Idiopathic arterial calcification of infancy; report of 2 cases occurring in siblings, and review of the literature.
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Calcification, Physiologic↗
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Phosphate overload accelerates vascular calcium deposition in end-stage renal disease patients.
Cardiovascular disease is a major problem in end-stage renal disease (ESRD) patients, with calcification being one of the conspicuous features of arteriosclerotic vessels. In the present study, clinical analysis and in vitro cell culture were used to investigate factors promoting vascular calcification in ESRD patients. The aortic arch calcification score (AACS) was the method used to estimate vascular calcification by evaluation of the simple posterior-anterior view chest X-rays. Factors that relate significantly to vascular calcification and the AACS are the Ca x Pi, age, dialysis period, blood pressure, smoking and diabetes mellitus, but not total cholesterol or triglyceride. The Ca x Pi, which depends on the serum phosphate concentration, is the only specific factor with the possibility for correction in ESRD patients, and so control of serum phosphate concentration is an important factor for reducing vascular calcification. The effects of phosphate overload on calcium deposition in human vascular smooth muscle cells (hVSMCs) using a primary cell culture system were also investigated. hVSMCs were harvested from the radial artery in ESRD patients and it was found that they could secrete extracellular matrix with a high affinity for calcium in a high phosphate medium (Pi=5.4 mg/dl). Therefore, phosphate overload might stimulate the hVSMCs to accelerate the calcium deposition in ESRD patients. These results suggest that the control of phosphate excess is important for prevention of calcium deposition on arteriole walls in ESRD patients.
Aorta, Thoracic↗
Phosphorus and uremic serum up-regulate osteopontin expression in vascular smooth muscle cells.
BACKGROUND: Dialysis patients have accelerated atherosclerosis, with extensive calcification of both the intima and media. Cross-sectional studies have implicated hyperphosphatemia in this process, but the mechanism is unclear. METHODS: To test the hypothesis that hyperphosphatemia and/or uremia induces vascular calcification, bovine vascular smooth muscle cells (BVSMC) were treated with increasing concentrations of beta-glycerophosphate, a phosphate donor, in the presence or absence of inhibitors for sodium/phosphate (Na/Pi) co-transport (foscarnet) or alkaline phosphatase (levamisole) for 48 hours. BVSMC also were incubated for various times with DMEM plus 15% pooled uremic sera from patients with low (LP) or high serum phosphorus (HP), or from pooled healthy control serum. Calcification in BVSMC was examined by quantitation of calcium deposition. Osteopontin expression and alkaline phosphatase activity were assessed by Western blotting and a colorimetric assay. RESULTS: beta-glycerophosphate increased osteopontin expression and alkaline phosphatase activity in BVSMC. Inhibition of either alkaline phosphatase activity or Na/Pi co-transport abolished this effect. Compared to incubation with control human serum, BVSMC cultured with uremic sera had increased mineral deposition. Uremic sera also increased alkaline phosphatase activity and osteopontin expression in BVSMC. The addition of beta-glycerophosphate to uremic HP or LP sera did not further augment osteopontin expression. Blocking Na/Pi co-transport or alkaline phosphatase activity only partially inhibited uremic sera-induced osteopontin expression, indicating that other non-Na/Pi co-transport dependent mechanisms also are involved. CONCLUSION: beta-glycerophosphate and uremic sera induce calcification and osteopontin expression in BVSMC. The uremic sera-induced osteopontin expression in BVSMC is partially mediated through alkaline phosphatase activity and a Na/Pi co-transporter dependent mechanism. However, other non-Na/Pi dependent mechanisms also contribute to accelerated vascular calcification in patients with ESRD.
Alkaline Phosphatase↗
Re-evaluation of risks associated with hyperphosphatemia and hyperparathyroidism in dialysis patients: recommendations for a change in management.
Hyperphosphatemia is a predictable consequence of chronic renal failure and is present in most patients on dialysis. Traditionally, the risk associated with elevated serum phosphorus has focused on its impact on renal osteodystrophy. A growing body of evidence, however, suggests that abnormalities in serum phosphorus, calcium-phosphorus product (CaxP), and parathyroid hormone (PTH) levels are resulting in vascular and visceral calcification, thereby contributing to the substantially increased risk of cardiovascular death in this population. In this analysis, we review in detail the literature that describes these associations. We show that the current treatment paradigm for serum phosphorus and secondary hyperparathyroidism is ineffective for a large segment of dialysis patients. Currently, 60% of hemodialysis patients have phosphorus greater than 5.5 mg/dL, and 40% have CaxP greater than 60 mg(2)/dL(2). It is our belief that prevention of uremic calcification, cardiac death, and vascular disease should assume primary importance when evaluating the risks associated with elevated levels of phosphorus, CaxP, and PTH. We recommend that target levels should become 9.2 to 9.6 mg/dL for calcium, 2.5 to 5.5 mg/dL for phosphorus, less than 55 mg(2)/dL(2) for CaxP product, and 100 to 200 pg/mL for intact PTH.
Calcinosis↗
Localised pulmonary metastatic calcification associated with pulmonary artery obstruction.
BACKGROUND: Metastatic pulmonary calcification, a complication of uraemia and disordered calcium metabolism, may be diffuse or localised. The factors that determine calcium precipitation are complex, but tissue alkalosis is thought to be important. As obstruction of the pulmonary artery theoretically causes local alkalosis a retrospective necropsy study was carried out to examine the relation between metastatic pulmonary calcification and vascular obstruction. METHODS: Five patients with focal and two with diffuse metastatic calcification in the lungs were identified over eight years. Lungs were studied macroscopically and by light microscopy, haematoxylin and eosin and histochemical stains being used for calcium. RESULTS: Underlying risk factors for calcification in these patients included renal failure in six and disseminated malignancy in five. In the five patients with localised calcification obstruction of the pulmonary artery by thrombus or tumour was found proximal or adjacent to areas of calcium deposition. In two patients metastatic calcification was confined to a lung with unilateral pulmonary artery thromboembolic occlusion. Calcification was not specifically associated with infarction, pneumonia, or diffuse alveolar damage. Lesions of the pulmonary artery were not seen in the two patients with diffuse bilateral metastatic calcification. CONCLUSION: In this small series there was a spatial association between pulmonary artery obstruction and localised metastatic calcification. It is proposed that pulmonary artery obstruction alters the microchemical environment of the lung, favouring tissue alkalosis and thereby enhancing parenchymal calcification in patients predisposed to this condition.
Adult↗
Manchester wasting disease: a disease of ruminants manifested by metastatic calcification especially of the cardio-vascular system.
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Calcification, Physiologic↗
[Diffuse, symmetric calcifications in the brain; idiopathic, non-arteriosclerotic, intracerebral blood vessel calcifications of Fahr].
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Brain↗
Histopathology of silicone oil keratopathy in humans.
Corneal endothelial decompensation is a frequent complication when silicone oil is used as a tamponade following vitrectomy for treatment of proliferative vitreoretinopathy in an aphakic eye. We evaluated the clinical, histopathological, and ultrastructural features of silicone oil-induced keratopathy in 10 patients who developed corneal complications requiring penetrating keratoplasty. Clinically, some cases showed corneal edema, corneal hypesthesia, endothelial opacification, band keratopathy, and peripheral corneal vascularization. Histopathologically, retrocorneal membranes were present, and different degrees of stromal hypercellularity, superficial stromal calcification, and vascularization were noted. The ultrastructural features of endothelial cell loss and retrocorneal membrane formation are consistent with changes previously reported in rabbits and cats receiving intracameral silicone oil injections.
Adult↗
Demonstration of a malignant soft-tissue lymphoma during triple-phase skeletal scintigraphy.
Malignant soft-tissue neoplasms may be demonstrated in the course of triple-phase skeletal scintigraphy due to the presence of either abnormal vascularity or calcifications. We report the unusual case of a malignant lymphoma which was detected in the vascular phases of a triple-phase skeletal scintigraphic study but was not visualized utilizing conventional radioangiographic techniques. Lymphoma should be included in the differential diagnosis of soft-tissue neoplasms demonstrable by scintiangiography.
Edema↗
Evaluation of calcific tendonitis of the rotator cuff: role of color Doppler ultrasonography.
OBJECTIVE: To use color Doppler ultrasonography to evaluate the morphology and vascularity of calcific tendonitis and to predict the formative and resorptive phases of the calcification. METHODS: Ninety-four patients with shoulder calcification on plain radiographs were enrolled in this study. Ultrasonography of the shoulder was focused on the rotator cuff. Color Doppler ultrasonography was applied in the calcific region. Patient symptoms were graded as painless, mild, moderate, and severe. The calcific plaques were classified as arc-shaped, fragmented or punctate, nodular, and cystic types. Color Doppler ultrasonographic signals were graded 0 to 3. The formative and resorptive phases of calcification were categorized by patient symptoms; acute onset of moderate or severe pain indicated the resorptive phase. RESULTS: The calcific plaques appeared arc shaped in 59 patients (20 painless, 19 mild, and 20 moderate), fragmented or punctate in 27 (2 painless, 3 mild, 20 moderate, and 2 severe), nodular in 6 (1 moderate and 5 severe), and cystic in 2 (severe). There was a significant difference between the morphology of the calcific plaques and clinical symptoms (P < .01). On color Doppler ultrasonography, grade 0 signals were found in 28 patients (22 painless and 6 with mild pain); grade 1 in 18 (16 mild and 2 severe); grade 2 in 41 (all moderate); and grade 3 in 7 (all severe). The correspondence between color Doppler ultrasonographic findings and clinical symptoms was excellent (P < .01). CONCLUSIONS: High-resolution ultrasonography with color Doppler imaging could differentiate the formative and resorptive phases of the calcification and could be used as a follow-up modality in calcific tendonitis of the shoulder.
Calcinosis↗
Bone morphogenic protein-4 expression in vascular lesions of calciphylaxis.
Calciphylaxis is characterized by an extensive media-calcification of cutaneous and subcutaneous arterioles and capillaries. Recent studies have provided evidence that vascular calcification is a process with similarities to bone metabolism. Bone morphogenic protein-4 (BMP-4) is physiologically involved in bone development and repair. The presence of BMP-4 in atherosclerosis and in sclerotic heart valves led us to suggest that BMP-4 is also involved in calciphylaxis. A 47-year-old male patient developed end-stage renal failure due to chronic glomerulonephritis. He has had two kidney transplants with an immunosuppressive regimen consisting of cyclosporine A and steroids. He was admitted to our hospital because of an increase in serum creatinine (Cr) and he subsequently developed progressive dermal ulcerations. A skin biopsy led to the diagnosis of calciphylaxis. Immunohistochemistry for BMP-4 of a skin specimen from our patient showed strong cytoplasmic immunoreactivity of intradermal cells with clear spatial association to arterioles and hair follicles. Whereas there are identified inhibitors and promoters of vascular calcification, the presence of BMP-4 has not been demonstrated in calcific uremic arteriolopathy. In contrast to atherosclerosis, BMP-4 in calciphylaxis cannot be found in vascular media, but in intradermal cells at the border of arterioles and hair follicles. Therefore, in calciphylaxis BMP-4 can play the role of a cytokine, a growth factor or a media-calcification promoter.
Bone Morphogenetic Protein 4↗
The mechanism of calcium deposition in soft tissues.
The current understanding of the mechanisms of calcium deposition in soft tissues in chronic kidney disease (CKD) patients has been deeply investigated in the last ten years. Because of higher morbidity and mortality due to cardiovascular disease in dialysis patients compared to general population, several studies showed that extraskeletal calcification may play a major role in the pathogenesis of cardiovascular events in CKD patients. Traditionally, the pathogenesis of vascular and soft tissue calcification has been associated with a passive calcium-phosphate deposition. Actually, it is well known that extraskeletal calcification is also related to an active process. In this review, we analyzed some of the factors potentially involved in the pathogenesis of vascular calcification in CKD patients.
Activin Receptors, Type I↗
[The Sturge-Weber syndrome. Tomodensitometric diagnosis].
Radiological diagnosis of Sturge-Weber's disease is based on the recognition of the characteristic "tram-line" type of calcification at routine skull X ray examination. Computerized tomography allows an earlier diagnosis since it shows smaller calcifications. It also provides a better appreciation of the associated parenchimal anomalies, such as cerebral atrophy, and an exact evaluation of the extent of the pial angiomatosis following intravenous injection of contrast. In four children with Sturge-Weber's disease CT clearly revealed the full extent of calcifications and vascular anomaly; in one of the children the diagnosis was possible before the appearance of the calcifications.
Angiomatosis↗
[Scleroderma, calcareous gout and arterial calcifications].
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Gout↗
Can the presence of carotid artery calcification on panoramic radiographs predict the risk of vascular diseases among 80-year-olds?
OBJECTIVE: The purpose of this study was to evaluate whether subsequent vascular diseases and related death could be predicted by the presence of carotid artery calcification detected on panoramic radiographs among elderly persons. STUDY DESIGN: We evaluated 659 panoramic radiographs from 262 male and 397 female 80-year-old subjects and their general medical examination data to assess the relationship between the presence of carotid artery calcification and vascular disease risk at baseline examination. Of these subjects, the occurrence of vascular diseases within 5 years after baseline examination was examined in 191 subjects. Further, the causes of death were examined in 108 subjects who died within 5 years after baseline examination. RESULTS: There was a significant difference in the history of past vascular diseases among subjects with and without carotid artery calcifications; however, no significant difference in the occurrence of subsequent vascular diseases was found among them. Further, there was no significant difference in the occurrence of vascular disease-related death within 5 years after baseline examination among subjects with and without carotid artery calcifications (P = 0.719). CONCLUSION: Our results suggest that the presence of carotid artery calcifications on panoramic radiographs may be related to the history of past vascular diseases; however, this is not a useful marker for subsequent vascular diseases and related death among 80-year-olds.
Aged, 80 and over↗
Three-dimensional analysis of a calciphylaxis plaque: clues to pathogenesis.
BACKGROUND: Calciphylaxis is a rare, life-threatening disorder associated with chronic renal failure, presenting with ulcerating plaques leading to death by sepsis in 60% of patients. Calcification of subcutaneous arterioles, thromboses, and extravascular calcification have been demonstrated in incisional biopsy specimens. However, the sequence of these pathologic events is unknown. OBJECTIVE: We examined a calciphylaxis plaque to document the wave of pathologic change from its center to its periphery. METHODS: A calciphylaxis plaque was excised postmortem from a female patient. It was examined histologically along 12 radii from the center of the lesion to its periphery. RESULTS: Calcification of small subcutaneous vessels was present in all histologically abnormal sections and extended further peripherally than extravascular calcification by up to 3.0 cm and further than subcutaneous thrombosis by up to 1.5 cm. CONCLUSION: Vascular mural calcification is an early and essential process in the development of a calciphylaxis plaque.
Autopsy↗
Effect of healing on small internal diameter arterial graft compliance.
Porosity is an essential component for long term function of small internal diameter synthetic vascular prostheses. Theoretically, porosity is required for healing by providing a scaffold for ingrowth of periprosthetic tissues. Porosity may be required for transfer of fluids and ions in prostheses even if tissue ingrowth does not occur. Increased permeability of vascular grafts has been shown to enhance tissue incorporation. Implants with pore sizes greater than 10 microns but less than 45 microns become ingrown with fibrohistiocytic tissue and capillaries. Implants with pore sizes greater than 45 microns are ingrown with organized fibrous tissue and minimal histiocytic response. The phenomenon of differential ingrowth may have important functional significance. Prostheses which heal with organized fibrous tissue have the potential for long term contracture, strangulation of vascularity and calcification. Fibrohistiocytic tissue has low mechanical strength and does not appear to contract or calcify. Elastomeric microporous vascular prostheses which are minimally ingrown or ingrown with fibrohistiocytic tissue maintain compliance after months of implantation. This study was designated to determine the effects of healing on the compliance of small internal diameter vascular replacements and to correlate the compliance to patency rates.
Animals↗
Progression of aortic valve stenosis: TGF-beta1 is present in calcified aortic valve cusps and promotes aortic valve interstitial cell calcification via apoptosis.
BACKGROUND: Aortic valve stenosis characteristically progresses due to cuspal calcification, often necessitating valve replacement surgery. The present study investigated the hypothesis that TGF-beta1, a cytokine that causes calcification of vascular smooth muscle cells in culture, initiates apoptosis of valvular interstitial cells as a mechanistic event in cuspal calcification. METHODS: Noncalcified and calcified human aortic valve cusps were obtained at autopsy or at the time of cardiac surgery. The distributions within cusps of TGF-beta1, latent-TGF-beta1-associated peptide, and TGF-beta receptors were studied using immunohistochemistry. The effects of TGF-beta1 on mechanistic events contributing to aortic valve calcification were also investigated using sheep aortic valve interstitial cell (SAVIC) cultures. RESULTS: Immunohistochemistry studies revealed that calcific aortic stenosis cusps characteristically contained within the extracellular matrix qualitatively higher levels of TGF-beta1 than noncalcified cusps. Noncalcified normal valves demonstrated only focal intracellular TGF-beta1. Addition of TGF-beta1 to SAVIC cultures led to a cascade of events, including: cellular migration, aggregation, formation of apoptotic-alkaline phosphatase enriched nodules, and calcification of these nodules. The time course of these events in the SAVIC culture system was rapid with nodule formation with apoptosis by 72 hours, and calcification after 7 days. Furthermore, ZVAD-FMK, an antiapoptosis agent (caspase inhibitor), significantly inhibited calcification and apoptosis induced by TGF-beta1, but had no effect on nodule formation. However, cytochalasin D, an actin-depolymerizing agent, inhibited nodule formation, but not calcification. CONCLUSIONS: TGF-beta1 is characteristically present within calcific aortic stenosis cusps, and mediates the calcification of aortic valve interstitial cells in culture through mechanisms involving apoptosis.
Aged↗