syndrome in association with severe secondary hyperparathyroidism. Fulminant gangrene led to the death of the first patient, while in the second, multiple amputations had to be performed after parathyroidectomy. In both patients, evidence of iron overload due to multiple blood transfusions was present and iron was histologically demonstrated in a calcification area in one case. The possibility of iron overload as a "challenger" for systemic calciphylaxis is discussed.

Acute Disease↗
PubMed2003

Vascular calcification in the uremic patient: a cardiovascular risk?

BACKGROUND: Several factors suggest that the presence of vascular calcification (VC) is associated with a high risk of cardiac events in uremic patients. The aim of this study was to analyze the influence of VC on cardiac morbidity and mortality in our hemodialysis (HD) patients. METHODS: We studied 79 patients on HD: 43 males, mean age 48 +/- 15 years old, mean time on HD 83 +/- 63 months. The presence of VC was evaluated by radiologic series. Other cardiovascular risk factors analyzed were arterial hypertension, diabetes mellitus, obesity, cigarette smoking, anemia, and dyslipidemia. All patients underwent M-mode, two-dimensional, Doppler echocardiography. Patients were followed for two years. During this time, clinical information collected included predialysis blood pressure, incidence of ischemic heart disease, episodes of congestive heart failure, and mortality due to cardiovascular event. RESULTS: VC was observed in 55.7% of patients. Left ventricular hypertrophy, diastolic dysfunction, and cardiac valve calcification were significantly associated with VC. Ischemic heart disease (71.4% vs. 28.6%) and episodes of cardiac failure (0.41 vs. 0.18 per year; P < 0.05) appeared more frequently in the patient group with VC. VC was present in 80.6% of patients who developed episodes of heart failure. Eight patients died from cardiac disease; each of them had VC. CONCLUSION: The presence of VC can help to identify those HD patients with a higher cardiovascular risk.

Aged↗
PubMed2006

Vascular calcification: Hardening of the evidence.

In the past several years, basic-science studies have shown that vascular calcification is an active, cell-mediated process. It is increased in the uremic milieu and with hyperphosphatemia and therefore should be preventable. Additional advances in imaging techniques have facilitated the diagnosis of arterial calcification, a critical initial step in the translation of this knowledge to patient care.

Calcinosis↗
PubMed2004

The clinical significance of vascular calcification in young patients with end-stage renal disease.

Mortality statistics of young adults with childhood-onset end-stage renal disease (ESRD) show that cardiovascular disease (CVD) is responsible for most deaths on dialysis and after transplantation. This is most likely explained by the presence of a multitude of traditional and non-traditional risk factors in uremia, promoting the combination of classical atherosclerosis, uremic vasculopathy, and uremic cardiomyopathy. Vascular (arterial) calcifications occur with a high prevalence in young adults and their presence correlates with non-traditional risk factors, markers of inflammation, intake of calcium-containing phosphate binders, and the calcium-phosphorus product in serum. This might be explained by a high positive calcium and phosphorus balance in ESRD patients, which may be comparatively higher in the young. In addition, treatment with active vitamin D preparations may enhance the positive calcium and phosphorus balance and have a direct calcifying effect on the arterial wall. The biological process of vascular calcification resembles osteogenesis. These data indicate that vascular calcifications are related to non-traditional risk factors, inflammatory mechanisms, and disturbances in calcium and phosphorus metabolism in uremia. They provide strong evidence for a change in the current management of renal osteodystrophy in children and adolescents with ESRD.

Adolescent↗
PubMed2006

Reversal of the adynamic bone disorder and decreased vascular calcification in chronic kidney disease by sevelamer carbonate therapy.

A model of chronic kidney disease (CKD)-induced vascular calcification (VC) that complicates the metabolic syndrome was produced. In this model, the metabolic syndrome is characterized by severe atherosclerotic plaque formation, hypertension, type 2 diabetes, obesity, and hypercholesterolemia, and CKD stimulates calcification of the neointima and tunica media of the aorta. The CKD in this model is associated the adynamic bone disorder form of renal osteodystrophy. The VC of the model is associated with hyperphosphatemia, and control of the serum phosphorus both in this animal model and in humans has been preventive in the development of VC. This article reports studies that demonstrate reduction of established VC by the addition of sevelamer carbonate to the diets of this murine metabolic syndrome model with CKD. Sevelamer, besides normalizing the serum phosphorus, surprisingly, reversed the CKD-induced trabecular osteopenia. Sevelamer therapy increased osteoblast surfaces in the metaphyseal trabeculae of the tibia and femur. It also increased osteoid surfaces and, importantly, bone formation rates. In addition, sevelamer was found to be effective in decreasing serum cholesterol levels. These results suggest that sevelamer may have important actions in decreasing diabetic and uremic vasculopathy and that sevelamer carbonate may be capable of increasing bone formation rates that are suppressed by diabetic nephropathy.

Animals↗
PubMed1983

Inhibition of vitamin D3-induced vascular calcification by carbocromen.

High doses of vitamin D3 induce myocardial lesions, necrotic alterations, and calcification of the vascular smooth muscle, (Mönckeberg arteriosclerosis) (6). These effects are accompanied by an increased calcium influx into the wall of the aorta and mesenterial vessels (1). Prophylactic application of MgCl2 nearly prevents this calcium overload, whereas KCl or calcium antagonists are less active. In our studies, the uptake of calcium-45 4 days after a single dose of vitamin D3 (90,000 IU/200 g) was increased in rat heart and aorta by a factor of 3 to 7, and up to 30-fold in mesenterial vessels. Application of carbocromen (10 mg/kg b.i.d.) for 4 days decreases the vitamin D3-induced radiocalcium uptake by 44 (aorta) to 67% (mesenterial vein), MgCl2 (15 mmol/kg b.i.d.) by 46 (mesenterial vein) to 92% (mesenterial artery), and verapamil (5 mg/kg b.i.d.) by 15 (aorta) to 44% (mesenterial vein).

Animals↗
PubMed2000

Osteoprotegerin reverses osteoporosis by inhibiting endosteal osteoclasts and prevents vascular calcification by blocking a process resembling osteoclastogenesis.

High systemic levels of osteoprotegerin (OPG) in OPG transgenic mice cause osteopetrosis with normal tooth eruption and bone elongation and inhibit the development and activity of endosteal, but not periosteal, osteoclasts. We demonstrate that both intravenous injection of recombinant OPG protein and transgenic overexpression of OPG in OPG(-/-) mice effectively rescue the osteoporotic bone phenotype observed in OPG-deficient mice. However, intravenous injection of recombinant OPG over a 4-wk period could not reverse the arterial calcification observed in OPG(-/-) mice. In contrast, transgenic OPG delivered from mid-gestation through adulthood does prevent the formation of arterial calcification in OPG(-/-) mice. Although OPG is normally expressed in arteries, OPG ligand (OPGL) and receptor activator of NF-kappaB (RANK) are not detected in the arterial walls of wild-type adult mice. Interestingly, OPGL and RANK transcripts are detected in the calcified arteries of OPG(-/-) mice. Furthermore, RANK transcript expression coincides with the presence of multinuclear osteoclast-like cells. These findings indicate that the OPG/OPGL/RANK signaling pathway may play an important role in both pathological and physiological calcification processes. Such findings may also explain the observed high clinical incidence of vascular calcification in the osteoporotic patient population.

Acid Phosphatase↗
PubMed1993

[Study on vascular calcification in patients on continuous ambulatory peritoneal dialysis (CAPD): special reference to active vitamin D (VD) treatment].

Cardiovascular complications, such as vascular calcification (VC), have been a major concern in patients undergoing chronic dialysis. The pathogenesis of this VC has been attributed to the altered calcium and phosphate metabolism, but the contributing factors have not been clarified. In order to investigate these factors, 38 CAPD patients were divided into two sub-groups according to the absence of aortic calcification (Group-A; n = 18) or the presence of aortic calcification (Group-B; n = 20). The number of elderly patients was larger and the duration of CAPD was longer in Group-B than in Group-A. Calcium and phosphate metabolism and serum lipids levels did not differ significantly between groups and the number of patients given VD was 8/18 in Group-A and 14/20 in Group-B. In order to explore the progression of VC in CAPD patients given long-term treatment with VD, 22 patients who were matched for the duration of CAPD were analyzed. These were divided into two sub-groups according to whether they were treated with VD (Group-C; n = 11) or not treated with VD (Group-D; n = 11). Radiological findings (such as the degree of aortic calcification), bone mineral content, divalent ions, parathyroid hormone levels and lipid profiles were examined. The prevalence of patients with aortic calcification was significantly higher in Group-D than in Group-C (7/11 v. s. 2/11, P < 0.05). However, lipids, mineral and endocrinological parameters did not differ between the sub-groups. No significant difference in the calcium and phosphate balance was observed. The bone mineral content revealed no difference between both of the sub-groups. VD administration by conventional mode, even without significant suppression of PTH or increase of bone mineral content, may enhance vessel calcification in patients on long-term CAPD.

Adult↗
PubMed1990

The impact of osteophytic and vascular calcifications on vertebral mineral density measurements in men.

To evaluate the influence of extravertebral calcification on spinal bone density determinations, we measured lumbar vertebral density in 71 hospitalized and 58 normal men using dual photon absorptiometry. The extent of vascular and osteophytic calcification was graded from lateral lumbar radiographs. Fifty-five (43%) of the subjects had identifiable osteophytes, and 86 (67%) had vascular calcifications. Despite similar ages and weights in subjects with and without ostephytes, those with osteophytes had greater spinal density (1.34 vs. 1.17 g/cm2; P less than 0.001), and there was a strong correlation between osteophyte severity and spinal density (r = 0.41; P less than 0.00001). Proximal femoral density was not different in those with and without osteophytes. The distribution of osteophytes in this population was not random, and as a result, the presence of osteophytes obscured the the relationship of bone density to age as well as the comparison of hospitalized to normal men. Vascular calcification had a minimal effect on vertebral density. In summary, osteophytic calcification exerted an important influence on the measurement of spinal bone density in men. This effect should be considered in both clinical and research applications of integral vertebral density measures.

Absorptiometry, Photon↗
PubMed1997

Vascular calcification as a source of hand pain and weakness in a patient with end-stage renal failure.

This article describes a unique case of vascular calcification of the hands complicated by pain and weakness. The case demonstrates the interaction of the skeletal and renal systems and the consequences of an unrecognized imbalance of calcium and phosphorus metabolism. Definitive medical management to keep the calcium-phosphate product below 70 through the judicious use of aluminum phosphate binders and diet should be coordinated to prevent and limit the extent of these calcifications.

Calcinosis↗
PubMed1985

Osteosclerotic myeloma complicated by diffuse arteritis, vascular calcification and extensive cutaneous necrosis.

Widespread, progressive skin necrosis developed in a 42-year-old male with a 5-year history of osteosclerotic myeloma. Biopsy of the necrotic lesions demonstrated a leucocytoclastic vasculitis with extensive vascular calcification. Radiological investigations demonstrated widespread arterial calcification. Clinical improvement of the established skin lesions followed the institution of a forced calciuresis and parathyroid hormone suppression by induced hypermagnesaemia and phosphate depletion. No further cutaneous necrosis developed. Subsequent treatment with oral immunosuppressive therapy and the diphosphonate, EHDP, has been associated with a complete 18-month remission. The relationship of this apparently unique pathological process to the osteosclerotic myeloma is discussed, together with the rationale for the therapeutic regime instituted.

Adult↗
PubMed2003

Vascular calcification in ex vivo carotid specimens: precision and accuracy of measurements with multi-detector row CT.

PURPOSE: To test the accuracy and precision of multi-detector row computed tomography (CT)-derived measurements of vascular calcification in ex vivo human carotid endarterectomy (CEA) specimens. MATERIALS AND METHODS: Sixteen ex vivo CEA specimens were imaged with multi-detector row CT. Multi-detector row CT-derived calcium scoring algorithms (ie, mineral mass and volume score) were compared with the mass and volume of ashed remnants of the CEA specimens. Bland-Altman analysis was performed to assess the mean (ie, bias) and SD (ie, precision) of differences between multi-detector row CT- and ashing-derived measurements. In addition, conventional Agatston score, volume score, mineral mass, and modified Agatston score were calculated for each specimen by using a number of scanning protocols. Images were obtained at a section thickness of 1.25 mm by using different tube energy settings and tube currents. Specimens were also imaged at different section thicknesses with fixed combinations of tube energy and tube current. To compare measurement variability of scoring methods, coefficients of variation for all protocols were calculated. RESULTS: Both mean multi-detector row CT-derived mineral mass and mean ashing-derived mineral mass were 0.129 g +/- 0.173 (r = 0.99, P <.001). Mean multi-detector row CT- and ashing-derived volumes were 339.94 mm3 +/- 395.4 and 39.48 mm3 +/- 55.76, respectively (r = 0.95, P <.001). Measurement bias relative to the reference ashing values was high (2,800.0%) for volume score and low (2.58%) for mineral mass. Measurement precision was 0.6% for volume score and greater than 0.0005% for mineral mass. Mean coefficients of variation for all CT protocols were 5.0% +/- 4.2 and 4.9% +/- 4.2 for mineral mass and modified Agatston score, respectively, and 16.0% +/- 9.2 and 14.5% +/- 3.9 for conventional Agatston and volume scores, respectively (P <.001). CONCLUSION: Compared with the conventional volume score, multi-detector row CT-derived mineral mass is a less biased and more precise measurement of the mineral content of nonmoving ex vivo CEA specimens. Mineral mass and modified Agatston score are more reproducible than conventional volume and Agatston scores.

Calcinosis↗
PubMed2005

Low turnover osteodystrophy and vascular calcification are amenable to skeletal anabolism in an animal model of chronic kidney disease and the metabolic syndrome.

LDL receptor (LDLR)-null mice fed high-fat/cholesterol diets, a model of the metabolic syndrome, have vascular calcification (VC) worsened by chronic kidney disease (CKD) and ameliorated by bone morphogenetic protein-7 (BMP-7), an efficacious agent in treating animal models of renal osteodystrophy. Here, LDLR-/- high-fat-fed mice without CKD were shown to have significant reductions in bone formation rates, associated with increased VC and hyperphosphatemia. Superimposing CKD resulted in a low turnover osteodystrophy, whereas VC worsened and hyperphosphatemia persisted. BMP-7 treatment corrected the hyperphosphatemia, corrected the osteodystrophy, and prevented VC, compatible with skeletal phosphate deposition leading to reduced plasma phosphate and removal of a major stimulus to VC. A pathologic link between abnormal bone mineralization and VC through the serum phosphorus was supported by the partial effectiveness of directly reducing the serum phosphate by a phosphate binder that had no skeletal action. Thus, in this model of the metabolic syndrome with CKD, a reduction in bone-forming potential of osteogenic cells leads to low bone turnover rates, producing hyperphosphatemia and VC, processes ameliorated by the skeletal anabolic agent BMP-7, in part through deposition of phosphate and increased bone formation.

Animals↗