维持性血液透析患者血管钙化情况及其与心血管疾病的关系

目的调查维持性血液透析（MHD）患者血管钙化的发生情况。方法应用x线摄片方法调查MHD患者胸主动脉及四肢血管发生的钙化情况,初步分析血管钙化与心血管疾病的关系。结果69例患者中38例有至少一处血管钙化,占55％（38／69）。23例有四肢血管钙化的患者中,大部分（14／23）为内膜、中膜钙化同时存在。有血管钙化患者与无血管钙化患者相比,年龄更大,既往有缺血性心脏病的患者更多（P〈0．05）。随访1年,有16例患者在此期间发生心衰。有血管钙化患者发生心衰的人数明显多于无血管钙化患者（P〈0．01）。结论血管钙化可能与MHD患者心血管疾病有关。     

血液透析患者血管钙化及相关影响因素的调查分析

目的 了解维持性血液透析（maintenance hemodialysis，MHD）患者血管钙化情况及相关影响因素分析。方法 记录72例MHD患者人口学特征、临床及实验性检查资料，根据腹主动脉钙化评分（abdominal aortic calcification score，AACs）分为无钙化/轻度钙化组和中重度钙化组。检测血钙、血磷、碱性磷酸酶（alkaline phosphatase，ALP）、C反应蛋白（C reactive protein，CRP）、全段甲状旁腺激素（intact parathyroid hormone，iPTH）、血清骨硬化蛋白、白介素（interleukins，IL）-37水平。结果 72例患者中有无钙化19例、轻度钙化11例、中度29例、重度13例。中重度钙化组年龄、透析龄、血钙、血磷、ALP、CRP及iPTH水平高于无钙化/轻度钙化组，差异均具有统计学意义（均有P<0.05）。中重度钙化组血清骨硬化蛋白、IL-37水平高于无钙化/轻度钙化组，差异均有统计学意义（均有P<0.05）。Logistic回归分析结果显示高龄、高血钙、iPTH水平增加是MHD患者腹主动脉中重度钙化的独立危险因素（均有P<0.05）。结论 MHD患者普遍存在血管钙化，对血管钙化相关影响因素分析研究可能为血管钙化防控提供新靶点。     

B型利钠肽对老年维持性血液透析患者左心功能评估的临床研究

目的 观察老年维持性血液透析(MHD)患者血浆B型利钠肽(BNP)水平与左心功能之间的关系.方法检测50例老年MHD患者(MHD组)和30例健康体检者(健康对照组)的BNP水平,以及彩色多普勒超声心动图测定的左室射血分数(LVEF).分析BNP水平与左心功能之间的关系.结果 MHD组透析前后血浆BNP中位数分别为213.5 ng/L及110.2 ng/L,健康对照组为20.2 ng/L,MHD组的BNP水平透析前后均较健康对照组显著增高(P<0.01),且透析后较透析前显著下降(P<0.01).Spearman等级相关分析结果提示,MHD组的血浆BNP水平与LVEF呈负相关(r=-0.4357,P<0.05).LVEF<50%者20例,透析前后血浆BNP中位数分别为386.5 ng/L和232.0ng/L,LVEF≥50%者30例,透析前后血浆BNP中位数分别为59.7 ng/L和29.1 ng/L,两组比较差异有统计学意义(P<0.01).结论 BNP可反映左心功能的动态变化,可能有助于MHD患者的心血管疾病早期诊断和治疗.     

老年维持性血液透析患者血管钙化与透析间低血压的相关性研究

目的探讨老年维持性血液透析(maintenance hemodialysis,MHD)患者血管钙化(vascular calcification,VC)和透析间低血压(intradialytic hypotension,IDH)的相关性,评估血管钙化对老年MHD患者合并透析间低血压的影响。方法回顾性选取沈阳军区总医院血液净化科403例老年患者,其中男性216例,女性187例。入选标准为:血液透析3次/周,每次4 h;年龄65~85岁;透析时限6个月~10年;病情稳定,无急性心血管事件。血管钙化可由胸部正位片检查判断,透析间低血压定义为收缩压90 mmHg或需要回输生理盐水或葡萄糖溶液。结果血管钙化的MHD患者52名(12.9%),IDH在血管钙化患者中发生率较无血管钙化高(34.6%vs 18.5%,P=0.005),血管钙化是透析间低血压发生的风险的独立影响因素。结论血管钙化与透析间低血压密切相关,良好的控制血管钙化进程可能对于防止透析间低血压的发生具有一定的意义。     

尿毒症患者外周血管钙化的临床相关因素分析

目的 研究尿毒症患者外周血管钙化的特点,并探讨血管钙化与临床相关因索之间的关系.方法 在行动静脉内瘘手术时留取尿毒症患者桡动脉0.5～1.0 cm,共43例.应用茜索红染色观察血管钙化情况.记录患者的临床及生化指标.结果 43例患者中有10例(23.3%)发生程度不同的血管钙化,均位于血管中膜.根据组织钙化积分将患者分为重度钙化组、轻中度钙化组与无钙化组.重度钙化组与轻中度钙化组血磷、钙磷乘积、C-反应蛋白、体重指数较无钙化组明显增高,差异有统计学意义;重度钙化组透析时间较无钙化组明显延长.相关性分析显示,组织钙化积分与血磷、C-反应蛋白、体重指数、透析时间及钙磷乘积呈正相关(P＜0.05或＜0.01).结论 尿毒症患者外周血管钙化发生在中膜,血磷、钙磷乘积、C-反应蛋白、体重指数、透析时间可能是发生血管钙化的非传统性危险因素.     

终末期肾脏病患者桡动脉钙化与骨保护素表达的关系

目的 检测终末期肾脏病患者桡动脉和血清中骨保护素(OPG)的表达,探讨其与血管钙化的关系.方法 终末期肾脏病患者43例(终末期肾脏病组),动静脉内瘘成形术时取废弃桡动脉,无钙化24例、轻中度钙化13例、重度钙化6例、透析患者20例、未透析患者23例.上肢外伤9例(对照组),取废弃上肢血管.血管行von Kossa染色、茜素红染色和OPG免疫组化染色,判断积分.同时检测血清OPG水平.结果 终末期肾脏病组血清OPG水平高于对照组[(216.47±83.78) ng/L比(57.15±23.22) ng/L],差异有统计学意义(P＜0.01).终末期肾脏病组无钙化、轻中度钙化、重度钙化患者血清OPG水平分别为(152.21±32.21)、(248.31±53.86)、(368.44±53.57) ng/L,血管OPG染色积分中位数分别为1、2、4分,随血管钙化程度的加重,血清OPG水平、血管OPG染色积分逐渐升高(P＜0.01).血清OPG水平与血管钙化值呈正相关(茜素红染色:r=0.517,P＜0.01;von Kossa染色:r=0.677,P＜0.01).透析患者血清OPG水平和血管OPG染色积分中位数要高于未透析患者[(283.57±79.02) ng/L比(152.46±30.89) ng/L;2分比1分],差异有统计学意义(P＜0.01).结论 终末期肾脏病患者血清OPG水平以及桡动脉上的OPG表达与血管钙化有关.     

蔗糖铁注射液治疗维持性血液透析患者肾性贫血临床观察

目的 观察蔗糖铁注射液治疗维持性血液透析(MHD)患者肾性贫血的疗效与安全性.方法 46例MHD患者按照进入透析时间顺序分为治疗组和对照组,每组各23例.治疗组:蔗糖铁注射液100 mg稀释于100 ml 0.9%Nacl溶液中,每周使用2～3次;对照组:维铁缓释片2片,每日1次口服.比较两组患者血红蛋白(Hh)、红细胞压积(Hct)、血清铁蛋白(SF)、转铁蛋白饱和度(TSAT)的变化及不良反应发生情况.结果 治疗后,治疗组与对照组Hb均较治疗前显著升高[分别为(70.5±7.3)g/L比(110.8±11.5)g/L和(70.5±8.2)g/L比(98.6±12.3)g/L],Hct也较治疗前明显升高,两组比较差异有统计学意义(P<0.05).治疗组治疗后SF、TSAT均较治疗前有明显升高,治疗组SF为(657.2±142.3)μg/L,TSAT为(28.1±6.5)%,上升幅度高于对照组(P<0.05).治疗组总有效率(91.3%,21/23)高于对照组(69.6%,16/23).治疗组无不良反应发生.结论 蔗糖铁注射液治疗.肾性贫血安全有效,且不良反应少.     

慢性肾脏病维持性血液透析患者血清SGK1 、SOST、OPN水平与钙磷代谢指标及血管钙化的关系

目的 研究慢性肾脏病维持性血液透析(MHD)患者血清糖皮质激素调节蛋白激酶1(SGK1)、骨硬化蛋白(SOST)、骨保护素(OPN)水平与钙磷代谢指标及血管钙化的关系.方法 选择本院2019年1月2日至2020年10月30日收治的慢性肾脏病MHD患者200例,按照血管钙化与否分作钙化组和无钙化组.比较两组血清SGK1、...     

尿毒症患者外周血管钙化的临床相关因素分析

目的研究尿毒症患者外周血管钙化的特点，并探讨血管钙化与临床相关因素之间的关系。方法在行动静脉内瘘手术时留取尿毒症患者桡动脉0．5-1．0cm，共43例。应用茜素红染色观察血管钙化情况。记录患者的临床及生化指标。结果43例患者中有10例（23．3％）发生程度不同的血管钙化，均位于血管中膜。根据组织钙化积分将患者分为重度钙化组、轻中度钙化组与无钙化组。重度钙化组与轻中度钙化组血磷、钙磷乘积、C-反应蛋白、体重指数较无钙化组明显增高，差异有统计学意义；重度钙化组透析时间较无钙化组明显延长。相关性分析显示，组织钙化积分与血磷、C-反应蛋白、体重指数、透析时间及钙磷乘积呈正相关（P〈0．05或〈0．01）。结论尿毒症患者外周血管钙化发生在中膜，血磷、钙磷乘积、C-反应蛋白、体重指数、透析时间可能是发生血管钙化的非传统性危险因素。     

维持性血液透析患者中MIA综合征的临床分析

目的 探讨血液透析患者MIA综合征的发生率、临床表现及与透析的充分性之间的相关性.方法 对142例血透患者进行了营养指标、慢性炎症状况、心血管疾病的横断面调查.结果 142例维持性血透患者普遍存在着营养不良,其发生率为轻中度42.3%(60/142),重度7.0%(10/142),总发生率为49.3%(70/142).142例血CRP为0.33～44(5.55±10.22)mg/L,慢性炎症35例(24.6%)超过正常值(8mg/L).142例有心血管疾病表现的总发生率为52.1%(74/142).提示维持性血透患者存在营养不良、炎症、心血管疾病是较常见的.而兼有营养不良、炎症、心血管疾病即MIA综合征者为19.0%(27/142),但MIA综合征的发生与透析充分性无明显关系.结论 血液透析患者中存在MIA综合征,且营养不良、心血管疾病及炎症之间可能是相互关联的.     

基质金属蛋白酶-9及其组织抑制剂-1与尿毒症患者桡动脉血管钙化的关系

目的 研究尿毒症患者桡动脉血管壁上基质金属蛋白酶-9及其组织抑制剂-1的血清含量以及在血管的表达与血管钙化的关系.方法 选择某院行动静脉内瘘术的尿毒症患者120例为尿毒症组,手术时留取废弃的桡动脉；另选择该院133例因上肢外伤行清创手术者为正常对照组,并留取废弃的上肢桡动脉.ELISA法测定血清TIMP-1和MMP-9浓度.应用von Kossa染色判断钙盐沉积程度；应用免疫组化方法测定MMP-9、TIMP-1在血管壁上的表达.结果 尿毒症患者桡动脉血管内膜厚度和桡动脉管壁/血管直径高于对照组,120例尿毒症桡动脉血管标本中出现血管钙化105例,发生率87.5％.钙化的血管中膜MMP-9、TIMP-1表达高于对照组,且和血管钙化程度呈正相关.结论 尿毒症患者普遍存在血管钙化,MMP-9、TIMP-1在尿毒症患者桡动脉的血管壁表达和血管钙化程度相关,提示组织基质金属蛋白酶系统和尿毒症血管钙化密切相关.     

Vitamin K status and vascular calcification: evidence from observational and clinical studies

Vascular calcification occurs when calcium accumulates in the intima (associated with atherosclerosis) and/or media layers of the vessel wall. Coronary artery calcification (CAC) reflects the calcium burden within the intima and media of the coronary arteries. In population-based studies, CAC independently predicts cardiovascular disease (CVD) and mortality. A preventive role for vitamin K in vascular calcification has been proposed based on its role in activating matrix Gla protein (MGP), a calcification inhibitor that is expressed in vascular tissue. Although animal and in vitro data support this role of vitamin K, overall data from human studies are inconsistent. The majority of population-based studies have relied on vitamin K intake to measure status. Phylloquinone is the primary dietary form of vitamin K and available supplementation trials, albeit limited, suggest phylloquinone supplementation is relevant to CAC. Yet observational studies have found higher dietary menaquinone, but not phylloquinone, to be associated with less calcification. Vascular calcification is highly prevalent in certain patient populations, especially in those with chronic kidney disease (CKD), and it is plausible vitamin K may contribute to reducing vascular calcification in patients at higher risk. Subclinical vitamin K deficiency has been reported in CKD patients, but studies linking vitamin K status to calcification outcomes in CKD are needed to clarify whether or not improving vitamin K status is associated with improved vascular health in CKD. This review summarizes the available evidence of vitamin K and vascular calcification in population-based studies and clinic-based studies, with a specific focus on CKD patients.     

Coronary calcification in patients with end-stage renal disease: a novel endocrine disorder?

Cardiovascular mortality is significantly increased among patients with end-stage renal disease. The commonly observed vascular calcification in such patients has been considered as one of the causative factors. In patients undergoing dialysis, the incidence of coronary artery calcification is 2-5 times higher compared to patients with normal renal function and angiographically demonstrated coronary artery disease. Moreover, epidemiological studies have revealed a significant correlation of the extent of coronary artery calcification with the severity of underlying atherosclerotic lesions. Vascular calcification was initially considered as a passive process of hydroxyapatite deposition due to elevated plasma concentrations of calcium and phosphate. Nevertheless, there is a growing body of evidence that vascular calcification is an actively regulated and cell-mediated process. This phenomenon includes phenotypic alterations of vascular smooth muscle cells mainly resulting from an imbalance between promoters (such as increased Ca x P product) and inhibitors (fetuin-A, GLA protein, osteoprotegerin) of mineral deposition. With regard to the therapeutic approach, despite the evident effectiveness of both traditional and innovative remedies in the management of metabolic and electrolytic abnormalities of patients with end-stage renal disease, an individualized intervention based on etiopathogenesis is really required.     

The Pathogenesis of the Mechanism of FGF23 in Chronic Kidney Disease Patients with Vascular Calcification

Fibroblast growth factor 23(FGF23)is a protein synthesized by bone cell and the osteoblast with endocrine function.The main role of FGF23 is to regulate serum phosphorus and 1,25(OH)2 D3 levels,it also plays an important role in calcium and phosphorus metabolism.The role of FGF23 in renal disease is to inhibit of phosphorus reabsorption,promote urinary phosphorus excretion and maintain a stable blood phosphorus level.Patients with chronic kidney disease(CKD)have more risk to suffer cardiovascular disease(CVD)which is related to the abnormal metabolism of calcium and phosphorus.FGF23,as newly discovered cardiovascular risk marker,several studies have shown that FGF23 level associates with multiple cardiovascular risk factors in CKD patients,especially in CKD patients with vascular calcification.To explore its pathogenesis of vascular calcification in CKD patients is particularly important,and that may help to take appropriate measures to improve the prognosis of CKD patients.     

Chronic hemodialysis patients with visceral obesity have a higher risk for cardiovascular events

The risk of cardiovascular disease is substantially high in hemodialysis patients. The risk factors for cardiovascular disease in dialysis patients include age, malnutrition, duration of dialysis, diabetes mellitus and hyperphosphatemia. However, it is not clear whether cardiovascular disease is associated with abdominal obesity in dialysis patients. The aim of the present study was to clarify the relationship among visceral fat area and cardiovascular complications in chronic dialysis patients. Area of visceral fat was measured using computed tomography scan in 94 patients. The abdominal aortic calcification index (ACI), blood lipid profile and complication of cardiovascular disease were evaluated in these patients. Compared to patients with smaller visceral fat area (<100 cm2), those with larger visceral fat area (≥100 cm2) showed significantly higher cardiovascular complication and higher serum levels of triglyceride and significantly lower serum levels of HDL-cholesterol. Patients with larger visceral fat area and longer duration of dialysis showed severer calcification by ACI analysis, and showed higher incidences of ischemic heart disease. This study suggested that chronic dialysis patients with higher visceral fat area have a higher risk for vascular events, especially ischemic heart disease.     

Correlation between Vascular Calcification and Serum Sclerostin in MHD Patients

Objective Investigate the correlation between serum sclerostinlevel and chronic kidney disease-mineral and bone disorder(CKD-MBD),especially vascular calcification,in maintenance hemodialysis(MHD)patients.Methods This is across-sectional study,a total of 72 MHD patients were included from the first affiliated hospital of Jinan university.Measure the biochemical indicators of mineral metabolism,renal function,and serum sclerostin level by ELISA.The abdominal aorta calcification score(AACS)was assessed according to Kauppila method on lateral spine imaging using DEXA.Patients were distributed into two groups according to the level of serum sclerostin:low sclerostingroup(≤125 pg/ml)and high sclerostingroup(>125 pg/ml).Analyze the association of serum sclerostin level with the indicators of CKD-MBD.Results There was significant difference in i PTH level between high sclerost in group and low sclerost in group.Multivariate Logistic regression analysis demonstrated that dialysis duration,male and anuria were independent risk factor of high sclerostin level,and i PTH and Kt/V were protective factors.Conclusion Dialysis duration,man,anuria was independent risk factors and i PTH,Kt/V were protective factors of high serum sclerostin level in MHD patients.There was no correlation between abdominal aorta calcification and serum sclerostin level.     

Vascular stiffness and aging in HIV

Large artery stiffening is a biological index of vascular aging. Vascular aging and atherosclerosis are two closely linked processes that develop in parallel and in synergy, sharing common aetiological determinants. Vascular stiffening increases left ventricular work and can lead to diminished coronary perfusion, and may therefore contribute to the development of cardiovascular disease. There is emerging evidence that large artery stiffness and vascular aging are accelerated in HIV infection because of the high prevalence of cardiovascular risk factors among HIV-infected patients. Moreover, the biological effects of HIV and the metabolic perturbations associated with antiretroviral therapies appear to accelerate vascular stiffening in HIV-infected patients. Further studies evaluating the effects of general and targeted therapies and various combinations of antiretroviral therapies on measures of large artery stiffness are urgently needed.     

Vitamin D receptor activation and prevention of arterial ageing

In chronic kidney disease (CKD) patients, cardiovascular (CV) morbidity and mortality rate is higher than in the general population, because of frequently concomitant hypertension, peripheral vascular disease, heart failure, vascular calcification (VC), diabetes and mineral bone disease. Recently, another important factor associated to CV risk in CKD has been deeply investigated: vitamin D deficiency. Vitamin D Receptors (VDRs) are present in several systems and tissues and VDR activation is associated to positive effects, resulting in better blood pressure control and prevention of diabetic nephropathy. Unfortunately, the natural, non-selective vitamin D receptor activator (VDRA), calcitriol, is associated to higher serum calcium and phosphate levels, thus worsening CV risk in CKD. Recent data showed that the selective VDRA paricalcitol might have ameliorative CV effects. The potential positive impact of the use of paricalcitol on diabetic nephropathy, cardiac disease, hypertension, and VC may open new paths in the fight against CV disease in CKD patients.