羟苯磺酸钙联合中药保留灌肠治疗慢性肾脏病疗效观察

目前我国慢性肾脏病(CKD)的患者逐年上升,而且预后差,医疗费用高,给社会和家庭带来沉重的经济负担,如何延缓或阻止慢性肾脏病的进展,是当前CKD非透析治疗急需解决的问题.     

慢性肾脏病高磷血症的研究进展CSCD

慢性肾脏病(chronic kidney disease,CKD)患病率高,随肾功能下降,磷代谢异常逐渐加重。我国CKD伴高磷血症呈患病率高、达标率低的特点。高磷血症是慢性肾脏病患者肾病进展、继发性甲状旁腺功能亢进(secondary hyperparathyroidism,SHPT)、心血管事件和全因死亡的独立危险因素。本文综述了慢性肾脏病时高磷血症的调控机制及其不良预后的机制。     

重视慢性肾脏病中的代谢性骨病

慢性肾脏病(chronic kidney disease,CKD)已成为全球的公共卫生问题,其发病率日益升高,且预后较差。矿物质代谢异常在CKD早期即可出现,患者如未得到及时的诊断和治疗,将发生代谢性     

慢性肾脏病蛋白质能量消耗的发病机制及防治策略

在慢性肾脏病(CKD)的众多并发症中,蛋白质能量消耗(PEW)的患病率较高,且在CKD各期中均可出现。PEW严重影响了CKD患者的生活质量,并与患者的不良预后密切相关。因此,早期诊断和及时干预PEW对CKD患者预后具有重大意义。本文综合PEW的病因、发病机制以及防治策略等方面,对近年来关于CKD并发PEW的研究进展予以综述。     

细胞内铁稳态失衡对慢性肾脏病患者心血管钙化和骨异常的影响

正慢性肾脏病(chronic kidney disease,CKD)是公共卫生的重大问题之一。我国流行病学调查显示,CKD的患病率为10.8%,而上海社区的调查数据显示CKD的患病率为11.8%。慢性肾脏病矿物质和骨异常(chronic kidney disease-mineral and bone disorders,CKD-MBD)是终末期肾脏病患者的常见并发症,包括矿物质代谢异常、骨异常及异位钙化,其与终末期肾脏病患者心血管疾病的发生、发展及预后密切相关。目前认为,心血管钙化是CKD患者     

慢性肾脏病患者脑血管事件危险因素分析和护理对策

目的：探讨CKD非透析患者脑血管事件的发生情况以及护理对策。方法：将45例确诊为慢性肾脏病住院患者进行调查,从分析CKD非透析患者的颈动脉超声、心脏超声、实验室检查等结果,调查CKD非透析患者脑血管事件的发生情况。结果：CKD患者中脑血管事件的发生率高。结论：对慢性肾脏病患者采取适时的护理对策,有助于改善肾功能,减少慢性肾脏病患者脑血管事件的发生。     

慢性肾脏病中血管钙化的早期诊治进展

心血管疾病（CVD）是慢性肾脏病（CKD）患者最主要的致病及致死原因,终末期肾脏病（ESRD）患者CVD的病死率显著高于普通人群[1]。研究显示血管钙化与CKD患者的缺血性心脏病、心血管死亡和全因死亡密切相关[2-4]。心血管钙化是CKD患者矿物质和骨代谢紊乱（CKD-MBD）的一部分,是慢性肾衰竭患者常见的合并症。早期预防和治疗血管钙化对于改善CKD患者的预后具有重要的临床意义。     

慢性肾脏病患者心血管疾病的现况、病因及治疗

慢性肾脏病（chronickidneydisease,CKD）和心血管疾病（cardiovasculardisease,CVD）的关系十分密切,且越来越被人们所重视。不仅慢性肾脏病是心血管疾病的一个危险因素,其存在也对心血管疾病的治疗增加了复杂性。CKD患者有很高的动脉硬化和心血管事件风险,常合并CVD,而CVD是CKD患者的主要死亡原因。CKD合并CVD患者常需要进行血运重建,     

慢性肾脏病合并结核分枝杆菌感染诊治进展

正我国成年人慢性肾脏病(Chronic Kidney Disease, CKD)发病率约为10.8%。CKD患者是一个免疫功能受损及肾功能异常的群体,研究表明CKD患者,尤其是透析患者,发生结核病的风险较普通人群高~([1])。2017年,全球估计有1 000万人感染结核(Tuberculosis, TB),其中有160万人因结核病而死亡~([2])。不典型的临床表现、诊断的延迟、不适当的抗     

慢性肾脏病患者血管及软组织钙化的评估

血管和软组织钙化是慢性肾脏病-矿物质骨异常（CKD-MBD）中的重要组成部分,是慢性肾脏病（CKD）患者心血管疾病（CVD）的危险因素,影响患者预后。随着改善全球肾脏病预后（KDIGO）组织指南的不断更新,特别强调血管/瓣膜钙化是发生心血管病的最高风险（2A）,要根据患者有无血管/瓣膜钙化指导CKD-MBD的治疗（未分级）。鉴于血管钙化的进展性特点,明确钙化情况对于有效预防和治疗非常重要。本文将主要讲述CKD患者血管和软组织钙化的评估。     

The treatment of coronary artery disease in patients with chronic kidney disease

Premature cardiovascular disease is the largest cause of mortality, and a major cause of morbidity, in patients with chronic kidney disease (CKD). Patients with end-stage kidney disease (ESKD) are at extreme risk, but cardiovascular event rates are increased even in early CKD. There is little controlled trial evidence on which to base treatment, as most therapeutic trials have excluded CKD patients. Current treatment strategies are therefore based upon small prospective studies or retrospective analyses of controlled trials and registry data. It is thus unclear whether CKD patients benefit from modern secondary preventive treatments in the same manner as patients with normal renal function. There is a need for randomized trials to identify effective drugs to prevent and treat coronary artery disease in CKD. Revascularization by CABG in CKD has been widely reported in registry data to provide better results than medical treatment or angioplasty. Recent angioplasty data in patients with CKD, however, show improving results, and the risks of CABG in CKD remain high. It is not clear which revascularization technique has a better outcome in patients 'equally suitable' on angiographic criteria for either procedure. The high rate of late adverse cardiovascular events after both CABG and angioplasty accentuates the need for effective secondary preventive therapy disease in these high-risk patients.     

Dyslipidemias in patients who have chronic kidney disease

Patients with CKD are at high risk for developing CVD. In fact, most CKD patients have a 10-year risk of coronary heart disease events greater than or equal to 20%, placing them in the highest risk category according to the National Cholesterol Education Program Adult Treatment Panel III guidelines. For this reason, the National Kidney Foundation K/DOQI guidelines for managing dyslipidemia suggest that CKD patients with LDL greater than or equal to 100 mg/dL (2.59 mmol/L) should be treated with diet and a statin. The K/DOQI guidelines also make it clear that the evidence supporting treatment in CKD populations is lacking however, and that additional placebo-controlled trials are needed. In the mean time, the high incidence of CVD makes intensive monitoring and treatment of dyslipidemias in patients with CKD a reasonable clinical approach.     

Statin therapy in patients with chronic kidney disease: to use or not to use

Dyslipdemia is a common complication of chronic kidney disease (CKD) and contributes to high cardiovascular morbidity and mortality of CKD patients. Experimental studies have demonstrated that lipids induce glomerular and tubulointerstitial injury and that lipid-lowering treatments ameliorate renal injury. Therapy with statins not only has the potential to lower cardiovascular morbidity and mortality in patients with CKD but also to slow progression of renal disease. Whereas the guidelines for treatment of hyperlipidaemia in nonrenal patients are based on prospective, randomized, placebo-controlled mega-trials, such data are not available for CKD patients. This review outlines the limited information currently available on the effect of statins among patients with CKD and summarizes the ongoing randomized trials designed to address this question.     

慢性肾脏病5期与5D期患者血清矿物质及骨代谢异常调查

目的比较慢性肾脏病(CKD)5期与5D期患者血清矿物质及骨代谢异常(MBD)状况。方法回顾性分析240例终末期肾脏病患者的临床资料。根据血液透析情况将患者分为CKD5期组(非透析)和CKD5D期组(已透析),比较2组血清矿物质及骨代谢相关指标(血清钙、磷、全段甲状旁腺素、碱性磷酸酶等),评估血钙、血磷和甲状旁腺激素的达标情况。结果CDK5D期组患者血清全段甲状旁腺素(iPTH)、校正血钙、钙磷乘积、血清白蛋白高于CKD5期组,估算肾小球滤过率(eGFR)低于CKD5期组,差异均有统计学意义(P<0.01)。CKD5期组、CDK5D期组患者高磷血症发生率分别为83.75%、91.25%,低钙血症发生率分别为31.25%、17.50%,高钙血症发生率分别为1.88%、30.00%,高甲状旁腺激素发生率分别为37.50%、63.75%。结论终末期肾脏病患者伴有严重的钙、磷和甲状旁腺激素指标异常,CKD5期患者突出表现为高磷、低钙和高甲状旁腺激素。CKD5D期患者的CKD-MBD状况并未因血液透析而得到改善,反而变得更加严重,突出表现为高磷、高钙和高甲状旁腺激素。     

三维斑点追踪技术评估慢性肾脏病患者左心收缩功能的进展

慢性肾脏病（CKD）因预后较差及高额医疗费用而成为严重影响公共健康的疾病之一。心脏损害是引起CKD患者死亡的首要病因,早期发现CKD患者左心收缩功能异常有助于治疗及评估病情。与传统超声心动图相比,新技术3D-STI能更准确、无创地评价左心室收缩功能。本文对3D-STI在评估CKD患者左心室收缩功能中的应用进展进行综述。     

CKD 3~5期患者血脂水平特点及其与肾功能指标的关系

目的:探讨慢性肾脏病(chronic kidney disease,CKD)3~5期血脂水平特点以及与肾功能指标的关系。方法:选取2018年8月至2020年10月皖西卫生职业学院附属医院肾内科收治的247例CKD患者(3期64例,4期34例,5期149例),记为CKD组。另选取70例体检健康志愿者记为对照组。比较不同分期CKD患者血清三酰甘油(triglyceride,TG)、总胆固醇(total cholesterol,TC)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)、高密度脂蛋白胆固醇(high density lipoprotein cholesterol,HDL-C)水平并归纳血脂异常构成情况,采用Pearson相关性分析CKD患者血脂水平与肾功能指标[血肌酐(serum creatinine,Scr)、肾小球滤过率(glomerular filtration rate,GFR)]的关系。结果:CKD 3~5期患者血清TC、LDL-C水平比较,差异无统计学意义(P>0.05),随CKD分期增加,血清TG、HDL-C水平逐渐下降(P<0.05),CKD 3期血清TG、HDL-C高于CKD 5期,CKD 4期血清HDL-C水平高于CKD 5期,差异有统计学意义(P<0.05)。CKD 3~5期血脂异常率59.92%,明显高于对照组的12.86%(P<0.05)。CKD3期、4期、5期血脂异常率分别为59.38%、61.76%、59.73%,差异无统计学意义(P>0.05)。CKD3~5期患者血脂异常类型以高三酰甘油血症、低高密度脂蛋白胆固醇血症为主,分别占17.41%、32.79%,且随CKD分期增加,低高密度脂蛋白胆固醇血症比重显著升高,差异有统计学意义(P<0.05)。Pearson相关性分析显示CKD 3~5期患者血清TG、HDL-C水平与血清Scr水平均呈负相关(r=-0.436、r=-0.850,P<0.05),与GFR均呈正相关(r=0.472、r=0.717,P<0.05)。结论:CKD3~5期患者血脂异常率较高,血脂异常类型以高TG、低HDL-C为主,且随CKD分期增加,低HDL-C愈发明显,血清TG、HDL-C水平与肾功能进展紧密相关。     

CKD非透析患者CVD的发生情况及影响因素分析

目的研究慢性肾脏病（CKD）非透析患心血管疾病（CVD）的发生情况及危险因素。方法分析695例cKD非透析患者基础资料、实验室指标、心脏彩色超声指标及其与既往CVD病史之间的关系,研究CKD非透析患者CVD的发生情况,探讨与其相关的危险因素。结果695例患者中226例（32．5％）有CVD既往史,Logistic回归分析显示,年龄、GFR、SBP、DBP、颈总动脉内径、颈总动脉IMT及分叉部IMT是cKD非透析患者CVD的独立危险因素。结论cKD非透析患者CVD的发生率较正常人显著升高,年龄、高血压、脂质代谢紊乱、微炎症状态、贫血、低蛋白血症、钙磷代谢紊乱等因素与CKD患者CVD的发生、发展密切相关。     

Protein recommendations for individuals with CKD stages 1-4.

In CKD Stages 1 and 2, diet and lifestyle interventions are key for their potential to delay progression of kidney failure and reduce CVD risk. The recommendations are to prudently lower protein in the diet to the RDA. Although the research supporting this data may still be considered uncertain about the efficacy of a low protein diet on slowing the progression of CKD, it may also be considered safe since it is the RDA (Levey et al., 2006). Other interventions may include control of proteinuria, of high blood pressure, and blood sugar, and the use of an ACE inhibitor or ARB. In CKD Stages 3 and 4, there are more enthusiastic recommendations regarding protein, potassium, and phosphorous that influence diet decision making but are not necessarily employed in the earlier stages of CKD. In addition, we cannot neglect that these patients, despite our best efforts, often progress to Stage 5 CKD treated with peritoneal dialysis or hemodialysis. We must maintain an optimum nutritional status along the continuum of CKD Stages 1 to 5. Protein energy malnutrition is a predictor of morbidity and mortality in patients on dialysis (NKF, 2000). The goal for these patients is to be well nourished and kidney protected, which is a balancing act. Medicare supports medical nutrition therapy for registered dietitian (RD) services for patients with GFRs of 15 to 50 mL/min/1.73m2 (NKF, 2007). The RDs in nephrology are effective in reviewing the diet options and providing necessary guidance and support to individuals with CKD. These RDs are the nutrition information resource for practitioners treating patients with Stages 1 to 4 CKD.     

Chronic kidney disease and vascular remodelling: molecular mechanisms and clinical implications

CKD (chronic kidney disease) is a severe and complex disease with a very high prevalence of CV (cardiovascular) complications. CKD patients are exposed to haemodynamic disturbances in addition to severe metabolic abnormalities that lead to a specific form of arterial remodelling, which contributes to the development of CV disease. Arterial calcification is a major event in the arterial remodelling process and is strongly linked to mineral metabolism abnormalities associated with CKD. Arterial remodelling is not limited to arterial calcification and modifications in arterial wall composition are also observed. Activation of the RAS (renin-angiotensin system), ET-1 (endothelin-1), endothelial dysfunction, oxidative stress and ADMA (asymmetric ω-NG,NG-dimethylarginine), as well as the anti-aging molecule Klotho, are implicated in this process. The present review details the mechanisms involved in arterial calcification and arterial remodelling associated with CKD, and provides the clinical consequences of large and small artery stiffness and remodelling in CKD patients.     

Chronic inflammation in peritoneal dialysis: the search for the holy grail?

Mortality and morbidity in chronic kidney disease (CKD) patients are unacceptably high. The annual mortality rate due to cardiovascular disease (CVD) is approximately 9%, which, for the middle-aged person, is at least 10- to 20-fold higher than for the general population. Classic risk factors for CVD are highly prevalent in CKD patients, but they cannot fully account for the excessive rate of CVD in this population. Instead, it has become increasingly clear that nontraditional risk factors, such as systemic inflammation, may play a key role in the development of atherosclerosis. It is well established that inflammatory markers are very powerful predictors of high CVD morbidity and mortality not only in the general population, but particularly in CKD patients. Signs of a sustained low-grade inflammation, such as increased levels of C-reactive protein (CRP), are present in the majority of stage 5 CKD patients, even in patients in clinically stable condition, and they are also commonly observed after the initiation of dialysis therapy. Dialysis therapy--hemodialysis as well as peritoneal dialysis (PD)--may itself contribute to systemic inflammation. Local intraperitoneal inflammation can also occur in patients treated with PD. These local effects may result in a low-grade inflammation, caused by the bioincompatibility of conventional glucose-based dialysis fluids, to intense inflammation associated with peritonitis. Given these circumstances, it is reasonable to hypothesize that strategies aiming to reduce inflammation are potentially important and novel, and could serve to reduce CVD, thereby lowering morbidity and mortality in patients with CKD. In this review we provide information supporting the hypothesis that systemic inflammation is tightly linked to the most common complications of CKD patients, in particular those on PD, and that local inflammation in PD may contribute to various related complications. The aims of this review are to discuss the reasons that make inflammation an attractive target for intervention in CKD, the particular aspects of the inflammation-CVD axis during PD treatment that are likely involved, and possible means for the detection and management of chronic inflammation in PD patients.