终末期肾脏病患者心血管钙化的研究进展

心血管疾病（CVD）在终末期肾脏病（ESRD）患者中的发病率和病死率均居于首位,约50％的ESRD患者死于CVD及其并发症。近年发表的肾脏疾病早期评估计划（KEEP）显示,慢性肾脏病（CKD）患者发生致死或非致死心血管事件的危险远远超过肾病进展的危险。血管钙化越严重,心血管事件发生率越高。因此,     

慢性肾脏病血管钙化的诊治进展

慢性肾脏病（chronic kidney disease,CKD）和心血管疾病（cardiovascular disease,CVD）为两大严重威胁人类健康的疾病,已成为全球性公共卫生问题。CVD是CKD患者特别是终末期肾病患者最常见的并发症和首位致死病因,心血管事件造成的死亡占总死亡原因的50%以上,其发病率比同年龄普通人群高出20～30倍[1]。2007年发表的肾脏疾病早期评估计划显示,CKD患者发生致死或非致死心血管事件的危险远超过肾病进展的危险[2]。血管钙化导致心血管疾病发生和发展,最终影响CKD患者的生存率。因此,早期发现CKD患者血管钙化,积极干预钙化危险因素,对于减少CKD患者心血管事件发生,提高生存质量有重要意义。     

成纤维细胞生长因子23在CKD患者心血管疾病中的新认识

并发心血管疾病（cardiavascular disease,CVD）是慢性肾脏病（chronic kidney disease,CKD）患者死亡的重要原因,传统的Framinghan危险因子（如高血压、糖尿病、高龄等）以及CKD患者体内的钙磷代谢失衡、血脂异常、长期血液净化治疗等因素是心肌病和血管硬化的促进因素,CKD患者心血管并发症发生率高,由于心血管事件引起的死亡占CKD总的死亡原因的50％以上。     

慢性肾脏病患者微炎症状态对心血管系统的影响

慢性肾脏病（chronic kidney disease，CKD）和心血管疾病（cardiovascular disease，CVD）均为威胁人类健康的重大疾病，现已成为全球性的公共卫生问题。CVD是CKD最常见的并发症和致死原因，CKD又加重原有的CVD，二者相互影响并形成恶性循环，共同的发病机制已引起广泛关注，其中CKD患者微炎症状态对心血管系统的影响不容忽视。     

慢性肾脏病血清β-脑钠肽、同型半胱氨酸与心血管病变的关系

目的探讨血清β-钠肽（BNP）、同型半胱氨酸（Hcy）与慢性肾脏病（CKD）35期心血管事件的发生和病死率的关系。方法本组77例CKD患者，按NKF-DOQI指南分为CKD3期（A组）17例，CKD4期（B组）21例和CKD5期（C组）39例。正常对照组30例，观察各组临床表现、生化指标，血清BNP、Hcy等变化。同时，将77例患者根据Hcy数值分为升高组和正常组，观察其与心血管疾病（CVD）的相关性。结果与正常对照组比较，A、B、C组血肌酐（SCr）、尿素氮（BUN）、BNP明显升高，B组与A组比较，C组与B组比较，各组数值差异均有统计学意义。与Hcy正常组比较，Hcy升高组发生CVD明显增加，具有正相关关系。结论本研究显示，BNP和Hcy可作为慢性肾衰竭早期心血管损害的指标之一，BNP，Hcy与CVD发生及病死率的关系密切，BNP、Hcy越高，CVD的发生率越高，病死率也越高。     

慢性肾脏病血管钙化的研究进展

心血管疾病（CVD）是慢性肾脏病（CKD）患者的主要并发症之一,血管钙化是透析患者心血管事件发生率和死亡率增加的重要危险因素。血管钙化实际上是血管平滑肌细胞发生骨样变化的主动调节过程。目前认为血管钙化的机制和调节包括血管平滑肌细胞的损伤、凋亡和囊泡的释放;血管平滑肌细胞的表型改变;血管钙化抑制物的减少;血管钙化的诱导和循环核复合物形成等五个方面。对血管钙化进展的研究将为防治CKD患者的心血管疾病提供了新的前景。     

调脂治疗对CKD患者CVD的防治

患有慢性肾脏病（CKD）的人数正在不断增长,美国约11％的成人患CKD,我国20岁以上人群中CKD患病率为79／6～13％,而大部分CKD患者（58％）死于心血管疾病（CVD）。美国肾脏病基金会一肾脏病生存质量指导（NKF-KDOQI）指南中将CVD定义为冠心病、脑血管疾病、肾动脉狭窄、周围血管疾病、充血性心力衰竭或左心室肥厚,并指出CKD患者是冠心病的最高危险因素人群。     

CKD患者血管钙化与钙磷代谢紊乱

<正>心血管疾病(cardiovascular disease,CVD)是慢性肾脏病(chronic kidney disease,CKD)患者死亡的主要原因,占CKD患者死亡率的50%以上。血管钙化已成为CKD患者CVD高发和心血管事件增加的独立危险因素。影响CKD患者血管钙化的因素错综复杂,除年龄、高血压、糖尿病、吸烟、血脂异常等传统危险因素有关外,钙磷代谢紊乱、继发性甲状旁腺功能亢     

新型心血管疾病相关生物标志物在慢性肾脏病患者的研究进展

正目前,心血管疾病(cardiovascular disease,CVD)仍然为终末期肾脏病(end-stage renal disease,ESRD)患者最主要的死亡原因[1]。早期识别慢性肾脏病(chronic kidney disease,CKD)患者是否存在心血管危险因素、及时干预、延缓病程进展对于减少CVD的发病率与死亡率均是非常重要的。然而,临床上对于CKD患者合并无症状的心血管疾病时,早期诊断与治疗     

慢性肾脏病患者钙磷代谢紊乱对心血管事件的影响

目的探讨钙磷代谢紊乱在慢性肾脏病（CKD）患者心血管事件发生中的作用。方法选取我科住院的225例CKD2～5期患者,分为4组,以是否发生心血管事件分为2组,比较各期CKD患者钙磷代谢的差异及发生心血管事件者与未发生心血管事件者之间的差异。结果CKD5期血清钙离子浓度低于CKD2～4期,CKD5期血清磷离子浓度高于CKD2～4期,CKD5期钙磷乘积高于CKD3、4期。225例CKD患者住院期间,64例发生心血管事件,发生率为28．44％。结论对CKD患者,尤其是终末期肾脏病患者存在低钙、高磷、高钙磷乘积;与既往高钙增加一般人群心血管事件发生风险不同的是,低钙是其独立心血管事件危险因素。     

Von Hippel-Lindau disease simulating polycystic kidney disease

Polycystic kidney disease and the renal manifestations of von Hippel-Lindau disease have much in common. Making the distinction between these two diseases is important. There is a strong association of renal cell carcinoma with von Hippel-Lindau disease, whereas renal cell carcinoma is rare in polycystic kidney disease. Furthermore, the many extrarenal manifestations of von Hippel-Lindau disease are serious and can be fatal while those of polycystic kidney disease are generally benign. Early diagnosis of the lesions of von Hippel-Lindau disease could lead to effective surgical treatment and prevent death. A case of von Hippel-Lindau disease is presented which was incorrectly diagnosed as polycystic kidney disease for sixteen years. The case is instructive in that the possibility of making the correct diagnosis prior to the patient's terminal illness was only through careful assessment of the family. The case is also remarkable in that the patient suffered from progressive renal failure requiring hemodialysis, which has not been associated previously with von Hippel-Lindau disease.     

Homocysteine and cardiovascular disease in renal disease

Elevated homocysteine (hyperhomocysteinaemia) in renal patients is a major concern for physicians. Although cause and effect between homocysteine and cardiovascular disease (CVD) has not been established in either the general population or renal patients, there is much evidence that this relationship does exist. Purported mechanisms that may explain this effect include increases in endothelial injury, smooth muscle cell proliferation, low-density lipoprotein oxidation and changes in haemostatic balance. Renal patients have a much greater incidence of hyperhomocysteinaemia and this may be explained by decreases in either the renal or extrarenal metabolism of the compound. We conclude that data from long-term placebo-controlled trials are urgently required to determine whether hyperhomocysteinaemia in renal patients is a cause of CVD events and requires therapeutic targeting.     

Associated neoplastic disease in inflammatory bowel disease

The development of intestinal carcinoma in the setting of inflammatory bowel disease (IBD) has been recognized as an unsavory outcome of chronic inflammation of the bowel. Numerous studies have recently documented the clinical and morphologic features of malignant transformation in this closely-followed group of patients. This article highlights the recent findings of these population-based studies with specific attention to surgical concepts and frames these data in the context of surgical approaches to cancer arising in inflammatory disease. Specifically, the authors address the pathobiology of malignant transformation, the management of colorectal cancer in inflammatory bowel disease, the development of dysplasia in ulcerative colitis, surveillance of patients who have IBD, chemoprevention of cancer, and special features of surgical oncologic management.     

Metabolic bone disease in chronic kidney disease

Metabolic bone disease is a common complication of chronic kidney disease (CKD) and is part of a broad spectrum of disorders of mineral metabolism that occur in this clinical setting and result in both skeletal and extraskeletal consequences. Detailed research in that past 4 decades has uncovered many of the mechanisms that are involved in the initiation and maintenance of the disturbances of bone and mineral metabolism and has been translated successfully from "bench to bedside" so that efficient therapeutic strategies now are available to control the complications of disturbed mineral metabolism. Recent emphasis is on the need to begin therapy early in the course of CKD. Central to the assessment of disturbances in bone and mineral metabolism is the ability to make an accurate assessment of the bone disease by noninvasive means. This remains somewhat problematic, and although measurements of parathyroid hormone are essential, recently recognized difficulties with these assays make it difficult to provide precise clinical practice guidelines for the various stages of CKD at the present time. Further research and progress in this area continue to evaluate the appropriate interventions to integrate therapies for both the skeletal and extraskeletal consequences with a view toward improving patient outcomes.     

Multicentric Castleman's disease mimicking adult-onset Still's disease

Castleman's disease is a rare lymphoproliferative disorder having two types of presentation: the localized and the multicentric form. Multicentric Castleman's disease (MCD) typically presents with constitutional symptoms, generalized peripheral lymphadenopathy, hepatosplenomegaly, and laboratory markers of inflammation. Rash and arthritis may also be initial complaints of this disease. In these cases, MCD can resemble adult-onset Still's disease (AOSD), especially if the arthritis precedes other manifestations.We describe a patient with initial clinical suspicion of AOSD. Eighteen months later evidence of MCD was ascertained when the patient developed insidiously growing axillary lymphadenopathies. Despite its rarity, MCD should be borne in mind in the differential diagnosis of patients with suspicion of AOSD.