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Objective:To investigate the correlation between serum Vitamin D, uric acid levels and arterial calcification in maintenance hemodialysis patients.Methods:A total of 120 patients who received MHD treatment in Daxing Teaching Hospital, Capital Medical University, from March 2019 to March 2021 were retrospectively selected as research subjects, and their general clinical data were recorded in detail. X-ray was used to detect the arterial calcification of patients. Multivariate Logistic regression was used to analyze the risk factors of arterial calcification in MHD patients.Results:According to the arterial calcification score, 120 MHD patients were divided into non-calcification group (43 cases, 35.83%), mild calcification group (16 cases, 13.33%), moderate calcification group (42 cases, 35.00%) and severe calcification group (19 cases, 15.83%). There were significant differences in dialysis years, serum Vitamin D, serum uric acid, serum calcium, serum phosphorus, intact parathyroid hormone (iPTH) and arterial calcification score among the four groups ( P<0.05). According to serum Vitamin D level, 120 MHD patients were divided into deficient serum Vitamin D group (84 cases, 70.00%) and normal serum Vitamin D group (36 cases, 30.00%), serum calcium and phosphorus levels in the deficient serum Vitamin D group were lower than those in the normal serum Vitamin D group: (2.53 ± 0.28) mmol/L vs. (3.15 ± 0.31) mmol/L, (1.83 ± 0.26) mmol/L vs.(2.07 ± 0.31) mmol/L; serum uric acid and arterial calcification scores in the deficient serum Vitamin D group were higher than those in the normal serum Vitamin D group: (512.41 ± 65.21) μmol/L vs.(311.94 ± 72.56) μmol/L, (6.92 ± 2.34) scores vs. (2.18 ± 2.01) scores, there were statistical differences ( P<0.05). One hundred and twenty MHD patients were divided into hyperuricemia group (77 cases, 64.17%) and uric acid normal group (43 cases, 35.83%) according to the level of serum uric acid, the serum Vitamin D level in the hyperuricemia group was lower than that in uric acid the normal group: (12.28 ± 5.18) μg/L vs. (28.84 ± 4.69) μg/L; and iPTH level and arterial calcification scores were higher than those in the uric acid normal group: (372.45 ± 90.31) ng/L vs. (291.60 ± 98.52) ng/L, (6.22 ± 2.52) scores vs. (2.72 ± 2.63) scores, there were statistical differences ( P<0.05). The results of multivariate Logistic regression showed that serum Vitamin D and uric acid levels were risk factors for arterial calcification in MHD patients ( P<0.05). Conclusions:Serum Vitamin D and uric acid levels are correlated with arterial calcification in MHD patients, and are the risk factors leading to arterial calcification in patients.
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Vascular calcification, including intimal and medial calcification, is closely associated with a significant increase in cardiovascular diseases. Although increased understandings were achieved, people still know much more about intimal calcification than medial calcification because the latter doesn't obstruct the arterial lumen, commonly considered as a non-significant finding. We clarified the pathologic characteristic of medial calcification, its difference from intimal calcification, principally focused on its clinical relevance, such as diagnosis, nosogenesis, and hemodynamics. We underline the importance of identifying and distinguishing medial calcification, understanding its effect to local/systematic arterial compliance, and relationship to diabetic neuropathy. Recent studies emphasize do not ignore its predictive role in cardiovascular mortality. It is of great clinical significance to summarize the mechanisms of occurrence, lesion characteristics, diagnostic methods, pathogenic mechanisms, hemodynamic changes, and the distinction as well as association of intimal calcification with intimal calcification.
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Humans , Cardiovascular Diseases , Tunica Intima , Vascular Calcification , Clinical Relevance , Diabetic NeuropathiesABSTRACT
Objective To investigate the correlation between serum uric acid and arterial calcification in maintenance hemodialysis patients.Methods 117 patients with maintenance hemodialysis were selected in our hospital.The blood uric acid and related clinical indexes were detected and the coronary artery calcification score (CACs) was measured by multislice spiral CT.The correlation between clinical indicators and coronary artery calcification score in hyperuricemia group and normal group was analyzed.Results The 117 patients with maintenance hemodialysis, 68 patients had elevated serum uric acid, and the incidence of hyperuricemia was 58.12％.The levels of DBP, SBP, TG, TC, hs-CRP and CACs in the hyperuricemia group were significantly higher than those in the normal group (P＜0.05).By correlation analysis, serum uric acid levels were positively correlated with TG, hs-CRP and CACs in patients (P＜0.05).The risk factors for severe vascular calcification (CACs＞400) in patients with persistent hemodialysis include hs-CRP levels, serum uric acid levels, and hypertension.Conclusion The incidence of hyperuricemia is high in continuous hemodialysis patients.There is a close relationship between serum uric acid level and coronary artery calcification.And the level of high blood uric acid is an important factor causing coronary artery calcification in patients.Therefore, the prevention of cardiovascular and cerebrovascular complications in maintenance hemodialysis patients should be paid more attention to the treatment of hyperuricemia.
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Objective To investigate the mechanism that receptor activator of NF-κB ligand (RANKL) promotes arterial calcification.Methods Firstly,RANKL was added into the culture media,in which the monocyte precursor cells alone were cultured.Morphological observation and tartrate resistant acid phosphatase(TRAP)stain were used to assess whether RANKL could induce the monocyte precursor cells to differentiate into osteoclast-like cells.During arterial calcification,both in vivo and in vitro expressions of RANKL and osteoprotegerin (OPG,as RANKL inhibitor)were measured via real-time PCR.The extent of osteoclast-like cell differentiation was also assessed.Results It was found that RANKL could induce osteoclast-like cell differentiation.There were no both in vivo and in vitro expressions of osteoclast-like cells in the early stage of calcification.At that time,the ratio of RANKL to OPG was very low.In the late stage of calcification,a small amount of osteoclast-like cell expression coincided with a relatively high ratio of RANKL to OPG.According to the results,the ratio of RANKL to OPG was very low during most of the arterial calcification period.This made it possible for OPG to completely inhibit RANKL-induced osteoclast-like cell differentiation.The ratio of RANKL to OPG was (0.36 ± 0.08) (F =36) and (1.68 ± 0.08) (F =36) respectively in the early and late subgroup of calcification group in the animal model,but was zero in the control group(both P＜0.05).The ratio of RANKL to OPG was(0.42±0.09) (F=16)and(1.50 ± 0.10)(F=16)respectively in the early and late subgroup of calcification group in the cell model,but was zero in the control group(both P＜0.05).Conclusions Our result likely explains why RANKL has the ability to induce osteoclast-like cell differentiation,but acts as a promoter of calcification.
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Objective To retrospectively analyze the relationship between the atherosclerosis plaques in abdominal aorta and superial mesenterial artery (SMA) and the development of ischemia bowel disease (IBD) in elderly patients. Methods Elderly patients diagnosed as IBD (n=20) and non-IBD elderly patients with coronary heart disease (n=20) were selected in our hospital from January 2010 to December 2015. Data of CT imaging of abdominal aorta and SMA were evaluated by Syngo.Via software in two groups. Results The calcified plaques were dominated by dots in control group, while they were the annular lesions in IBD group, according to the CT imaging data. The mean sum of calcification in SMA was significantly increased in IBD group than that in control group (χ2=5.010,P=0.025). The stenosis of SMA was more significant in IBD group compared to that of control group (Z=3.370,P=0.001). The degree of SMA lesion was positively correlated with its opening stenosis in the IBD group (rs=0.650,P=0.002). Conclusion The basic vascular lesion is dot calcification in elderly patients with coronary heart disease, and the opening stenosis in SMA induced by mass calcification is the main cause of atherosclerosis-induced ischemic intestinal disease in elderly people.
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Objective To retrospectively analyze the relationship between the atherosclerosis plaques in abdominal aorta and superial mesenterial artery (SMA) and the development of ischemia bowel disease (IBD) in elderly patients. Methods Elderly patients diagnosed as IBD (n=20) and non-IBD elderly patients with coronary heart disease (n=20) were selected in our hospital from January 2010 to December 2015. Data of CT imaging of abdominal aorta and SMA were evaluated by Syngo.Via software in two groups. Results The calcified plaques were dominated by dots in control group, while they were the annular lesions in IBD group, according to the CT imaging data. The mean sum of calcification in SMA was significantly increased in IBD group than that in control group (χ2=5.010,P=0.025). The stenosis of SMA was more significant in IBD group compared to that of control group (Z=3.370,P=0.001). The degree of SMA lesion was positively correlated with its opening stenosis in the IBD group (rs=0.650,P=0.002). Conclusion The basic vascular lesion is dot calcification in elderly patients with coronary heart disease, and the opening stenosis in SMA induced by mass calcification is the main cause of atherosclerosis-induced ischemic intestinal disease in elderly people.
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A 1-year-old male meerkat was found dead by the owner. The animal was clinically healthy and was regularly vaccinated for distemper virus. Necropsy revealed multifocal to confluent dry white areas in the myocardium, pneumonia and congestive hepatopathy. All the other organs, including gross vessels, were macroscopically normal. The heart showed histologically large, multifocal to confluent areas of mineralization of the myocardium and the wall of small coronary artery. Vascular calcifications were also observed in the hepatic portal tracts and kidneys arteries of small/medium sizes. The arterial lumen appeared narrowed and the wall thickened due to the calcification of the tunica media. In veterinary medicine, arterial mineralization is regarded as a metastatic calcification, as the result of hypercalcemia and/or hyperphosphatemia. However, today, the pathogenesis of medial artery calcification in humans seems to be the results of an active process resembling embryonic osteogenesis, rather than a mere passive process.
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Objective To detect the correlation between the periodontal bone loss and carotid calcifications by using MSCT.Methods Imaging materials of 270 patients who were suspected atherosclerosis and underwent MSCT were retrospectively studied.According to the score of carotid calcification,the patients were divided into three groups:slight calcification group (carotid calcification score <100),severe calcification group (carotid calcification score ≥100),and normal control group (carotid calcification score=0).The original images were post-processed with volume rendering(VR),multi planar reformation(MPR),curved planar reformation(CPR)and maximum intensity projection (MIP)by using EBW4.5 workstation,and then the residual teeth number and the periodontal bone loss teeth were recorded in different groups.Results On MSCT,the carotid calcification score and the number of periodontal bone loss were displayed clearly.The number of the periodontal bone loss teeth in the calcification groups were significantly higher than those in the normal control group(P<0.01).Furthermore,the number of the periodontal bone loss teeth was positively correlated with the severity of carotid calcification.Conclusion The periodontal bone loss is highly correlated with the severity of the carotid calcification.The volume reconstruction technique of MSCT is a non-invasive diagnostic testing to detect the periodontal desease and to quantify carotid calcifications.
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Intracranial arterial calcification (IAC) is an easily identifiable entity on plain head computed tomography scans. Recent studies have found high prevalence rates for IAC worldwide, and this may be associated with ischemic stroke and cognitive decline. Aging, traditional cardiovascular risk factors, and chronic kidney disease have been found to be associated with IAC. The severity of IAC can be assessed using different visual grading scales or various quantitative methods (by measuring volume or intensity). An objective method for assessing IAC using consistent criteria is urgently required to facilitate comparisons between multiple studies involving diverse populations. There is accumulating evidence from clinical studies that IAC could be utilized as an indicator of intracranial atherosclerosis. However, the pathophysiology underlying the potential correlation between IAC and ischemic stroke-through direct arterial stenosis or plaque stability-remains to be determined. More well-designed clinical studies are needed to explore the predictive values of IAC in vascular events and the underlying pathophysiological mechanisms.
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Aging , Arteries , Constriction, Pathologic , Head , Intracranial Arteriosclerosis , Methods , Prevalence , Renal Insufficiency, Chronic , Risk Factors , Stroke , Weights and MeasuresABSTRACT
Intracranial arterial calcification (IAC) is an easily identifiable entity on plain head computed tomography scans. Recent studies have found high prevalence rates for IAC worldwide, and this may be associated with ischemic stroke and cognitive decline. Aging, traditional cardiovascular risk factors, and chronic kidney disease have been found to be associated with IAC. The severity of IAC can be assessed using different visual grading scales or various quantitative methods (by measuring volume or intensity). An objective method for assessing IAC using consistent criteria is urgently required to facilitate comparisons between multiple studies involving diverse populations. There is accumulating evidence from clinical studies that IAC could be utilized as an indicator of intracranial atherosclerosis. However, the pathophysiology underlying the potential correlation between IAC and ischemic stroke-through direct arterial stenosis or plaque stability-remains to be determined. More well-designed clinical studies are needed to explore the predictive values of IAC in vascular events and the underlying pathophysiological mechanisms.
Subject(s)
Aging , Arteries , Constriction, Pathologic , Head , Intracranial Arteriosclerosis , Methods , Prevalence , Renal Insufficiency, Chronic , Risk Factors , Stroke , Weights and MeasuresABSTRACT
Osteoclast-like cells are known to inhibit arterial calcification. Receptor activator of NF-κB ligand (RANKL) is likely to act as an inducer of osteoclast-like cell differentiation. However, several studies have shown that RANKL promotes arterial calcification rather than inhibiting arterial calcification. The present study was conducted in order to investigate and elucidate this paradox. Firstly, RANKL was added into the media, and the monocyte precursor cells were cultured. Morphological observation and Tartrate resistant acid phosphatase (TRAP) staining were used to assess whether RANKL could induce the monocyte precursor cells to differentiate into osteoclast-like cells. During arterial calcification, in vivo and in vitro expression of RANKL and its inhibitor, osteoprotegerin (OPG), was detected by real-time PCR. The extent of osteoclast-like cell differentiation was also assessed. It was found RANKL could induce osteoclast-like cell differentiation. There was no in vivo or in vitro expression of osteoclast-like cells in the early stage of calcification. At that time, the ratio of RANKL to OPG was very low. In the late stage of calcification, a small amount of osteoclast-like cell expression coincided with a relatively high ratio of RANKL to OPG. According to the results, the ratio of RANKL to OPG was very low during most of the arterial calcification period. This made it possible for OPG to completely inhibit RANKL-induced osteoclast-like cell differentiation. This likely explains why RANKL had the ability to induce osteoclast-like cell differentiation but acted as a promoter of calcification instead.
Subject(s)
Animals , Male , Rats , Acid Phosphatase , Genetics , Metabolism , Aorta , Metabolism , Pathology , Cell Differentiation , Coculture Techniques , Gene Expression Regulation , Isoenzymes , Genetics , Metabolism , Monocytes , Cell Biology , Metabolism , Myocytes, Smooth Muscle , Metabolism , Pathology , Osteoclasts , Metabolism , Pathology , Osteoprotegerin , Genetics , Metabolism , RANK Ligand , Genetics , Metabolism , Pharmacology , Rats, Sprague-Dawley , Signal Transduction , Tartrate-Resistant Acid Phosphatase , Vascular Calcification , Genetics , Metabolism , PathologyABSTRACT
El estudio de la enfermedad metabólica ósea es amplio y complejo. La enfermedad ósea más reconocida por médicos de todas las especialidades es la osteoporosis, probablemente debido a su elevada frecuencia. No obstante, es importante reconocer que existen numerosas entidades que afectan el metabolismo óseo de diferentes formas, llevando a fragilidad ósea, aumento del riesgo de fractura, osteoporosis u osteocondensación, de acuerdo a cada caso particular. Tanto el diagnóstico clínico como el reconocimiento de la alteración metabólica subyacente son importantes porque la identificación de la anormalidad específica se constituye en la base para el tratamiento. Se presentan 5 casos diferentes en los que un trastorno metabólico conlleva a una patología ósea específica; se discute la patogenia de las calcificaciones arteriales y se presenta una entidad mixta que nosotros llamamos osteoporomalacia.
The study of metabolic bone disease is broad and complex. The most widely recognized bone disease by physicians of all specialties is osteoporosis, probably due to its high frequency. However, it is important to recognize that there are numerous entities that affect bone metabolism in different ways, leading to brittle bones, increased risk of fracture, osteoporosis or osteocondensation, according to each particular case. Both the clinical diagnosis and recognition of the underlying metabolic abnormality are important because they identify the specific abnormality that will be the base for treatment. There were 5 different cases in which a metabolic disorder leads to specific bone pathology, we discuss the pathogenesis of arterial calcifications and presents a mixed entity we call osteoporomalacia.
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Humans , Female , Adult , Middle Aged , Aged , Bone Diseases, Metabolic , Osteoporosis , Pathology , Therapeutics , Bone and Bones , Clinical Diagnosis , Risk , Fractures, BoneABSTRACT
OBJECTIVE: The purpose of this study was to investigate the relationship between the breast arterial calcification (BAC) detected by mammograms and the hypertensive retinopathy (HR) in hypertensive women who underwent ophthalmologic examination. MATERIALS AND METHODS: Screening mammography was performed in 99 hypertensive women and these women also underwent an ophthalmologic examination. The presence of arterial calcification and the number of calcified blood vessels in each breast were evaluated. The grade of HR was determined. The presence of BAC and the number of blood vessels involved was compared according to the presence of HR and the grade of HR. RESULTS: Among the 99 patients, HR was detected in 70 patients, and of these 70 patients, 42 patients had grade I HR and 28 had grade II HR. BAC was detected in 54 cases. Forty-six patients with HR (66%) and eight patients without HR (27%) were diagnosed with BAC after they underwent mammographic examination. The prevalence of BAC in the subjects who had HR was statistically higher than that in those subjects who did not have HR (p 0.05). The positive predictive value of the BAC detected on mammography for HR was 0.80 in those subjects who were > or = 60 years old. CONCLUSION: The detection of BAC by mammography is associated with an increased risk of HR, and particularly for patients after the age of 60. The findings of BAC may be related to hypertensive end-organ damage, and performing mammograms might contribute to predicting the presence of ophthalmologic hypertensive complications in these patients.
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Adult , Aged , Female , Humans , Middle Aged , Age Factors , Arteries/pathology , Breast/blood supply , Calcinosis/complications , Hypertension/complications , Mammography , Retinal Diseases/complicationsABSTRACT
90? superficial calcium is low.