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PubMed2003

Cardiac valve calcification as an important predictor for all-cause mortality and cardiovascular mortality in long-term peritoneal dialysis patients: a prospective study.

Calcification complications are frequent among long-term dialysis patients. However, the prognostic implication of cardiac valve calcification in this population is not known. This study aimed to determine if cardiac valve calcification predicts mortality in long-term dialysis patients. Baseline echocardiography was performed in 192 patients (mean +/- SD age, 55 +/- 12 yr) on continuous ambulatory peritoneal dialysis (mean +/- SD duration of dialysis, 39 +/- 31 mo) to screen for calcification of the aortic valve, mitral valve, or both. Valvular calcification was present in 62 patients. During the mean follow-up of 17.9 mo (range, 0.6 to 33.9 mo), 46 deaths (50% of cardiovascular causes) were observed. Overall 1-yr survival was 70% and 93% for patients with and without valvular calcification (P < 0.0001, log-rank test). Cardiovascular mortality was 22% and 3% for patients with and without valvular calcification (P < 0.0001). Multivariable Cox regression analysis showed that cardiac valve calcification was predictive of an increased all-cause mortality (hazard ratio [HR], 2.50; 95% CI, 1.32 to 4.76; P = 0.005) and cardiovascular death (HR 5.39; 95% CI, 2.16 to 13.48; P = 0.0003) independent of age, male gender, dialysis duration, C-reactive protein, diabetes, and atherosclerotic vascular disease. Eighty-nine percent of patients with both valvular calcification and atherosclerotic vascular disease, 23% of patients with valvular calcification only, 21% of patients with atherosclerotic vascular disease only, and 13% of patients with neither complication died at 1-yr (P < 0.0005). The cardiovascular death rate was 85% for patients with both complications, 13% for patients with valvular calcification only, 14% for patients with atherosclerotic vascular disease only, and 5% for those with neither complication (P < 0.0005). The number of calcified valves was associated with all-cause mortality (P < 0.0005) and cardiovascular death (P < 0.0005). One-year all-cause mortality was 57% for patients with both aortic and mitral valves calcified, 40% for those with either valve calcified, and 15% for those with neither valve calcified. In conclusion, cardiac valve calcification is a powerful predictor for mortality and cardiovascular deaths in long-term dialysis patients. Valvular calcification by itself has similar prognostic importance as the presence of atherosclerotic vascular disease. Its coexistence with other atherosclerotic complications indicates more severe disease and has the worst outcome.

Aged↗
PubMed1980

Bilateral basal ganglia calcifications visualised on CT scan.

Thirty-eight cases of basal ganglia calcification imaged on computed axial tomography were reviewed. Most cases were felt to represent senescent calcification. The possibility of a vascular aetiology in this group is discussed. A less common group of patients was identified with calcification secondary to abnormalities in calcium metabolism or radiation therapy. Three cases of basal ganglia calcifications were detected in juvenile epileptic patients receiving chronic anticonvulsants. These cases may be related to abnormalities in calcium metabolism and alkaline phosphatase activity. Clinical evidence of basal ganglia abnormality was generally absent demonstrating the preservation of neuronal pathways in most cases.

Adolescent↗
PubMed1982

Joint problems in patients on maintenance hemodialysis.

A questionnaire about joint symptoms was sent to 130 maintenance hemodialysis patients. All patients had a skeletal survey to assess the degree of hyperparathyroidism. 40 patients had no joint symptoms, 31 had mild joint symptoms, and 59 had severe joint symptoms. A higher proportion of these patients had radiological evidence of hyperparathyroidism, vascular or soft tissue calcification. Several different patterns of joint symptoms evolved including calcification problems, carpal tunnel syndrome, avascular necrosis, ruptured tendon and infection. We also describe a new syndrome of recurrent hemarthroses progressing to chronic capsulitis occurring in patients who have been on dialysis for more than 10 years.

Adult↗
PubMed1988

[Cell kinetics of oligodendroglioma and oligo-astrocytoma--Ki-67 PaP study].

In order to determine the principal histologic features in distinguishing the "anaplastic" from the "well differentiated" oligodendroglioma and mixed glioma (oligo-astrocytoma), correlations between the growth fraction, and histologic grade and 6 histologic variables (vascular proliferation, cytologic pleomorphism, calcification, necrosis, cellularity, mitotic index) were studied in 24 patients. The growth fraction was calculated as the percentage of Ki-67-immunostained nuclei in frozen sections using Ki-67 monoclonal antibody. 6 histologic variables were checked with HE stain of paraffin-embedded tissue sections. The growth fraction was in general agreement with the histologic grade, in order of decreasing mean percentage, ranging from 11.1% (anaplastic mixed glioma) to 5.3% (anaplastic oligodendroglioma), 2.8% (isomorphic oligo.) and 1.9% (mixed, grade II). There was a significant association between the growth fraction and 3 histologic variables (vascular proliferation, cytologic pleomorphism, mitotic index) out of 6. Thus, even though there exist some gaps between these parameters in paraffin-embedded tissues and those in frozen sections, the percentage of Ki-67-immunostained nuclei is likely to be very valuable as a supplement information of histological grading and a prognostic indicator.

Adult↗
PubMed1994

Fetal myocardial calcification associated with maternal cocaine use.

Two cases of fetal myocardial calcification confirmed postnatally are reported. In contrast to other reports, both infants survived with resolution of calcification by 6 and 12 months. Diagnostic investigations failed to confirm the presence of congenital infection. Both pregnancies were complicated by early cocaine use leading to the speculation that myocardial necrosis with subsequent calcification related to the toxic and/or vascular effects of cocaine was responsible. The finding of fetal myocardial calcification on prenatal ultrasound should prompt a search for causes, which may include cocaine exposure.

Adult↗
PubMed2005

Effects of adipocyte-derived cytokines on endothelial functions: implication of vascular disease.

Adipose tissue has recently emerged as an active endocrine organ that secretes a variety of metabolically important substances, collectively called adipocytokines or adipokines. In this review we summarize the effects of the adipokines leptin, adiponectin, and resistin on the vasculature and their potential role for pathogenesis of vascular disease. Leptin is associated with arterial wall thickness, decreased vessel distensibility, and elevated C reactive protein (CRP) levels. Leptin possesses procoagulant and antifibrinolytic properties, and it promotes thrombus and atheroma formation, probably through the leptin receptors by promoting vascular inflammation, proliferation, and calcification, and by increasing oxidative stress. Research for development of pharmacologic antagonism for the leptin receptor is currently under way. Adiponectin inhibits the expression of the adhesion molecules ICAM-1, VCAM-1, and P selectin. Therefore, it interferes with monocyte adherence to endothelial cells and their subsequent migration to the subendothelial space, one of the initial events in the development of atherosclerosis. Adiponectin also inhibits the transformation of macrophages to foam cells in vitro and decreases their phagocytic activity. Resistin, discovered in 2001, represents the newest of the adipokines and was named for its ability to promote insulin resistance. Resistin increases the expression of the adhesion molecules VCAM-1 and ICAM-1, up-regulates the monocyte chemoattractant chemokine-1, and promotes endothelial cell activation via ET-1 release. Although many aspects of its function need further clarification, it appears that resistin will add significantly to our knowledge of the pathophysiology of vascular disease and the metabolic syndrome.

Adiponectin↗
PubMed1992

Widespread cutaneous and systemic calcification (calciphylaxis) in patients with the acquired immunodeficiency syndrome and renal disease.

BACKGROUND: Calciphylaxis is a form of widespread calcification that may occur in patients with renal disease and hyperparathyroidism. The skin is often affected secondary to vascular compromise and ischemia. Patients infected with the human immunodeficiency virus (HIV) are predisposed to renal failure and thus may develop this serious complication. OBJECTIVE: The purpose of this article is to describe two cases of fatal calciphylaxis in patients with the acquired immunodeficiency syndrome and renal disease. METHODS: Two patients were examined clinically and through the performance of serologic studies and skin biopsies. RESULTS: Both patients had a widespread livedo reticularis-like eruption, which rapidly progressed to cutaneous gangrene. Patient 1 had elevated serum calcium and phosphorus levels whereas patient 2 had normal values but had markedly elevated serum parathyroid hormone levels. Biopsy specimens in both cases showed vascular thrombosis and soft tissue calcification. CONCLUSION: Widespread calcification may develop in patients with HIV infection and renal failure and, in some cases, calcium and phosphorus levels may be normal.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Diffusely calcified renal cell carcinoma: CT features.

Calcifications of renal masses are common. They are usually dense, partial, small, punctate, and linear opacities. Diffuse calcification is an extremely rare feature of renal masses. Generally, calcified renal cell carcinomas are hypovascular, with calcifications in the interstitium, and they also contain fibrotic capsules, necrotic areas, or hyalinization. We recently observed a renal neoplasm with diffuse calcification on CT and intermediate vascularity on angiography, which was diagnosed histologically as renal cell carcinoma, clear cell type. Interestingly, there were numerous calcific deposits within the tumor cells.

Adult↗
PubMed1990

Raised vascular calcium in an animal model: effects on aortic function.

STUDY OBJECTIVE - The aim of the study was to develop an animal model to study the relationships between raised tissue calcium and vascular function. DESIGN - Ectopic calcification was developed in the animal model using chronic vitamin D2 intoxication, after which functional studies were performed in isolated superfused aortic rings. Results were compared with control preparations. EXPERIMENTAL ANIMALS - 160 female Sprague-Dawley rats weighing 200-225 g were randomly divided into experimental (vitamin D2 1 mg.d-1) and control (vehicle only) groups. MEASUREMENTS and RESULTS - Aortas from vitamin D treated animals had a higher calcium content than control aortas, without concomitant increases in cardiac calcium. Aortas with high calcium content were found to develop greater tension than control aortas when exposed to noradrenaline in the absence of extracellular calcium, but the tension maxima achieved in response to noradrenaline in calcium containing media or to high potassium depolarising solution were the same. The rate of development of contraction in response to noradrenaline was greater in aortas from the vitamin D treated animals than in controls. Isoprenaline and sodium nitroprusside produced less relaxation in the animal model aortas than in the controls. CONCLUSIONS - The results suggest that increased aortic calcium affects the response of the tissue to vasoactive agents. It appears that the additional vascular calcium may be stored in an agonist releasable pool, probably within the sarcoplasmic reticulum. The enlarged or newly developed pools appear to be refillable from the extracellular medium but not by intracellular reuptake of calcium, suggesting a bicompartmental model of intracellular calcium release and reuptake.

Animals↗
PubMed2003

Angiogenesis in the distal femoral chondroepiphysis of the rabbit during development of the secondary centre of ossification.

In the developing chondroepiphyses of long bones, the avascular cartilaginous anlage is invaded by numerous blood vessels, through the process of angiogenesis. The objective of this study was to investigate the chronology of this vascular invasion with the spontaneous calcification of the cartilaginous epiphysis during development of the secondary ossification centre in the rabbit distal femur. The time-course of chondroepiphyseal vascular invasion was determined histologically and standardized for eight gestational and four postnatal intervals by plotting kit body mass against crown-rump length. Similarly, microcomputed tomography (micro-CT) helped to visualize calcification at those same gestational and postnatal intervals. To confirm the angiogenic nature of the avascular chondroepiphysis, such samples were assayed on the chick chorio-allantoic membrane (CAM). Neovascular outgrowths from the CAM were apparent 48 h following introduction of an 18-day (gestational) chondroepiphyseal sample. Chondroepiphyseal samples were assayed for the potent developmental angiogenic factors bFGF and VEGF, with the mRNA expression for both these mediators being confirmed using RT-PCR. As angiogenesis and calcification during chondroepiphyseal development occur in a defined tissue environment initially devoid of blood vessels and mineral, those processes provided a unique opportunity to study their progression without complication of injury-related inflammation or extant vasculature and mineral. Furthermore, the discovery of angiogenic, angiostatic or mineral-regulating mediators specific to developing connective tissue may prove useful for analysing the regulation of vascular and mineral pathogenesis in articular tissues.

Actins↗
PubMed2006

[Ultrasound diagnostics of upper urinary tract calculi].

The review is dedicated to ultrasonography of the upper urinary tract in patients with nephrolithiasis. Ultrasonographic semiotics of urolithiasis, the ability of unlrasonography to detect nephrolithiasis, and methods of the optimization of these diagnostic techniques in patients with upper urinary tract calculi are covered. The author discusses difficulties that may be faced while differentiating between nephrolithiasis and such conditions as spongious kidney, nephrocalcinosis, calcification of renal papillae, cysts, tumors, and vascular walls, as well as other kinds of renal calcification, associated with ultrasonographic acoustic path phenomenon. The advantages and disadvantages of ultrasonography in cases of X-ray urolithiasis are evaluated in the paper. The article describes hardships in ultrasound visualization of ureteral calculi causing acute upper urinary tract obstruction, and the ways of getting over them.

Diagnosis, Differential↗
PubMed2005

Heart valve calcification in young patients with systemic lupus erythematosus: a window to premature atherosclerotic vascular morbidity and a risk factor for all-cause mortality.

The objective of the study was to evaluate the association between heart valve calcification and atherosclerosis and outcome in systemic lupus erythematosus (SLE). One-hundred and seven patients with SLE (mean age 45.9 +/- 14.7 years) were studied by 2D transthoracic echocardiography. Mitral annulus calcification (MAC) was detected in 24 patients (22.6%) and aortic valve calcification (AVC) in 22 (20.1%). Both MAC and AVC were associated with older age (r = 0.2, p = 0.02; r = 0.40, p <or= 0.001, respectively), high SLE damage index (r = 0.3, p = 0.005; r = 0.40, p = 0.001, respectively), diabetes mellitus (r = 0.2, p = 0.05; r = 0.3, p = 0.003, respectively), hyperlipidemia (r = 0.03, p = 0.01; r = 0.03, p = 0.001, respectively), hypertension (r = 0.20, p = 0.07; r = 0.20, p = 0.08, respectively), serum IgA isotype of anticardiolipin antibody (r = 0.03, p = 0.03; r = 0.04, p = 0.02, respectively), increased serum creatinine (r = 0.03, p = 0.0005; r = 0.12, p = 0.02, respectively), and stroke (r = 0.3, p = 0.0008; r = 0.35, p = 0.0002, respectively). In addition, MAC was associated with coronary artery disease (r = 0.2, p = 0.05). Both MAC and AVC were significantly associated with death during the follow-up period (n = 9, 8.6%) (r = 0.20, p = 0.05; r = 0.20, p = 0.03, respectively). On stepwise logistic regression analysis, MAC and AVC are independently associated with hyperlipidemia and antiphospholipid antibodies. In conclusion, MAC and AVC are prevalent among young SLE patients, positively correlate with premature diffuse atherosclerosis, and are a risk factor for subsequent all-cause mortality.

Aortic Valve↗
PubMed1993

Cortical vascular abnormalities in the syndrome of celiac disease, epilepsy, bilateral occipital calcifications, and folate deficiency.

The pathological changes in the syndrome of celiac disease, folate deficiency, bilateral occipital calcifications, and intractable epilepsy have not been previously described. A child with this disorder had a field defect correlating with active lateralized epileptic discharges and asymmetrical lesions. After resection of the right occipital lobe she was seizure free for 4 years. A cortical vascular abnormality with patchy pial angiomatosis, fibrosed veins, and large jagged microcalcifications was found. These pathological abnormalities were similar though not identical to those found in the Sturge-Weber syndrome.

Calcinosis↗
PubMed2004

Renal osteodystrophy.

Patients with chronic renal failure suffer from four different kinds of typical bone lesions which are summarized as renal osteodystrophy (ROD). These changes can occur early during renal disease and are dependent on several factors, such as the calcium-phosphorus homeostasis, the type of renal disease or the frequency and dose of potentially harmful drugs administered. ROD usually gets worse as renal failure progresses, and during hemodialysis, and culminates, in the case of kidney transplantation, in the early post-transplant phase. Although the decrease of parathyroid hormone (PTH) and the dose of immunosuppression administered subsequently permit a certain restitution of bone stability, ROD persists lifelong in the majority of cases and is associated with a high rate of bone fractures. However, the abnormalities of mineral metabolism that lead to ROD are not only confined to bone morphology but also predispose to vascular or soft tissue calcification. This might lead to severe tissue or coronary artery calcification. It is therefore not surprising that life expectancy on hemodialysis is correlated to the expression and form of ROD. The awareness and early diagnosis of renal osteodystrophy are therefore of great importance, in particular since a number of new treatment options have recently evolved. Previously-used phosphate binders, which contain either aluminium or calcium, might be replaced by non-absorbable drugs which bind phosphate through ion exchange. In addition, PTH production can be reduced efficiently by administration of recently developed calcimimetic agents that increase the sensitivity of calcium-sensing receptors in the parathyroid gland. In patients with high-turnover bone disease or after transplantation, bisphosphonates might prevent or restore bone loss.

Biopsy↗
PubMed2000

Morphology of vascular, renal, and heart lesions in the antiphospholipid syndrome: relationship to pathogenesis.

A growing body of evidence suggests that aPL are not only serological markers of the antiphospholipid syndrome (APS), but may also directly contribute to the development of thrombosis and other manifestations, including the APS vasculopathy. The latter has been documented in leptmeninges, lung, skin, myocardium, peripheral arteries, and kidney. Renal lesions, a common feature of primary antiphospholipid syndrome (PAPS), include occlusion of principal renal arteries or their main branches, TMA, cortical ischemia, and renal vein thrombosis. Within the cardiac manifestations associated with aPL, valvular involvement is the most common. Histologic findings in valve specimens are consistent with a noninflammatory lesion characterized by intravalvular capillary thrombosis, laminar or verrucous superficial thrombosis, vascular proliferation, fibrosis, and calcification. Even though there is general consensus that endothelial damage triggers the chain of events that results in valve thickening, fusion, rigidity, and ultimately functional abnormalities, we believe that more experimental work remains to be done on the initial valve insult in APS.

Antibodies, Antiphospholipid↗
PubMed1990

Skin necrosis associated with acquired protein C deficiency in patients with renal failure and calciphylaxis.

PURPOSE: To determine if the natural anticoagulant protein C plays a role in the pathogenesis of systemic calciphylaxis, a syndrome characterized by extensive vascular and soft tissue calcification and skin necrosis, which is similar to that seen in warfarin-induced skin necrosis. PATIENTS AND METHODS: The study population included five patients with end-stage renal disease and systemic calciphylaxis undergoing hemodialysis, 12 patients without evidence of calciphylaxis undergoing dialysis, eight patients with nephrotic syndrome, and eight normal healthy volunteers. Protein C antigen levels were measured by rocket immunoelectrophoresis, and functional activity was quantitated by a chromogenic assay and an anticoagulant assay utilizing the venom of Agkistrodon contortrix. RESULTS: Skin biopsy specimens of involved areas in three patients showed thrombotic occlusion of venules identical to that seen in warfarin-induced skin necrosis. Protein C antigen levels were normal in all groups. However, protein C activity was significantly reduced as measured by chromogenic (p less than 0.01) or anticoagulant assays (p less than 0.01) in patients with calciphylaxis compared with the other three groups. CONCLUSION: These findings suggest that hypercoagulability due to functional protein C deficiency may contribute to thrombosis, resulting in skin necrosis and digital gangrene in systemic calciphylaxis.

Adult↗
PubMed1986

Atherosclerotic involvement of coronary branch vessels.

The atherosclerotic involvement of coronary branch vessels (first diagonal, first septal, posterior descending, left and right marginals, conus and the vessels supplying the conduction system) was investigated in 450 apparently healthy subjects aged 11-55 years who died of accidental causes. In subjects 35-55 years old, 1 out of every 3 persons with atherosclerotic plaques in the major coronary arteries also had atherosclerotic plaques in coronary branch vessels; the respective relation for fatty streaks was 1 out of every 12 subjects, for intimal necrotic areas 1 out of every 7 subjects and for incorporated microthrombi 1 out of every 9 subjects. One out of every 3 subjects 51-55 years old had more than 50% lumen reduction in the undistended major coronary arteries, compared to 1 out of every 6 subjects in undistended coronary branch vessels. A small subgroup (8.2%) showed more severe stenotic lesions in coronary branch vessels than in coronary major arteries. The atherosclerotic plaques of coronary branch vessels appeared as 'underdeveloped', lacking a thick fibrohyaline cap, a large detritus cavity, abundant lipid deposition, cholesterol crystals, basal vascularization, intraplaque hemorrhage, ulceration, calcification, occlusive thrombosis. On the other hand the stenotic character of these plaques was often severe (more than 75% lumen reduction). The questionable value of the estimation of the ischemic significance of a coronary stenosis in the absence of available data on the development of a compensatory collateral circulation is discussed.

Adolescent↗