Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vascular Calcification”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1982

Parathyroid surgery in chronic renal insufficiency. Subtotal parathyroidectomy versus total parathyroidectomy with autotransplantation to the forearm.

During the period 1970 to 1980 48 parathyroidectomies were performed in 46 patients with chronic renal insufficiency. Thirty patients underwent 31 subtotal parathyroidectomies and 17 patients underwent total parathyroidectomy with parathyroid autotransplantation to the forearm. Ten patients were on conservative renal treatment, 26 were on chronic haemodialysis and 12 had functioning kidney transplants at the time of parathyroid surgery. The indication for parathyroidectomy were clinical symptoms such as pruritus, bone and joint pain, neuromuscular disorders and radiological skeletal abnormalities pointing to hyperparathyroidism (HPT). Hypercalcaemia was present in 38 patients. The clinical symptoms and radiological findings were favourably affected by parathyroid surgery but vascular calcification was not affected by the operation in any of the patients. Normocalcaemia was achieved after surgery in all patients except one, who had residual parathyroid tissue in the neck. Vitamin D substitution was required in about 30% of the patients regardless of the type of operation that was performed. Recurrent HPT occurred in 9% with similar rates after both types of surgery. However, recurrence was more easily managed after a total parathyroidectomy with autotransplantation to the forearm than after a subtotal parathyroidectomy.

Adolescent↗
PubMed1983

[Uremic arteriopathy and ischemic skin changes].

The syndrome of uremic arteriopathy with ischemic skin manifestations--livedo reticularis, skin infarction and ulcerative necrosis--is described in a series of 6 patients. In all patients (3 female and 3 male, age 53-73 years) the syndrome occurred after slowly progressive renal failure and in 5 cases during temporary exacerbation of chronic renal failure and after alkalinizing treatment for marked metabolic acidosis. All patients had evidence of secondary hyperparathyroidism. In 4 the Ca X P product was in excess of 4.90, but only once above the critical product of 5.60 (greater than 70 when conventional units are used). Diagnosis was based on the clinical appearance of the skin involvement and the finding of vascular calcifications (x-ray and skin biopsy). The secondary hyperparathyroidism appears to play an important role in the pathogenesis of the syndrome. An increase in plasma phosphate or Ca X P product, calciphylaxis and/or alkalinizing therapy may release the precipitation of calcium salts in the interstitium or in the vessel walls. Therapy is confined to decreasing plasma phosphate and therewith the Ca X P product by means of phosphate binders or a diet low in phosphate. The unpredictable, often rapid success of parathyroidectomy awaits further clarification.

Aged↗
PubMed1983

Substitution of aluminium hydroxide by high doses of calcium carbonate in patients on chronic haemodialysis: disappearance of hyperaluminaemia and equal control of hyperparathyroidism.

Al(OH)3 was discontinued in 26 patients on chronic haemodialysis as well as vitamin D metabolites in eight. Oral CaCO3 was progressively increased from 4 +/- 3 to 10 +/- 5g/d to keep plasma PO4 less than 6.0mg/dl and P Ca less than 10.5mg/dl. This treatment had to be discontinued in three cases because of diarrhoea and/or uncontrolled hyperphosphataemia. In the remaining patients the control of hyperphosphataemia and of PTH values was as good or even better. Hyperaluminaemia disappeared in most patients demonstrating the role of oral Al(OH)3 in the induction of hyperaluminaemia. Because of frequent transient hypercalcaemia and of the occurrence of vascular calcification in two patients, high doses of CaCO3 after discontinuation of Al(OH)3 are advised only in cases of hyperaluminaemia.

Aluminum↗
PubMed1982

[5-year controlled therapy study on the prevention of diabetic angiopathy with the platelet-function inhibitor acetylsalicylic acid].

In a 5-year prospective double blind study on 120 diabetics at the age from 30 to 59 years the influence of 1.5 (1.0) g acetyl salicylic acid on the progression of the macro- and microangiopathy compared to a placebo was investigated. With regard to the total mortality, the cardiovascular death rate and the incidence of myocardial infarction, apoplectic insult and gangrene no advantages were the results for the group of intervention. Also the 74 test persons of the acetyl salicyl acid group and 88 test persons of the control group who remained after subtraction of all deceased and dismissed patients in the semiquantitative judgment of the progression of macroangiopathy (ischaemic heart disease, chronic venous insufficiency, arterial occlusive disease, vascular calcification) and in the development of retinopathy no significant differences in the sense of the effect of acetyl salicyl acid expected could be recognized. After the discussion of possible sources of error the result of the investigation is regarded as so reliable that one must dissuade from a primary prevention of the diabetic angiopathy by a middle-term application of acetyl salicyl acid in usual dosage.

Adult↗
PubMed1981

Total parathyroidectomy and parathyroid autotransplantation in patients with chronic renal failure.

Sixteen patients with chronic renal failure underwent total parathyroidectomy and parathyroid autotransplantation into the muscle of the forearm. Pertinent preoperative medical history of these patients included renal osteodystrophy, metastatic vascular calcifications, intractable itching and uncontrollable hyperphosphatemia. Efforts to control preoperative serum calcium and elevated serum parathormone levels were unsuccessful. The mass of parathyroid tissue implanted, in most instances, was approximately half that used in other series. Postoperatively, all patients received vitamin D and calcium orally, which were gradually decreased. Fourteen of the 16 patients had relief of symptoms, and all had restoration of parathormone levels to normal or slightly above normal, although in two patients, partial excision of hyperfunctioning tissue from the forearm was subsequently required because of recurring symptoms of secondary hyperparathyroidism. All patients had evidence of functioning grafts six to 40 months postoperatively or until death, attributable to intercurrent causes. The success of total parathyroidectomy and parathyroid autotransplantation in patients with chronic renal failure and symptomatic secondary hyperparathyroidism makes this a viable approach to the disease in such patients.

Female↗
PubMed1993

[A long-term hemodialysis patient complicated with systemic calciphylaxis].

A 46-year-old male patient underwent long-term hemodialysis treatment had suffered from calciphylaxis (defined by Selye), such symptoms as advanced systemic vascular calcification, rapid progression of gangrene on both fingers and toes, disturbance of consciousness, and sclerosis and obstruction of the superficial vein after venipuncture during 11.5 years of dialysis. Furthermore, he had a long history (30 years) of heavy smoking. He died as a result of sepsis due to pneumonia after 12.5 years of dialysis. He had received dialysis treatment using a small amount of dialysate (50 liters on a recirculating system) for 8.5 years and had been dialysed 2 and 2 or 3 times a week for 10 years. As a result of this insufficient dialysis treatment, his characteristic laboratory data showed hypocalcemia, hyperphosphatemia, elevated calcium-phosphorus product, advanced metabolic acidosis, hyperalkaliphosphatemia and elevated serum parathyroid hormone. Autopsy revealed the following: 1) enlargement parathyroid gland enlarged in two (4.0 g and 2.0 g, respectively) showing adenomatous hyperplasia presenting cord-like arrangement of chief cells and water-clear cells, 2) systemic medial calcification in radial, ulnar, renal, mesenteric and brain arteries, and 3) Berline-blue positive iron deposit in calcified arteries in mesenteric and parathyroid tissue. From these results, we concluded that factors (challengers) related to the appearance of calciphylaxis might be as follows: 1) advanced secondary hyperparathyroidism, 2) long-term uremic state, 3) administration of VD2 and VD3, 4) iron salt injection, and 5) a long history of heavy smoking. We speculated that these challengers might act synergistically to cause calciphylaxis.

Calciphylaxis↗
PubMedDate not supplied

Foot alterations in the hemodialyzed patient.

On the basis of their experience, the authors refer to complications observable at the foot level in chronic uremic patients in long-term hemodialytic treatment. These complications, termed renal osteodystrophy, are attributed to alterations in the phosphocalcium metabolism and to hyperparathyroidism. From an anatomopathologic viewpoint, they are characterized by alteration in bone tissue (osteomalacia and/or fibrous osteitis) and by soft tissue alterations. Alterations in the foot are the same as those observed in other osteoarticular regions. They consist of bone subperiosteal reabsorption of the phalanges, vascular calcifications, articular and para-articular calcifications, spontaneous disinsertion of the Achilles tendon and peripheral canalicular neuropathies specifically represented by the tarsal tunnel syndrome. Another complication of this pathology is represented by "Calciphylaxis," characterized by calcifications of the middle tunica of arteries and small arteries, by ulcerations and tissue necrosis at the foot level.

Chronic Kidney Disease-Mineral and Bone Disorder↗
PubMed1995

A longitudinal study of the effect of spinal degenerative disease on bone density in the elderly.

OBJECTIVE: To describe the relationship between spinal degenerative disease and bone density in the elderly both cross sectionally and longitudinally. METHODS: Random population based sample of 113 men and 187 women over 60 yrs of age participating in the Dubbo Osteoporosis Epidemiology Study (a longitudinal population based study of fracture risk factors) who had bone density measured on 2 occasions (average interval 2.5 yrs) and spinal radiographs on one occasion (performed according to a standardized approach). RESULTS: Spinal degenerative disease, of varying severity, was common in this population (osteophytes 69%, disc narrowing 67%, posterior element disease 99%). Scores for osteophytosis, disc narrowing, and posterior element disease (together with age and body mass index) independently explained 43% of the variation in spinal bone density in men (p < 0.00001) and 26% in women (p < 0.00001). The rate of change at the spine increased with increasing severity of osteophytosis in both men (p = 0.03) and women (p = 0.05), but not the other measures, and the total amount of variation explained by these measures was modest. In comparison, severity of spinal degenerative disease had only a modest but significant relationship with femoral neck bone density in both sexes, but not its rate of change. Subjects with any degree of osteophytosis had higher bone density compared to those without osteophytes at both the lumbar spine (men 21% higher, 95% CI 12-31; women 16% higher, 95% CI 9-23) and, to a lesser extent, femoral neck (men 12% higher, 95% CI 4-20; women 6% higher, 95% CI 1-13). Vascular calcification had no relationship with bone density at either spine or hip. CONCLUSION: Spinal bone density measurement and its sequential followup may be erroneous in the elderly due to concomitant degenerative disease. Bone density at the femoral neck was much less affected by spinal degenerative disease, which suggests that this site may be more efficacious for both monitoring response to treatment and determining fracture risk in the elderly.

Absorptiometry, Photon↗
PubMed1995

[Calcified intertrigo, a rare cause of cutaneous calcinosis].

INTRODUCTION: Calcinosis cutis is classically described in patients presenting chronic renal failure with secondary hyperparathyroidism. There are three clinical types described in the literature: cutaneous necrosis (secondary to vascular calcification), panniculitis with calcification of the adipose tissue and necrosis of the skin and dermo-hypodermic calcinosis without necrosis usually called metastatic calcinosis. The latter can affect all tissues but skin involvement is rare. CASE REPORT: A case of calcinosis cutis is presented in a 50 years old woman with moderate secondary hyperparathyroidism and chronic renal failure caused by renal amyloidosis. She was referred by the renal unit to our service for erythematous, woody-hard, infiltrated plaques with petechial purpura satellite lesions, involving the flexural areas, that appeared within a few weeks. DISCUSSION: This observation is original by the topography of the cutaneous lesions the involvement of the fexural areas is unusual and by the histologic aspect of pseudoxanthome elastic-like. We must notice that the hyperparathyroidism had always been very moderate (normal parathormonemia) compared to the rapid development of an important dermic calcinosis.

Aged↗
PubMed1996

Peripheral microcirculatory blood flow in haemodialysis patients treated with erythropoietin.

BACKGROUND: Haemodialysis patients have abnormal blood vessels, and increased morbidity from vascular causes, effects which may potentially be enhanced by erythropoietin (EPO) therapy. METHODS: Microcirculatory blood flow was assessed using a laser-Doppler flowmeter in a group of 19 haemodialysis patients before and during treatment with recombinant human (EPO). RESULTS: Haemodialysis patients had significantly impaired microcirculatory blood flow under both basal (25 degrees C) and hyperaemic (44 degrees C) conditions by comparison with 19 normal controls (baseline flow, median and range: patients 1.54 (0.28-2.54) volts, controls 3.39 (0.94-5.23) volts, p < 0.001 Mann Whitney U Test; hyperaemic flow, patients 2.69 (1.08-3.82) volts, controls 3.81 (1.32-8.00) volts, p < 0.001). There was no significant influence on microcirculatory blood flow of patient age, duration of haemodialysis, short-term EPO therapy (subcutaneous or intravenous), therapy with a calcium-channel blocker/vasodilator (nifedipine), or radiological evidence of vascular calcification. CONCLUSIONS: Haemodialysis patients have an abnormal peripheral microvasculature, which may be relevant to their increased risk of ischaemic tissue damage and poor wound healing.

Anemia↗
PubMed1996

[Peusoxanthoma elasticum with multiple calcinosis and hyperphosphoremia].

INTRODUCTION: Subcutaneous and vascular calcifications are classical manifestations of pseudoxanthoma elasticum. Visceral calcifications sometimes associated with unbalanced phosphocalcium leels are uncommon. CASE REPORT: We observed pseudoxanthoma elasticum in a French Caribbean patient who had extensive acneiform skin lesions with transepidermal elimination. Multivisceral calcifications were associated hyperphosphoremia alone. DISCUSSION: The pathogenic sequence of phosphocalcium disorders in this disease are discussed on the basis of calcifications and hyperphosphoremia observed in this case and from data in the literature.

Adult↗
PubMed1998

[Werner's syndrome].

BACKGROUND: Werner's syndrome associates early aging in young adults, small height, cataract, glucose intolerance, hypogonadism, skin ulcers, vascular calcifications and osteoporosis. CASE REPORT: We report a new case of Werner's syndrome in a 34-year-old man with suggestive alterations of the skin and endocrine anomalies in addition to hypospadias, urethral stenosis, bilateral mega-ureter and chronic renal failure. DISCUSSION: The diagnosis of Werner's syndrome in our patient was unquestionable because of the clinical presentation and the familial context. However, the urology anomalies have not been reported in this syndrome. A simple coincidence cannot be excluded.

Adult↗
PubMed2004

[Statins, and the vascular and valvular calcification].

Statins are currently approved for reducing the risk of cardiovascular diseases, clinically. These evidences were thought to be due to the lipid-lowering effects of the statins. But recently, the growing evidences showed the various effects of statins, such as inhibition of vascular and valvular calcification. How statins affects the bone forming proteins and genes are still not known.

Blood Vessels↗
PubMed2006

Calcification of human vascular smooth muscle cells: associations with osteoprotegerin expression and acceleration by high-dose insulin.

Arterial medial calcifications occur often in diabetic individuals as part of the diabetic macroangiopathy. The pathogenesis is unknown, but the presence of calcifications predicts risk of cardiovascular events. We examined the effects of insulin on calcifying smooth muscle cells in vitro and measured the expression of the bone-related molecule osteoprotegerin (OPG). Human vascular smooth muscle cells (VSMCs) were grown from aorta from kidney donors. Induction of calcification was performed with beta-glycerophosphate. The influence of insulin (200 microU/ml or 1,000 microU/ml) on calcification was judged by measuring calcium content in the cell layer and by von Kossa staining. OPG was measured in the medium by ELISA. Histochemistry was used for determination of alkaline phosphatase (ALP). Bone sialoprotein (BSP) and OPG mRNA expressions were done by RT-PCR. beta-Glycerophosphate was able to induce calcification in human smooth muscle cells from a series of donors after variable time in culture. Decreased OPG amounts were observed from the cells during the accelerated calcification phase. High dose of insulin (1,000 microU/ml) accelerated the calcification, whereas lower concentrations (200 microU/ml) did not. Calcified cells expressed ALP and BSP activity in high levels. In conclusion, high concentration of insulin enhances in vitro-induced calcification in VSMCs. Altered OPG levels during the calcification raise the possibility that OPG may have a potent function in regulating the calcification process or it may represent a consequence of mineralization. Effects of insulin and modulations by OPG on the calcification process in arterial cells may play a role in the development of calcifications as part of the diabetic macroangiopathy.

Alkaline Phosphatase↗
PubMed1991

Architecture of implanted bone matrix gelatin influences heterotopic calcification and new bone formation.

Heterotopic bone formation in skeletal muscle induced by compacted demineralized bone matrix gelatin (BMG) was studied histologically and biochemically. BMG was obtained by dehydrating diaphyseal shafts of femora and tibiae of 4-week-old male Sprague-Dawley rats, cutting the bone into chips, and demineralizing and extracting the chips with various solutions. The BMG was treated with 4 M guanidine-HCl, and compacted BMG was prepared by centrifugation. The compacted BMG was implanted into the rectus abdominis muscle of 5-week-old male Sprague-Dawley rats. The resulting specimens were examined histologically, and their alkaline phosphatase activity and the calcium content of the tissues were measured 3, 5, 7, 10, and 15 days after implantation. The BMG (separated BMG) with 75- to 500-microns particle sizes were implanted into control rats. The results showed that calcification, alkaline phosphatase activity, and bone formation were suppressed by implantation of the compacted BMG and that scarcely any vascularization occurred. Calcification, vascularization, and alkaline phosphatase activity were related and were indispensable for bone formation. In the control group, bone formation was observed at sites of high activity of alkaline phosphatase and well-developed vascularization. These results suggested that compacting of BMG suppressed vascularization, decreased calcification, and consequently reduced the induction of bone formation.

Alkaline Phosphatase↗
PubMed1992

Calcification of implanted vascular tissues associated with elastin in an experimental animal model.

We have previously studied the process of calcification in bioprosthetic porcine heart valves crosslinked with glutaraldehyde. Observations using light microscopy had indicated that calcification of elastic fibers occurs in implanted heart valves, in addition to calcification associated with collagen fibers. To determine the contribution of elastin to the process of calcification, small pieces of rabbit aorta were cross-linked with 0.2% glutaraldehyde, rinsed in buffer, and implanted subcutaneously in young adult male rats. Cross-linked jugular vein implants were included as controls. After an implantation period of 1 month or longer, we observed many areas of calcification in the aortic media associated with elastin and fewer such areas associated with collagen. The elastin-rich aortic tissues accumulated more calcium than venous tissues. Calcium deposits appeared similar in both allogenic and xenogeneic implants. Calcified areas viewed under the electron microscope included intercellular nonfibrous material. Calcified areas involved predominantly the outer layers of elastic fibers. Calcific deposits included needle-like crystals of hydroxyapatite but often consisted of an amorphous flocculant material surrounded by crystals. The close spatial relationship of hydroxyapatite crystals and elastic membranes seen in this study may be relevant to the initiation of dystrophic calcification in glutaraldehyde cross-linked aortic grafts.

Animals↗
PubMed2005

Cardiovascular calcification in end stage renal disease.

Extensive atherosclerosis and heavy vascular and valvular calcifications are common complications of end stage chronic kidney disease (CKD-V) and are related to a high incidence of cardiovascular events. In CKD-V vascular calcifications occur both in the subintimal space and in the runica media. Intimal calcification is associated with atherosclerosis and is therefore a universal finding. On the contrary, medial calcification is characteristically associated with advanced CKD and diabetes mellitus. Numerous metabolic and endocrine abnormalities, primarily involving calcium and phosphorus metabolism, are found in CKD. Furthermore, CKD-V is believed to be a state of heightened inflammation and oxidative stress. All of these dysfunctions occur early in the course of the renal failure and likely contribute to the development and progression of vascular calcification and atherosclerosis. This review is centred on the pathobiology of vascular calcification in CKD-V, its detection with modern imaging modalities and the therapeutic approaches currently available to slow its progression.

Calcinosis↗
PubMed2000

Phosphorylation of osteopontin is required for inhibition of vascular smooth muscle cell calcification.

Osteopontin (OPN) is a non-collagenous, glycosylated phosphoprotein associated with biomineralization in osseous tissues, as well as ectopic calcification. We previously reported that osteopontin was co-localized with calcified deposits in atherosclerotic lesions, and that osteopontin potently inhibits calcium deposition in a human smooth muscle cell (HSMC) culture model of vascular calcification. In this report, the role of phosphorylation in osteopontin's mineralization inhibitory function was examined. The ability of OPN to inhibit calcification completely depended on post-translational modifications, since bacteria-derived recombinant OPN did not inhibit HSMC mineralization. Following casein kinase II treatment, phosphorylated OPN (P-OPN) dose-dependently inhibited calcification of HSMC cultured in vitro about as effectively as native OPN. The inhibitory effect of osteopontin depended on the extent of phosphorylation. To determine the specific structural domains of OPN important for inhibition of calcification, we compared OPN fragments (N-terminal, C-terminal, and full-length), and compared the inhibitory effect of both phosphorylated and non-phosphorylated fragments. While none of the non-phosphorylated OPN fragments effected calcification, P-OPN caused dose dependent inhibition of HSMC calcification. P-OPN was treated with alkaline phosphatase to create dephosphorylated OPN. Dephosphorylated OPN did not have an inhibitory effect on calcification. The expression of OPN mRNA and P-OPN secretion by HSMC were decreased in a time-dependent manner during culture calcification. These results indicate that phosphorylation is required for the inhibitory effect of OPN on HSMC calcification, and that regulation of OPN phosphorylation represents one way in which mineralization may be controlled by cells.

Alkaline Phosphatase↗