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PubMed2001

Tissue characterization and calcification potential of commercial bioprosthetic heart valves.

BACKGROUND: Tissue properties may contribute to intrinsic calcification of bioprosthetic heart valves. Phospholipids have been proposed as potential nucleation sites for calcification. Other tissue properties might also be important in calcification. METHODS: Commercial and control bioprosthetic valve tissues were characterized by shrinkage temperature, moisture content, free amine content, phospholipid content, and calcification level after 90-day rat subcutaneous implantation as described. RESULTS: Shrinkage temperature, moisture content, and free amine content were typical for glutaraldehyde-cross-linked tissues. Phospholipid and calcium levels varied considerably among valve types. There was a significant correlation between phospholipid levels and calcification (r = 0.63, p = 0.04). Sulzer Carbomedics Mitroflow and Toronto SPV valve tissues had significantly more calcification than other commercial bioprostheses in this study (p < 0.01). Carpentier-Edwards Duraflex, CE SAV, and CE PERIMOUNT valve tissues had significantly less calcification than Medtronic Mosaic in this animal model (p < 0.02). CONCLUSIONS: Processes that reduce phospholipid levels are associated with reduced calcification in the rat subcutaneous model. Significant differences in calcification level were found among commercially available valves. The clinical significance of these results is unknown.

Bioprosthesis↗
PubMed1985

Relation of calcification to torn leaflets of spontaneously degenerated porcine bioprosthetic valves.

The gross appearance of 54 spontaneously degenerated porcine bioprosthetic valves was evaluated to determine the relation of calcium deposition to cusp disruption. Tears or perforations were shown in 89% (48) of the degenerated valves. The most common site of tears or perforations was near the commissural attachment (60% of all tears). Grossly visible deposits of calcium salts that ruptured to the surface of the cusps or caused changes in the topography were observed in 70% (38) of the 54 valves. Calcification was adjacent to tears or perforations in 56% (27) of the 48 valves with torn cusps. Among the valves that showed calcification, the deposits of calcium salts were adjacent to tears or perforations in 71% (27 of 38). The location of deposits of calcium did not relate to the age or sex of the patient or to the position of the valve, but valves with calcium were inserted longer than valves with no calcium (87 +/- 4 versus 58 +/- 7 months; p less than 0.001). The outflow surfaces showed more calcification than the inflow surfaces, irrespective of whether the valves were in the aortic or mitral position. Among the 38 valves with calcification, 92% (35) showed calcification at the commissural attachments, 53% (20) showed calcification in the body of 1 or more cusps, 11% (4) near the base, and 8% (3) near the free edge. In conclusion, most patients with spontaneous porcine valve degeneration showed calcification. The calcification was associated with tears or perforations of the cusps in 50% of all degenerated valves, in 56% of valves with torn cusps, and in 71% of valves that showed gross calcification.

Adult↗
PubMed1999

Further characterization of ATP-initiated calcification by matrix vesicles isolated from rachitic rat cartilage. Membrane perturbation by detergents and deposition of calcium pyrophosphate by rachitic matrix vesicles.

Although membrane associated enzymes such as ATPase, alkaline phosphatase, and NTP pyrophosphohydrolase in matrix vesicles (MVs) may underlie the mechanisms of ATP-promoted calcification, prior to the current investigation, the role of the MV membrane in calcification had not been addressed. In this study, various perturbations were introduced to the MV membrane in in vitro calcification systems to determine ideal conditions for ATP-initiated calcification by MVs isolated from rachitic rat epiphyseal cartilage. Membrane integrity appears to be required, since the rupture of the vesicular membrane by vigorously mixing with 10% butanol abolished calcification. In contrast, a mild treatment of MVs with low concentrations (e.g., 0.01%, which is much below the critical concentration for micelle formation) of either neutral Triton X-100 or anionic deoxycholate stimulated calcification by >2-fold, without inducing obvious changes in vesicular appearance. Fourier transform infrared spectroscopic studies were done to identify the mineral phase formed in these experiments. For the first time, rachitic MVs were shown to induce the formation of a calcium pyrophosphate dihydrate-like phase after their exposure to calcifying medium with 1 mM ATP. The integration of spectral areas indicated that calcification was enhanced by Triton X-100. The detergent effect was reversible and appeared to be not mediated through activation of ATPase, alkaline phosphatase, or ATP pyrophosphohydrolase. In contrast to neutral Triton X-100 and anionic deoxycholate, cationic cetyltrimethylammonium bromide inhibited both ATPase activity (I50=10 microM) and ATP-initiated calcification. These observations suggest that membrane perturbations can affect calcification and that the presence of NTP-pyrophosphohydrolase in MVs may play a role in the deposition of CaPPi in rachitic cartilage.

Adenosine Triphosphate↗
PubMed2004

Coronary calcification score: the coronary-risk impact factor.

CONTEXT: Identification of asymptomatic high-risk individuals is integral to current policies for preventing coronary heart disease, but existing methods of estimating risk lack sensitivity. To overcome this limitation increasing use is being made of non-invasive methods to detect subclinical coronary artery disease--eg, computed tomography (CT) to scan for coronary artery calcification. The location and extent of calcification correlate closely with pathological and angiographic abnormalities, but whether such calcification predicts clinical events, especially in younger individuals, is equivocal. Most data on coronary calcification have been obtained with electron-beam CT, but recently multislice CT, which is more versatile, less expensive, and available in most large hospitals, has been increasingly used. STARTING POINT: Leslee Shaw and colleagues (Radiology 2003; 228: 826-33) showed that the coronary calcification score predicted total mortality within subsets of patients classified at low, intermediate, or high risk according to Framingham criteria. In a cohort of over 10000 individuals, 5-year risk-adjusted survival was 95% when the score was over 1000 compared with 99% for scores of 10 or less. These results agree with other recent studies showing strong correlations between coronary calcification and coronary heart disease events. WHERE NEXT? The increasing use of multislice CT scanners should generate more data for comparison with those obtained from electron-beam CT. Radiation dose, which is higher with multislice than with electron-beam procedures, needs to be reduced, and calcification in scans needs to be quantified more accurately than with existing computer-based analyses. Further studies are needed to establish the predictive power of the coronary calcification score for clinical events and the effects of therapeutic intervention on both these outcomes. It would also be worth investigating the relation between coronary calcification and risk factors not quantified in Framingham-based estimates, including familial and racial predisposition to premature coronary heart disease.

Calcinosis↗
PubMedDate not supplied

Involvement of matrix metalloproteinases and tenascin-C in elastin calcification.

Elastin degeneration and calcification occur in many cardiovascular diseases, including medial arterial elastocalcinosis, atherosclerosis, and bioprosthetic heart valve mineralization. In the present study, we tested the hypothesis that the onset and progression of elastin-oriented calcification is associated with matrix remodeling and elastin degradation events. We studied whether aluminum ions inhibit elastin calcification by reducing elastin degradation and altering remodeling events. Subdermal implantation of pure elastin in juvenile rats resulted in a time-dependent calcification of elastin, reaching high levels 21 days after implantation. In situ hybridization showed that elastin calcification was associated with an up-regulation of matrix metalloproteinase (MMP) mRNA expression, specifically MMP-9 and MMP-2. Gelatin zymography demonstrated increased MMP-9 and MMP-2 enzyme activities in early stages of elastin calcification. Calcified elastin displayed a time-dependent pattern of tenascin-C (TN-C) and alkaline phosphatase (AP) expression. Pretreatment of pure elastin with aluminum ions prior to implantation resulted in complete inhibition of elastin calcification. Aluminum ion binding to elastin was found to protect elastin against MMP-mediated degradation in vitro. Noncalcified, explanted aluminum-pretreated elastin exhibited reduced activities of MMPs. TN-C expression in elastin implants exhibited a time-dependent pattern that was also affected by pretreatment of elastin with aluminum ions. In conclusion, elastin calcification is accompanied by matrix remodeling events, and the efficacy of aluminum pretreatment in inhibiting elastin calcification may be related in part to its effects on elastin remodeling.

Alkaline Phosphatase↗
PubMed2000

When have mammographic calcifications been adequately sampled at needle core biopsy?

AIMS: To determine if the number of flecks of calcification retrieved at stereotaxic core needle biopsy or the number of core samples obtained containing calcification are related to biopsy sensitivity, and to determine how many calcifications or cores containing calcification the radiologist should aim to retrieve when sampling mammographic microcalcification. MATERIALS AND METHODS: A retrospective review was performed of core specimen radiographs from 57 consecutive patients who had stereotaxic core needle biopsies of impalpable malignant microcalcifications without an associated mammographic mass. The total number of calcifications retrieved and the numbers of cores containing calcification were correlated with findings at core and surgical histology. RESULTS: Increasing retrieval of calcification elements visible on specimen radiography was associated with increasing sensitivity of the biopsy. Five or more flecks of calcium gave an absolute sensitivity of 100%. Increasing numbers of core samples obtained containing radiographically demonstrable calcification was also associated with increasing sensitivity. Three or more cores containing calcium resulted in a 100% absolute sensitivity for malignancy. CONCLUSION: To ensure adequate sampling of calcification at core biopsy, an optimum of either three or more cores containing calcium or five or more flecks of calcium in total is required. Achieving this target ensures a high pre-operative diagnosis rate for malignant microcalcifications.Bagnall, M. J. C. (2000). Clinical Radiology 55, 548-553.

Aged↗
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↗
PubMed2004

Coronary artery calcification measured with electron-beam computerized tomography correlates poorly with coronary artery angiography in dialysis patients.

BACKGROUND: Coronary artery calcification measured by electron-beam computerized tomography (EBCT) correlates with plaque burden and vessel stenosis and is predictive of future cardiac events in the general population. Uremic vascular calcification is common and widespread, tends to be medial as well as intimal, and may not relate solely to atherosclerotic lesions. Despite this difference and in the absence of any direct evidence in uremic patients, it is generally implied that coronary artery calcification equates to occlusive atherosclerosis. METHODS: We set out to compare the predictive value of coronary artery calcification assessed by EBCT with contemporaneous coronary angiography. We studied 18 patients with end-stage renal disease undergoing maintenance dialysis. Seventy-two coronary vessels were analyzed for angiographic evidence of stenotic disease and correlated with individual vessel calcification score. RESULTS: There was no significant correlation between degree of vessel stenosis and calcification score for individual vessels in patients with a positive calcium scan. Specificity was 48% and the positive predictive value was 53%. However, a calcification score <20 strongly correlated with the absence of significant luminal narrowing, and a 0 calcification score had a negative predictive value of 87.5%. CONCLUSION: Coronary artery calcification measured by EBCT is not an accurate marker of the degree of vessel stenosis in coronary artery disease in uremic patients and should not be used as a single screening test for atherosclerotic coronary disease.

Calcinosis↗
PubMed2005

Hyperphosphatemia and vascular calcification in end-stage renal disease.

Vascular calcification is a common finding in atherosclerosis and a serious problem in uremic patients. Because of the correlation of hyperphosphatemia and vascular calcification, the ability of extracellular inorganic phosphate levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization in vitro was examined. HSMC cultured in media containing normal physiologic levels of inorganic phosphate (1.4 mM) did not mineralize. In contrast, HSMC cultured in media containing phosphate levels comparable with those seen in hyperphosphatemic individuals (>1.4 mM) showed dose-dependent increases in mineral deposition. Mechanistic studies showed that elevated phosphate treatment of HSMC also enhanced the expression of the osteoblastic differentiation markers osteocalcin and osf2/Cbfa-1. The effects of elevated phosphate on HSMC were mediated by a sodium-dependent phosphate cotransporter (NPC) as indicated by the ability of the specific NPC inhibitor phosphonoformic acid to dose-dependently inhibit phosphate-induced calcium deposition as well as osteocalcin and Cbfa-1 gene expression. The NPC in HSMC was identified as Pit-1, a member of the novel type III NPCs. These data suggest that elevated phosphate may directly stimulate HSMC to undergo phenotypic changes that predispose to calcification and offers a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. Furthermore, we examined the factors affecting peripheral vascular calcification in 332 nondiabetic hemodialysis patients. There were 45 nondiabetic patients with vascular calcification. In multivariate logistic regression, the significant factors affecting vascular calcification were advanced age, longer duration of hemodialysis, increased phosphate concentrations, male gender, and lower predialysis diastolic pressure. Our findings suggest that an elevated phosphate level may directly stimulate HSMC to undergo phenotypic changes that predispose to calcification and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions.

Aorta↗
PubMed1977

[Calcification in mass lesions in the kidney (author's transl)].

In 80 mass lesions of the kidney, we found 11 cases with calcification; six of these occurred amongst 48 tumours and five amongst 32 solitary cysts. In particular, the following were found: 1. The frequency of calcification of 12 to 14% corresponds with that given in the literature. If other radiological signs fail indicate the nature of the space-occupying lesion, then calcification may be of diagnostic value. 2. Calcified cyst walls appear as fine, even, curvi-linear lines, Dense, irregular and extensive calcification indicates a solid tumour. 3. Ring or curvi-linear calcification in not a reliable sign of a cyst. Tumours may also show this type of calcification indicates a solid tumour. 3. Ring or curvi-linear calcification is not a reliable sign of cyst. Tumours may also show this type of calcification. Calcification occurs in solitary cyst with about the same frequency as in tumours. 4. Histologically all calcified tumours were clear cell carcinomas, mostly hypervascular. Only one case showed central necrosis.

Adenocarcinoma↗
PubMed2001

[Calcifications after operations of the subacromial space].

OBJECTIVE: Although there are several studies on the development of periarticular calcifications after different operation procedures of the joints, such calcifications have only seldomly been described in connection with operations in the subacromial space. Therefore, the present study was aimed at investigating the incidence of periarticular calcifications after operations in the subacromial space and to assess their clinical relevance. PATIENTS AND METHODS: In a retrospective study we examined 152 patients (51 female, 101 male) who had been operated on for primary shoulder impingement by open or arthroscopic procedures. The average follow-up time was 32.5 months. The assessment of the outcome of the treatment was performed using the criteria of the Constant score, different shoulder tests, a visual-analog scale for the evaluation of pain, and by evaluation of radiographs. RESULTS: Our study revealed good clinical results in the operative treatment of different stages of primary shoulder impingement and thus confirmed the results of similar studies before. However, in 25.6% of all patients we found periarticular calcifications. Hereby, calcifications occurred significantly more often after open procedures (56.8%) than after arthroscopic procedures (12.9%). There was non correlation between the occurrence of such calcifications and the stage of the disease. Moreover, comparison of the clinical results and the Constant scores at follow-up did not reveal any differences between patients with and without periarticular calcifications. CONCLUSION: Our study shows that the presence of periarticular calcifications after operations in the subacromial space is not necessarily associated with clinical symptoms. Therefore, routine prophylactic measurements against such calcifications are not justified.

Acromioclavicular Joint↗
PubMed2004

Coronary calcification in long-term type 1 diabetic patients -- a study with multi slice spiral computed tomography.

The risk for cardiovascular disease in diabetes is excessive. Multislice spiral computed tomography (MSCT) is a new technique for the assessment of coronary calcification in coronary artery disease. The aim of the study was to evaluate the presence of coronary calcium in asymptomatic long-term type 1 diabetic patients. Seventy-one type 1 diabetic patients (age 48 +/- 9 y, HbA1c 7.7 +/- 1.2, BMI 24.4 +/- 2.8, duration of diabetes 26 +/- 9 y) without clinical evidence for coronary artery disease were assessed with MSCT. A volumetric score was used to calculate the coronary calcification (CC) score. Five cardiac reflex tests were performed to study patients for cardiac autonomic neuropathy. Coronary calcifications were detectable in 22 (31 %) type 1 diabetic patients (CC-score > 0, mean CC-score 174 +/- 228 [X+/-SD]). Fourty-nine (69 %) type 1 diabetic patients demonstrated no coronary calcifications (CC-score= 0). In patients with coronary calcifications, both cardiac autonomic neuropathy and retinopathy were detected more frequently than in those without (64 % vs. 29 %, p < 0.02; 59 % vs. 31 %; p < 0.02). Duration of diabetes was longer in patients with than without coronary calcification (32 +/- 10 y vs. 24 +/- 8 y, p < 0.01). Age, BMI, and HbA1c were not significantly different between patients with and without coronary calcification. The study demonstrates that nearly one third of asymptomatic long-term type 1 diabetic patients present with coronary calcifications. In the patients, there is evidence for an association between coronary calcification and both cardiac autonomic neuropathy and retinopathy. MSCT is a promising non-invasive approach to analyze early alterations of the coronary system in diabetic patients.

Age of Onset↗
PubMed2001

Dynamic in vitro calcification of bioprosthetic porcine valves: evidence of apatite crystallization.

OBJECTIVE: Calcification is the most important cause of structural deterioration of glutaraldehyde-fixed bioprosthetic valves. Devitalization of tissue favors calcium deposits in the shape of apatite crystals. Host factors influence the extent and progression of calcification, but the phenomenon can also occur in vitro in the absence of a viable milieu. Whether calcific deposits obtained in vitro are similar to those found in vivo is unknown. METHODS: Four porcine frame-mounted bioprostheses (St Jude Medical Bioimplant; St Jude Medical, Inc, St Paul, Minn) were tested in vitro by using a pulsatile accelerated calcification testing device at a frequency of 300 cycles per minute at 37 degrees C for 19 x 10(6) cycles with a rapid synthetic calcification solution (final product [calcium x phosphate], 130 mg/dL(2)). Three of the same type of xenografts explanted from human subjects because of calcific failure (time in place, 108 +/- 25.63 mo) served as control grafts. Each sample underwent gross and x-ray examination, histology, transmission and scanning electron microscopy, atomic absorption spectroscopy, electron microprobe analysis, and x-ray powder diffraction methods. RESULTS: All in vitro bioprostheses were heavily calcific, with intrinsic Von Kossa stain-positive deposits and a mean calcium content of 205.285 +/- 64.87 mg/g dry weight. At transmission electron microscopy, nuclei of calcification involved mostly collagen fibers and interfibrillar spaces and, more rarely, cell debris and nuclei. Electron microprobe analysis showed a Ca/P atoms ratio of 4.5:3, a value intermediate between hydroxyapatite and its precursor, octacalciumphosphate. X-ray powder diffraction showed a well-separated and sharp peak, which is typical of hydroxyapatite. Aggregates of plate-like crystals up to 8 microm in size were observed at scanning electron microscopy, with a typical tabular hexagonal shape consistent with apatite. The morphologic and chemical findings in human explants were similar. CONCLUSIONS: Intrinsic calcification of glutaraldehyde-fixed porcine valves was induced in vitro. Electron microprobe analysis and x-ray powder diffraction findings were in keeping with apatite crystallization, such as that occurring in valve xenografts implanted in vivo. The model may be of value to accelerate the screening of anticalcific agents and may reduce the need for animal experiments.

Apatites↗
PubMedDate not supplied

As you like it, Part 3: A critique and historical review of calcification as seen with the electron microscope.

As You Like It, Part 3, is a continuation of the lectures given by the author (Ultra Path VIII and Ultra Path IX). It is a critical historical review of topics of interest to electron microscopists, attempting to show what went wrong and perhaps also why. The topics chosen this time demonstrate the prominent role electron microscopy has played in elucidating the diverse ways in which calcification can occur. The classic concept of dystropic and metastatic calcification is now inadequate to explain all observed phenomena. The electron microscope shows that calcification occurs in many different intracellular and extracellular sites and that each has its own morphology and etiology. Thus, a new classification based on ultrastructural morphology is born, but few seem to be aware of it. The author examines the ubiquitous but not too well-known phenomenon of cell remodeling, which often, but not always, leads to calcification. Topics are presented under the following headings: (1) matrical lipidic debris, (2) spherical microparticles, (3) matrix vesicles, (4) intramitochondrial calcification, (5) intralysosomal calcification, (6) calcification of collagen, (7) calcification of elastic fibers, and (8) calcification of secretory products.

Adenocarcinoma↗
PubMed2003

In subtotally nephrectomized rats 22-oxacalcitriol suppresses parathyroid hormone with less risk of cardiovascular calcification or deterioration of residual renal function than 1,25(OH)2 vitamin D3.

BACKGROUND: Although it effectively suppresses parathyroid hormone (PTH) secretion, vitamin D [1,25(OH)(2)D(3)] therapy often causes tissue calcification over the long term. In patients on chronic dialysis, cardiovascular calcification is clearly linked to an unfavourable prognosis. In pre-dialysis patients, renal calcification of the kidney leads to the deterioration of renal function. METHODS: We compared the propensities of 22-oxacalcitriol (OCT), with lesser calcaemic action, and 1,25(OH)(2)D(3) for producing their potential side effects in rats: (i) metastatic calcification of heart and aorta, and (ii) renal dysfunction with nephrocalcinosis, using the same effective doses for hyperparathyroidism. OCT (1.25 and 6.25 micro g/kg) or 1,25(OH)(2)D(3) (0.125 and 0.625 micro g/kg) solutions were administered intravenously to subtotally nephrectomized (SNX) rats three times weekly for 2 weeks. RESULTS: Despite the suppression of PTH to comparable levels, the calcification of the hearts, aortas and kidneys in the 1,25(OH)(2)D(3)-treated group was significantly greater than in the OCT-treated group. Of interest was that, in the OCT (6.25 micro g/kg) group, the degree of calcification in hearts, aortas and kidneys were distinctly lower than those in the 1,25(OH)(2)D(3) (0.125 micro g/kg) group despite the comparable serum Ca x Pi products. Therefore, there may be different mechanisms behind the calcifications resulting from OCT and 1,25(OH)(2)D(3). Deterioration of renal function, tubular changes, and atypical hyperplasia of proximal tubules associated with calcification were more severe in the 1,25(OH)(2)D(3)-treated group than in the OCT-treated group. CONCLUSIONS: These results indicate that OCT may be an effective agent for the suppression of PTH with a lesser risk of cardiovascular calcification or deterioration of residual renal function.

Animals↗
PubMed2004

Vascular calcification in patients with end-stage renal disease.

Vascular calcification is the most common type of extra-osseous calcification in end-stage renal disease (ESRD), manifesting as both medial and intimal calcification of large arteries. It is highly prevalent, often progressive and is associated with reduced arterial elasticity and increased mortality. Risk factors for calcification in ESRD include age, duration of dialysis, diabetes mellitus, most probably an elevated calcium-phosphorus product (Ca x P) level, the dose of calcium-containing phosphate binders and the induction of the systemic inflammatory response. Uraemic calcification was thought to be a largely physico-chemical process facilitated by elevated Ca x P (i.e. "metastatic" calcification). It is now well established, however, that vascular smooth muscle cells actively take up phosphate to form bioapatite. This process is associated with a phenotypic transformation of vascular smooth muscle cells during which they express osteoblast markers. In addition to phosphate, various other factors are likely to increase bioapatite formation, e.g. lipids and inflammatory cytokines. There have also been relatively new insights relating to the role of endogenous inhibitors of calcification [i.e. matrix Gla protein and fetuin-A (alpha(2)-Heremans-Schmid glycoprotein)], in particular the downregulation of fetuin-A in systemic inflammation. Decreased serum fetuin-A has been shown to be associated with a reduced capacity to inhibit calcium phosphate precipitation in vitro and is predictive of mortality in dialysis patients. These new insights into pathogenesis may lead to better prevention and treatment of calcification (e.g. with calcimimetics, anti-cytokines, etc.). However, the only preventive approach to have been established prospectively to date is the replacement of calcium-containing phosphate binders with sevelamer HCl, a non-calcaemic phosphate binder. Yet, it remains unclear whether sevelamer HCl reduces vascular calcification by preventing episodes of hypercalcaemia and/or by reducing low-density lipoprotein (LDL)-cholesterol levels.

Blood Proteins↗
PubMed2005

Aortic calcification in haemodialysis patients with diabetes mellitus.

BACKGROUND: Certain metabolic disorders, such as hyperphosphatemia induce vascular calcification in haemodialysis patients; it is unclear, however, whether these disorders contribute to aortic calcification in diabetic haemodialysis patients. This study examined the risk factors of aortic calcification in a large number of haemodialysis patients, and compared risk factors between diabetic and non-diabetic patients. METHODS: The subjects were 667 patients on maintenance haemodialysis: 184 with type 2 diabetes and 483 without. Aortic calcification was measured semi-quantitatively using a plain computed tomography image of the abdominal aorta, and an aortic calcification index (ACI) was calculated. RESULTS: The ACI of the diabetic subjects was significantly higher than that of those without diabetes (57.3+/-22.1 vs 44.8+/-28.3%, P < 0.0001), although the dialysis vintage of the former was significantly shorter (P < 0.001). Multiple regression analyses showed that diabetes was a significant independent risk factor for increased ACI. Multiple regression analyses, performed separately in diabetics and non-diabetics, revealed that advanced age, higher systolic blood pressure, smoking and longer haemodialysis vintage were common independent risk factors significantly associated with increased ACI in both patient groups (R2 = 0.296, P < 0.0001 for non-diabetics; R2 = 0.193, P < 0.0001 for diabetics). Higher serum phosphate concentration was not significantly associated with increased ACI in diabetic patients (P = 0.429), although it was a significant independent factor in non-diabetic patients (beta = 0.150, P < 0.0005). CONCLUSION: Aortic calcification in diabetic haemodialysis patients is more advanced, compared with non-diabetic patients, even with short haemodialysis vintage. Since disorders of mineral metabolism are not significantly associated with aortic calcification in diabetic haemodialysis patients, aortic calcification in these patients could be affected by metabolic abnormalities associated with the diabetic state per se, independent of other confounding factors; and aortic calcification may be advanced even before haemodialysis induction.

Adult↗
PubMed2006

The relationship between four single nucleotide polymorphisms in the promoter region of the osteoprotegerin gene and aortic calcification or coronary artery disease in Koreans.

OBJECTIVE: Osteoprotegerin (OPG) is a recently identified cytokine that acts as a decoy receptor for the receptor activator of the NF-kappaB ligand (RANKL). OPG has been shown to be an important inhibitor of osteoclastogenesis and arterial calcification in animal models. OPG has been proposed as a link molecule between osteoporosis and arterial calcification, but the relationship between the OPG gene and the cardiovascular system in human populations is unclear. Thus, the aim of this study was to investigate the relationship between OPG gene polymorphisms and aortic calcification or coronary artery disease in Koreans. DESIGN AND PATIENTS: Genotyping of four polymorphisms, A163G, G209A, T245G and T950C, in the promoter region of the OPG gene was performed in 251 healthy Korean women (mean age 51.3 +/- 6.9 years) and in a second study population consisting of 100 patients who underwent coronary angiography (mean age 57.0 +/- 11.9 years), by allelic discrimination using the 5' nuclease polymerase chain reaction assay. Cardiovascular risk factors and serum OPG levels were measured and aortic calcification in thoracic and abdominal aorta was examined by simple radiological methods. RESULTS: In the first study population, the prevalence of aortic calcification increased significantly as the subjects grew older. The frequencies of mutant alleles were significantly higher in the subjects with aortic calcification compared with those without aortic calcification in G209A and T950C polymorphisms, although these significances were lost after adjustment for age. No significant relationship was found between OPG gene polymorphisms and serum OPG levels or cardiovascular risk factors. In the second study group, there were no associations between OPG promoter genotypes and aortic calcification, serum OPG levels, or coronary artery disease. CONCLUSIONS: We observed that the four polymorphisms in the promoter region of the OPG gene were not associated with aortic calcification or coronary artery disease in Koreans. Further studies are needed to clarify this relationship.

Adult↗