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PubMed1982

[Extraskeletal calcification in chronic renal failure during hemodialysis and after renal transplantation (author's transl)].

The frequency of calcifications in vessels and soft tissue was 39% in 184 patients with chronic renal failure. Non-dialyzed patients and dialyzed patients at the start of dialysis treatment had most frequently calcifications of the aorta and larger vessels. Renal transplant recipients, who developed osteonecrosis or spontaneous fractures after transplantation, showed at the time of transplantation a higher frequency of calcifications compared to renal transplant recipients, who did not develop these complications. The frequency of calcifications increased with increasing age not only in the aorta, but also in the other vessels. In nondialyzed patients and in dialyzed patients at the start of dialysis treatment the calcifications were more commonly found in women and in renal transplant recipients in men. In all groups of patients a significant, higher frequency of calcifications was found in patients with radiologic evidence of bone resorption compared to patients without resorptive bone changes. Before and during chronic hemodialysis and following renal transplantation the frequency of calcifications increased. Calcification was most pronounced in the larger vessels in nondialyzed and dialyzed patients and in small vessels in renal transplant recipients. Increase in frequency of calcifications occurred slowly in nondialyzed patients and in renal transplant recipients, whereas an accelerated increase occurred in the first 15 months of the dialysis period in hemodialyzed patients.

Adult↗
PubMedDate not supplied

Medial arterial calcification and diabetic neuropathy.

The aim of this study was to detect linear arterial calcification (Mönckeberg's sclerosis) localized in feet, ankles, legs, knees and hands in an attempt to correlate the extent of calcification with the presence and severity of autonomic neuropathy as well as with microangiopathy (proliferative retinopathy, proteinuria greater than 200 mg/die) and peripheral neuropathy. Typical linear calcification were observed in 37 out of 41 (90.2%) patients with autonomic neuropathy and in none of those without autonomic neuropathy (p less than 0.001). These 37 patients were divided into two subgroups by cluster analysis: Subgroup A, including 18 subjects with calcification length ranging from 8 to 26 cm and moderate autonomic neuropathy, and Subgroup B, including 19 subjects with calcification length between 58 and 126 cm and severe autonomic neuropathy (p less than 0.0001 by Spearman's test). No difference in the length of arterial calcification was detected between patients with proteinuria greater than 200 mg/24h and/or proliferative retinopathy and patients without these complications. A possible relationship between arterial calcification and peripheral neuropathy is difficult to evaluate; in fact, the majority of subjects having autonomic neuropathy had peripheral neuropathy, too. Vice versa, around 10% of patients without peripheral neuropathy but with autonomic neuropathy did not have Mönckeberg's sclerosis. Autonomic neuropathy is the principal factor responsible for calcification of the arterial media, and in addition the severity of the neuropathy, rather than the patient's age or the known disease duration seems to determine the extent of calcification.

Adult↗
PubMed1999

[Intrahepatic calcification--a differential diagnostic problem].

HISTORY AND CLINICAL FINDINGS: A 57-year-old woman was admitted for investigation of intrahepatic calcifications. Intrahepatic cholangiolithiasis was suspected. In 1993 she underwent cholecystectomy because of lithiasis. The examination with endoscopic retrograde cholangiography (ERC) was planned. INVESTIGATIONS: The laboratory findings were normal except for a mild elevation of alkaline phosphatase and gammaglutamyl transpeptidase. The sonographic examination of the abdomen showed multiple hyperechoic calcifications along non-dilated bile ducts. In the spleen of normal size there were found a lot of intraparenchymatous calcifications. The abdominal roentgenography revealed calcifications also in the pancreas. In ERC, the intra- and extrahepatic bile ducts were normal with simultaneous proof of parenchymatous calcifications. TREATMENT AND COURSE: Because of the medical history of the patient and the radiologic findings the multiple parenchymatous calcifications could be referred to a miliary tuberculosis during childhood. In miliary tuberculosis, the liver almost always is involved by acute granulomatous inflammation. The therapy of hepatic tuberculosis follows the guidelines of systemic tuberculostatic therapy according to other presentations of this disease. Under sufficient therapy, tuberculotic granulomas normally heal without cicatrization. Sometimes tissue reactions in form of local fibrosis and calcification lead to a mild reduction in hepatic function as seen in this case. CONCLUSION: In the European population, intrahepatic cholangiolithiasis is a rare cause of focal hyperechoic liver lesions. In differential diagnosis, numerous diseases of possible systemic course have to be considered, which may induce calcifications of the liver or other organs. Among systemic diseases characterized by granulomatous inflammation and possible calcification tuberculosis and sarcoidosis have to be mentioned first.

Calcinosis↗
PubMed2002

Different risk factors for peripheral vascular calcification between diabetic and non-diabetic haemodialysis patients--importance of glycaemic control.

AIM/HYPOTHESIS: Although derangements of calcium and phosphate control have been emphasized as important risk factors for vascular calcification in non-diabetic haemodialysis patients, similar risk factors for diabetic haemodialysis patients are not known. We compared factors affecting peripheral vascular calcification between haemodialysis patients with and without diabetes. METHODS: We examined 421 patients on maintenance haemodialysis. There were 89 patients with Type II (non-insulin-dependent) diabetes mellitus (53 men and 36 women, 62+/-10 years old) and 332 patients without diabetes (192 men and 140 women, 59+/-13 years old). Hand roentgenography was carried out, and visible vascular calcification of the hand arteries was evaluated. RESULTS: There were 42 diabetic patients and 45 non-diabetic patients with vascular calcification. The prevalence of vascular calcification in diabetic patients (47.1%) was higher than in non-diabetic patients (13.6%) ( p<0.001). In multivariate logistic regression, the main factors affecting vascular calcification in non-diabetic patients were advanced age, longer duration of haemodialysis, increased phosphate concentrations, male gender, and lower predialysis diastolic pressure. In diabetic patients, predictors for vascular calcification were higher values of HbA(1C) and longer duration of haemodialysis. In diabetic patients, a 1% increase in HbA(1C) increased the risk of calcification by 2.1-fold (95% CI 1.282-3.575, p=0.0029). CONCLUSION/INTERPRETATION: We have shown that poor glycaemic control, rather than calcium and phosphate concentrations, is a predictor of peripheral vascular calcification in diabetic patients on haemodialysis. This study emphasizes that glycaemic control remains critical even in diabetic patients with end-stage renal disease.

Blood Glucose↗
PubMed2005

Mitigation of ectopic calcification in osteopontin-deficient mice by exogenous osteopontin.

Ectopic calcification is a major cause of bioprosthetic heart valve failure. New therapeutic opportunities are offered by the growing understanding that ectopic calcification is an actively regulated process involving several key gene products. One of these products, osteopontin (OPN), is a glycosylated phosphoprotein previously shown to inhibit apatite crystal formation, induce carbonic anhydrase II, and promote mineral resorption. In this study, OPN-deficient mice (OPN-/-) were utilized as an in vivo model to stimulate the ectopic calcification of glutaraldehyde-fixed bovine pericardium (GFBP) tissue and to examine OPN delivery and structure-function relationships with respect to its anti-calcific activity. Significant calcification of GFBP tissue was obtained within 7 days of subcutaneous implantation in OPN-/- mice. Direct rescue of the calcification phenotype was achieved by the administration of exogenous recombinant rat, histidine-fused OPN (rat His-OPN) to the implant site via soluble injection (up to 72% mitigation achieved) or adsorption onto the implant materials (up to 91% mitigation achieved). Effects were specific, since neither fibronectin nor polyhistidine alone could mitigate calcification of GFBP. The maximum anti-calcific effect was achieved only when rat His-OPN was adequately phosphorylated and contained a functional arginine-glycine-aspartate (RGD) cell adhesive domain. Furthermore, CAII levels in host cells surrounding GFBP were greatest when phosphorylated, RGD-containing rat His-OPN was adsorbed. These data suggest that both physical inhibition, mediated by phosphorylation sites in OPN, as well as the induction of CAII and mineral regression, mediated by the RGD domain, contribute to the unique ability of OPN to mitigate ectopic calcification of bioprosthetic valve tissue.

Animals↗
PubMed1996

Rotator cuff calcifications: treatment with ultrasound-guided percutaneous needle aspiration and lavage.

OBJECTIVE: To analyze the results of ultrasound (US)-guided needle puncture, aspiration and lavage in the treatment of symptomatic calcific tendinitis of the rotator cuff. DESIGN AND PATIENTS: Atraumatic pain in 61 shoulders of 58 patients was resistant to conservative therapy. The average age of the treated patients was 42 years (range 26-49 years), follow-up was 12 months, and the mean diameter of the calcifications was 1.6 cm (range 1.1-2.9 cm). With US guidance and local anesthesia, two needles were placed within each calcification. The calcification was punctured 10-15 times and saline solution injected and aspirated using the needles until the aspirate was free of calcific particles. RESULTS AND CONCLUSIONS: Based on radiographs at 1 year follow-up. 74% (45 of 61) of the calcifications decreased, including 28% (17 of 61) which disappeared totally, and 26% (16 of 61) were unchanged. Calcifications with a faint or absent shadow on US proved to be nearly liquid (slurry calcification in 93% (14 of 15) of cases and could be aspirated. Clinical results were excellent in 74% (45 of 61), moderate in 16% (10 of 61) and poor in 10% (6 of 61) of cases. US offers technical advantages over fluoroscopy, and the typical US image of a slurry calcification helps to select the most suitable patients for aspiration treatment. The results are comparable with those using fluoroscopic guidance.

Adult↗
PubMed1996

Association of gastrocnemius tendon calcification with chondrocalcinosis of the knee.

OBJECTIVE: Chondrocalcinosis of the knee is a common radiological finding in the elderly. However, visualization of chondrocalcinosis may be difficult in patients with advanced cartilage loss. The purpose of this study was to determine sensitivity, specificity, and accuracy of gastrocnemius tendon calcification that might serve as a radiographic marker of chondrocalcinosis in patients with painful knees. DESIGN AND PATIENTS: We prospectively evaluated 37 knee radiographs in 30 consecutive patients (29 men, 8 women; mean age 67 years, age range 37-90 years) with painful knees who had radiographic evidence of chondrocalcinosis. The frequency of fibrocartilage, hyaline cartilage, and gastrocnemius tendon calcification was determined. For a control group, we evaluated knee radiographs in 65 consecutive patients with knee pain (54 men, 11 women; mean age 59 years, age range 40-93 years) who had no radiological signs of chondrocalcinosis. The frequency of gastrocnemius tendon calcification in the control group was determined. RESULTS: Gastrocnemius tendon calcification was 41% sensitive, 100% specific, and 78% accurate in predicting chondrocalcinosis. The gastrocnemius tendon was calcified on 15 of 37 (41%) radiographs in the experimental group and on 0 of 67 radiographs in the control group. In the chondrocalcinosis group, 23 (62%) had posterior hyaline cartilage calcification, 14 (38%) had anterior hyaline cartilage calcification, 31 (84%) had medial meniscus calcification, and 36 (97%) had lateral meniscus calcification. CONCLUSIONS: Our results show that gastrocnemius tendon calcification is an accurate radiographic marker of chondrocalcinosis in patients with knee pain.

Adult↗
PubMed2006

Testicular calcification and microlithiasis: association with primary intra-testicular malignancy in 3,477 patients.

The prevalence of all forms of scrotal and testicular calcification and their association with testicular tumour in a symptomatic paediatric and adult population was investigated. A retrospective study of all testicular ultrasound examinations performed at a single centre over a 5-year period was undertaken. All studies were performed by experienced operators, recorded in a standard method, using high-frequency linear array transducers (> or =10 MHz). All available images (95.2%) were reviewed by experienced operators, recording the location and type of scrotal and testicular calcification according to a pre-determined schedule. A total of 3,854 studies were reviewed on 3,477 patients (age range: 1 month to 91 years). In the adult group, 3,279 examinations were analysed. Prevalence of testicular microlithiasis (TM) was 2.0%, and the prevalence of other non-microlithiasis testicular calcification (non-TM calcification) was 1.7%. Testicular tumour was associated with TM (odds ratio 9.5, P<0.001) and non-TM calcification (odds ratio 11.4, P<0.001) but not with other types of scrotal calcification. A total of 198 paediatric examinations were analysed. Prevalence of TM was 2.0% and the prevalence of non-TM calcification was 0.5%. One tumour (lymphoma) was identified, with no associated calcification. This study confirms the reported association between TM and testicular tumour and finds a previously unreported association between non-TM calcification and testicular tumour.

Adolescent↗
PubMed2000

Atherosclerotic carotid arteries--calcification and radio-morphological findings.

OBJECTIVES: Are there any predictable factors influencing the process of calcification in carotid arteries? BACKGROUND: The carotid arteries and especially the carotid bifurcation are one of the predisposed regions of atherosclerotic disease. Whether topography of the carotid sinus, flow patterns or different patient characteristics (e.g., diabetes mellitus, age, sex) are a factor determining calcification of atherosclerotic lesions is still hardly understood. METHODS: Morphological and morphometrical analysis including radiographic classification of different degrees of calcification on postmortal carotid arteries (90 men and 19 women) and 306 surgical samples after intramural desobliterations of carotid arteries (202 patients with diabetes, 104 patients without diabetes). RESULTS: Most common localization of radiographically identified calcified deposits are the carotid bulb (76%) especially on the lateral wall opposite the flow divider and the internal carotid artery (55%) especially the proximal 1 cm section. No difference in degree of calcification was found when comparing patients with and without diabetes (intermediate calcification in 59% of patients with diabetes and 50% without diabetes). More female patients with diabetes show calcification when compared to the group of patients without diabetes. Females produce calcification in atherosclerotic carotid lesions at an older age compared to male patients. CONCLUSIONS: Calcification is a frequent finding in advanced atherosclerotic carotid lesions. There is no difference in regard to degree, pattern of calcification or age distribution when comparing patients with and without diabetes mellitus. Atherosclerotic lesions more frequently found in female patients with diabetes may be due to less vasoprotection by estrogens.

Adult↗
PubMed1993

Effects of metallic ions and diphosphonates on inhibition of pericardial bioprosthetic tissue calcification and associated alkaline phosphatase activity.

This study focused on the association of extrinsic alkaline phosphatase (AP) activity with both early and advanced calcification of glutaraldehyde-pretreated bovine pericardial bioprosthetic (GPBP) tissue, and the inhibition of both calcification and AP activity by pre-incubation in diphosphonates (sodium-ethanehydroxydiphosphonate [NaEHDP], aminopropanehydroxydiphosphonate [APD]) and metallic salts (FeCl3, Ga(NO3)3, AICI3). GPBP specimens were implanted subcutaneously in 3 wk old male rats after pre-incubation. Following explantation of the tissue at 72 h and 21 d, calcification was assessed morphologically by light microscopy and chemically by atomic adsorption spectroscopy for calcium content and by molybdate complexation for phosphorus. AP activity was characterized by enzymatic hydrolysis of paranitrophenyl phosphate and by histochemical studies. In both control and pretreated groups, AP levels were greater in 72 h explants than 21 d retrievals, which demonstrated extensive calcification in control explants. All pre-incubations that resulted in inhibition of calcification after 21 d, except for APD, were associated with 72 h AP content which was lower than control specimens. The typical time of initiation of calcification was 72 h, as determined by previous studies with this model system. Covalently bound APD inhibited calcification. Increased AP activity in the APD group may be due to the toxicity of this agent with resultant acute inflammation, or other incompletely understood effects of diphosphonates on calcification and AP. Furthermore, EHDP and Ga3+ incubations were also associated with decreased GPBP AP at 72 h compared to control, but were not effective for inhibiting calcification after 21 d. We concluded that inhibition of peak GPBP AP activity is not necessarily associated with the prevention of GPBP mineralization.

Alkaline Phosphatase↗
PubMedDate not supplied

Brain calcification in hypoxic-ischemic lesions: an autopsy review.

Calcification of ischemic lesions in a child's brain is well recognized by pathologists; however, clinicians and radiologists usually associate cerebral calcification with infections, particularly the TORCH organisms. We illustrate this phenomenon in a 5-month-old infant with extensive, calcified, multicystic encephalomalacia without evidence of a cerebral infection. In order to ascertain the incidence of cerebral calcification in pure hypoxic-ischemic lesions, we retrospectively analyzed 486 consecutive autopsies. Ninety-nine patients had histologic evidence of cerebral hypoxic-ischemic lesions and hypoxia or ischemia. Thirty-nine of these patients displayed microscopic calcification; 23 patients had slight, 12 had minor, and 4 had prominent calcifications. Prominent calcification lesions were large enough to be detected by routine radiologic methods. Correlations between degree of calcification and the underlying disease process and between the gestational age and the length of survival were not statistically significant. This study illustrates the very frequent occurrence of brain calcification in ischemic brain lesions in children. It is necessary to include this diagnosis in the differential diagnosis of cerebral calcification.

Adolescent↗
PubMed2006

Consensus review: A method of assessment of calcifications that appropriately undergo a six-month follow-up.

RATIONALE AND OBJECTIVES: Breast calcifications seen on mammography may be associated with benign conditions or malignancies. Accurate characterization of these calcifications is crucial to providing optimal care that may spare women unnecessary biopsies and appropriately allow interval mammography. The purpose of this study is to determine if consensus characterization of calcifications by two breast imaging experts using standardized criteria can establish that follow-up is a safe option. MATERIALS AND METHODS: For this retrospective study, our breast imaging database was reviewed and the cases imaged between the years 1999 and 2001 were used to identify patients with calcifications who were recommended for a six-month follow-up or biopsy. All cases had been prospectively assessed by at least two expert breast imagers using standardized features to assess the findings before a recommendation for follow-up or a biopsy was made. A retrospective chart review examining the radiology reports was done to determine the percentage of women from each of the two groups who developed malignancies. RESULTS: Of 744 patients who had mammographically identified clusters of calcifications, 490 clusters (409 single and 81 multiple) were diagnosed as probably-benign, and a short-interval 6-month follow-up was recommended. Of these calcifications followed for three years, only two (0.5%) of the single clusters proved to be malignant, and malignancy was diagnosed at the 12-month follow-up examination. In both cases, the women were diagnosed with ductal carcinoma in situ (DCIS). Of 254 clusters recommended for biopsy, 242 (215 single and 27 multiple) underwent biopsy. A total of 70 cancers were diagnosed: 54 (77.1%) were DCIS and 16 (22.9%) were primary invasive mammary carcinoma (10 cases of invasive ductal carcinoma, 3 cases of invasive lobular carcinoma, 2 cases of invasive ductal carcinoma with DCIS, and one case of invasive mucinous carcinoma with DCIS). Twenty-nine percent of women who had a biopsy performed had calcifications associated with malignancy. In contrast, in the women whose calcifications were followed by mammography, only 0.5% went on to develop malignancies. CONCLUSION: Consensus review of calcifications by two breast imagers using standardized criteria is a safe follow-up option.

Breast Diseases↗
PubMed2004

Localization of osteopontin at calcification sites of cholesteatoma: possible role as a regulator of deposition of calcium phosphate in the middle ear.

OBJECTIVE: Recently, we showed that osteopontin (OPN), a major acidic phosphorylated glycoprotein of bone, participates in the pathological calcification that occurs as a result of chronic otitis media. To investigate the possibility of OPN as a common regulator of the pathological calcification in the middle ear, we here examined whether or not OPN is localized at the calcification sites of cholesteatoma, which is clearly different from chronic otitis media in the pathogenesis. METHODS: Middle ear tissues including cholesteatoma were obtained from 32 cases who underwent tympanoplasty. The tissues of 29 cases were used for the immunohistochemistry of OPN and CD68, the marker of macrophages, and in situ hybridization of OPN mRNA. And those of the other three for reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: Middle ear tissues including cholesteatoma were histologically classified as to the degree of calcification. In hyalinized tissues with macroscopic calcification, OPN was immunohistochemically found at the calcification sites. In inflammatory tissues with microscopic calcification, OPN was also found in the calcifying foci, and many OPN mRNA-expressing cells, as determined by in situ hybridization, were located near the foci. Moreover, immunohistochemical double staining for OPN and CD68 showed that the OPN-expressing cells were CD68-positive, indicating the cells were macrophages. In inflammatory tissues without calcification, immunohistochemistry of CD68 and in situ hybridization of OPN mRNA revealed that most OPN mRNA-expressing cells were CD68-positive. The expression of OPN mRNA in cholesteatoma tissues was also demonstrated by means of RT-PCR. CONCLUSION: OPN secreted by exudate macrophages was localized in the pathological calcification that occurs in association with cholesteatoma. These results are consistent with the observations in chronic otitis media. Therefore, it is suggested the possibility that OPN might contribute as a common regulator of the deposition of calcium phosphate in the middle ear.

Adolescent↗
PubMed2005

Smooth muscle cells deficient in osteopontin have enhanced susceptibility to calcification in vitro.

OBJECTIVE: Vascular calcification is an actively regulated process, correlating with cardiovascular morbidity and mortality especially in patients with diabetes and chronic renal diseases. Osteopontin (OPN) is abundantly expressed in human calcified arteries and inhibits vascular calcification in vitro and in vivo. How OPN functions in vascular calcification, however, is less clear. METHODS: Smooth muscle cells (SMCs) were isolated from aortas of OPN knock-out (OPN-/-) and wild type (OPN+/+) mice. RESULTS: OPN-/- SMCs were identical to OPN+/+ SMCs in morphology and stained positively for SM lineage proteins, desmin, smooth muscle alpha-actin and SM22alpha. No spontaneous calcification was observed in OPN-/- SMCs under normal culture conditions or in medium containing 1%, 3%, or 5% fetal bovine serum. However, when cultured in medium containing elevated concentrations of inorganic phosphate, an inducer of vascular calcification, a significantly higher calcification was observed in OPN-/- SMCs compared to OPN+/+ SMCs that, in response to elevated phosphate, synthesized and secreted OPN into the culture. Finally, retroviral transduction of mouse OPN cDNA into OPN-/- SMCs rescued the calcification phenotype of the cells. CONCLUSION: These results are the first to demonstrate an inhibitory role of endogenously produced OPN on SMC calcification, suggesting a novel feedback mechanism where OPN produced locally by the SMCs may serve as an important inducible inhibitor of vascular calcification.

Animals↗
PubMed2005

Ghrelin blunted vascular calcification in vivo and in vitro in rats.

Ghrelin is a new peptide with regulatory actions in growth hormone secretion in the anterior pituitary gland and in energy metabolism. Currently, ghrelin has potently protective effects in cardiovascular diseases. We used an in vivo model of rat vascular calcification induced by vitamin D3 and nicotine and one of cultured rat vascular smooth muscular cells (VSMCs) calcification induced by beta-glycerophosphate to study the possible mechanism in the regulatory action of ghrelin in vascular calcification. Calcification increased total Ca2+ content and 45Ca2+ deposition in aortas and VSMCs and alkaline phosphatase (ALP) activation in plasma, aortas and VSMCs. However, calcified aortas and VSMCs showed a significant decrease in osteopontin (OPN) mRNA expression and a marked reduction of ghrelin levels in plasma and its mRNA expression in aortas. The aortic calcification was significantly attenuated by subcutaneous administration of ghrelin 30 and 300 nmol kg(-1) day(-1) for 4 weeks, and the latter dosage was more potent than the former. Ghrelin treatment at the two dosages reduced the total aorta Ca2+ content by 24.4% and 28.1%, aortic 45Ca2+ deposition by 18.4% and 24.9%, plasma ALP activity by 36.6% and 76.7%, and aortic ALP activity by 10.3% and 47.6% (all P < 0.01 or 0.05), respectively. Ghrelin at 10(-8)-10(-6) mol/L attenuated the calcification in cultured VSMCs, with decreased total Ca2+ content, 45Ca2+ deposition and ALP activity and increased OPN mRNA expression, in a concentration-dependent manner. In addition, endothelin levels in plasma and aortas and its mRNA expression in aortas significantly increased with calcification, but ghrelin treatment significantly decreased endothelin levels and mRNA expression, with the high dosage being more potent than the lower dosage. These results indicate that local ghrelin in vascular was down-regulated during vascular calcification, whereas administration of ghrelin effectively attenuated vascular and VSMCs calcification.

Animals↗
PubMed2004

C-reactive protein is a significant predictor of vascular calcification of both aorta and hand arteries.

Although evidence has accumulated indicating a close relationship between inflammation and atherosclerosis, the relationship between inflammation and vascular calcification in patients with chronic renal failure is unclear. In the present study, the relationship between C-reactive protein (CRP) and vascular calcification in dialysis patients was examined. Vascular calcification of the aorta and hand arteries of 512 hemodialysis patients without significant infection (age 58.8 +/- 10.1 y; 305 men, 207 women) were examined by roentgenography of the lateral abdomen and hands, respectively. Patients with a mean CRP level greater than 1.0 mg/L (n = 254) were older than those with a CRP level less than or equal to 1.0 mg/L (n = 258) and had a longer duration of dialysis, lower serum albumin level, and higher phosphate level ( P < .01, P < .05, P < .001, and P < .01, respectively). Prevalence of vascular calcification of aorta and hand arteries in the former group was significantly higher than in the latter (65.0% versus 43.8% for aorta, P < .0001; and 25.0% versus 14.7% for hand arteries, P < .01). In a multivariate logistic regression analysis adjusted for age, hemodialysis duration, sex, levels of calcium and phosphate, and presence of diabetes, CRP level was a significant predictor for the presence of aortic calcification (odds ratio for highest versus lowest quartile, 2.669; 95% confidence interval, 1.539-5.421, P = .0010) and of calcification of hand arteries (odds ratio, 2.243; 95% confidence interval, 1.039-4.841; P = .0395). In conclusion, the present study shows that increased levels of CRP are significantly associated with the presence of vascular calcification in both aorta and hand arteries (ie, with both atheromatous and medial forms of calcification), indicating evidence for a relationship between inflammation and vascular calcification in hemodialysis patients.

Aortic Diseases↗
PubMed2000

Inhibition of matrix metalloproteinase activity attenuates tenascin-C production and calcification of implanted purified elastin in rats.

Elastin, a major extracellular matrix protein present in arterial walls provides elastic recoil and resilience to arteries. Elastin is prone to calcification in a number of cardiovascular diseases including atherosclerosis and bioprosthetic heart valve mineralization. We have recently shown that purified elastin when implanted subdermally in rats undergoes severe calcification. In the present study, we used this elastin implant model to investigate the molecular mechanisms underlying elastin calcification. Intense matrix metalloproteinase (MMP-2) and tenascin-C (TN-C) expression were seen in the proximity of the initial cal-cific deposits at 7 days. Gelatin zymography studies showed both MMP-2 (latent and active form) and MMP-9 expression within the implants. To investigate the role of MMPs in calcification, rats were administered a MMP inhibitor, (2S:-allyl-N:-hydroxy-3R:-isobutyl-N:-(1S:-methylcarbamoyl-2-ph enylet hyl)-succinamide (BB-1101) by daily injection, either systemically or at the implant site. The site-specific BB-1101 administration almost completely suppressed TN-C expression, as shown by immunohistochemical staining, within the implants. The systemic BB-1101 injections also significantly reduced TN-C expression within the elastin implants. Moreover, calcification of elastin implants was significantly reduced in the site-specific administration group (5.43 +/- 1.03 microg/mg Ca for BB-1101 group versus 21.71 +/- 1.19 for control group, P: < 0.001). Alizarin Red staining clearly showed that the elastin fibers were heavily calcified in the control group, whereas in BB-1101 group the calcification was scarce with few fibers showing initial calcification deposits. The systemic administration of BB-1101 also significantly reduced elastin calcification (28.07 +/- 5.81 control versus 16.92 +/- 2.56 in the BB-1101 group, P: < 0.05), although less than the site-specific administration. Thus, the present studies indicate that MMPs and TN-C play a role in elastin-oriented calcification.

Alkaline Phosphatase↗
PubMed1999

Role of glutaraldehyde in calcification of porcine aortic valve fibroblasts.

Glutaraldehyde-treated porcine aortic valve xenografts frequently fail due to calcification. Calcification in the prostheses begins intracellularly. In a previous study, various types of cell injury to canine valvular fibroblasts, including glutaraldehyde treatment, led to calcification. An influx of extracellular Ca2+ into the phosphate-rich cytosol was theorized to be the mechanism of calcification. To test the Ca2+ influx theory, cytosolic Ca2+ and Pi concentrations were assessed in glutaraldehyde-treated porcine aortic valve fibroblasts, and their relationship to a subsequent calcification was studied. Glutaraldehyde caused an immediate and sustained massive cytosolic Ca2+ increase that was dose dependent and a several-fold increase in Pi. Calcification of cells followed within a week. The earliest calcification was observed in blebs formed on glutaraldehyde-treated cells. Live control cells or cells fixed with glutaraldehyde in Ca2+-free solution did not calcify under the same conditions. Concomitant increases in Ca2+ and Pi in glutaraldehyde-treated cells appear to underlie the mechanism of calcification, and the presence of extracellular Ca2+ during glutaraldehyde fixation promotes calcification.

Animals↗